Regioselective synthesis, physicochemical properties and anticancer activity of 2-aminomethylated estrone derivatives

The unique estrogen receptor (ER)-independent antiproliferative and apoptotic activity of 2-methoxyestradiol (2ME2) is well known, however, its use has been limited because of its poor oral bioavailability. In this study, novel 2-aminomethylated estrone (E) and estradiol (E2) derivatives structurally related to 2ME2 were synthesized, and their physicochemical properties as well as their in vitro cytotoxic effects were investigated in the hope to find more selective antiproliferative agents with improved pharmacokinetic profile. The target compounds were synthesized from 2-dimethylaminomethylated E obtained regioselectively by a three-component Mannich reaction. Quaternization with methyl iodide followed by reacting the ammonium salt with various dialkyl and alicyclic secondary amines afforded the desired products in good yields.
The reactions proceeded via a 1,4-nucleophilic addition of the applied secondary amines to the ortho-quinone methide (o-QM) intermediates, generated in situ from the salt by base-promoted β-elimination. The compound library has been enlarged with structurally similar E2 analogues obtained by stereoselective reduction and with some 17β-benzylamino derivatives prepared by reductive amination. The potential values of the novel E and E2 derivatives were characterised by means of three different approaches. At the first step compounds were virtually screened using physicochemical parameters. Physicochemical characterization was completed by kinetic solubility and in vitro intestinal-specific permeability measurement. Antiproliferative effects were additionally determined on a panel of malignant and non-cancerous cell lines. The evaluation of the pharmacological profile of the novel E and E2 derivatives was completed with the calculation of lipophilic efficacy (LiPE).

The Role of Estriol and Estrone in Keratoconic Stromal Sex Hormone Receptors

Keratoconus (KC) is a progressive corneal thinning disease that manifests in puberty and worsens during pregnancy. KC onset and progression are attributed to diverse factors that include: environmental, genetics, and hormonal imbalances; however, the pathobiology remains elusive. This study aims to determine the role of corneal stroma sex hormone receptors in KC and their interplay with estrone (E1) and estriol (E3) using our established 3D in vitro model. Healthy cornea stromal cells (HCFs) and KC cornea stromal cells (HKCs), both male and female, were stimulated with various concentrations of E1 and E3.
Significant changes were observed between cell types, as well as between males and females in the sex hormone receptors tested; androgen receptor (AR), progesterone receptor (PR), estrogen receptor alpha (ERα), and estrogen receptor beta (ERβ) using Western blot analysis. E1 and E3 stimulations in HCF females showed AR, PR, and ERβ were significantly upregulated compared to HCF males. In contrast, ERα and ERβ had significantly higher expression in HKC’s females than HKC’s males. Our data suggest that the human cornea is a sex-dependent, hormone-responsive tissue that is significantly influenced by E1 and E3. Therefore, it is plausible that E1, E3, and sex hormone receptors are involved in the KC pathobiology, warranting further investigation.

Algorithms with Area under the Curve for Daily Urinary Estrone-3-Glucuronide and Pregnanediol-3-Glucuronide to Signal the Transition to the Luteal Phase

Background and Objectives: Home fertility assessment methods (FAMs) for natural family planning (NFP) have technically evolved with the objective metrics of urinary luteinizing hormone (LH), estrone-3-glucuronide (E3G) and pregnanediol-3-glucuronide (PDG). Practical and reliable algorithms for timing the phase of cycle based upon E3G and PDG levels are mostly unpublished and still lacking. Materials and Methods: A novel formulation to signal the transition to the luteal phase was discovered, tested, and developed with a data set of daily E3G and PDG levels from 25 women, 78 cycles, indexed to putative ovulation (day after the urinary LH surge), Day 0. The algorithm is based upon a daily relative progressive change in the ratio, E3G-AUC/PDG-AUC, where E3G-AUC and PDG-AUC are the area under the curve for E3G and PDG, respectively.
To improve accuracy the algorithm incorporated a three-fold cycle-specific increase of PDG. Results: An extended negative change in E3G-AUC/PDG-AUC of at least nine consecutive days provided a strong signal for timing the luteal phase. The algorithm correctly identified the luteal transition interval in 78/78 cycles and predicted the start day of the safe period as: Day + 2 in 10/78 cycles, Day + 3 in 21/78 cycles, Day + 4 in 28/78 cycles, Day + 5 in 15/78 cycles, and Day + 6 in 4/78 cycles. The mean number of safe luteal days with this algorithm was 10.3 ± 1.3 (SD). Conclusions: An algorithm based upon the ratio of the area under the curve for daily E3G and PDG levels along with a relative PDG increase offers another approach to time the phase of cycle. This may have applications for NFP/FAMs and clinical evaluation of ovarian function.

The 3-oxoacyl-(acyl-carrier-protein) reductase HSD-X1 of Pseudomonas citronellolis SJTE-3 catalyzes the conversion of 17β-estradiol to estrone

Background: Pseudomonas citronellolis SJTE-3 can efficiently degrade 17β-estradiol (E2) and other estrogenic chemicals. However, the enzyme responsible for E2 metabolism within strain SJTE-3 has remained unidentified.
Objective: Here, a novel 3-oxoacyl-(acyl-carrier protein) (ACP) reductase, HSD-X1 (WP_009617962.1), was identified in SJTE-3 and its enzymatic characteristics for the transformation of E2 were investigated.
Methods: Multiple sequence alignment and homology modelling were used to predict the protein structure of HSD-X1. The concentrations of different steroids in the culture of recombinant strains expressing HSD-X1 were determined by high performance liquid chromatography. Additionally, the transcription of hsd-x1 gene was investigated using reverse transcription and quantitative PCR analysis. Heterologous expression and affinity purification were used to obtain recombinant HSD-X1.
Results: The transcription of hsd-x1 gene in P. citronellolis SJTE-3 was induced by E2. Multiple sequence alignment (MSA) indicated that HSD-X1 contained the two consensus regions and conserved residues of short-chain dehydrogenase/reductases (SDRs) and 17β-hydroxysteroid dehydrogenases (17β-HSDs). Over-expression of hsd-x1 gene allowed the recombinant strain to degrade E2. Recombinant HSD-X1 was purified with a yield of 22.15 mg/L and used NAD+ as its cofactor to catalyze the oxidization of E2 into estrone (E1), while exhibiting a Km value of 0.025 ± 0.044 mM and a Vmax value of 4.92 ± 0.31 mM/min/mg. HSD-X1 could tolerate a wide range of temperature and pH, while the presence of divalent ions exerted little influence on its activity. Further, the transformation efficiency of E2 into E1 was over 98.03% across 15 min.
Conclusion: Protein HSD-X1 efficiently catalyzed the oxidization of E2 and participated in estrogen degradation by P. citronellolis SJTE-3.

Estrone(Estrone) ELISA Kit

EU3107 FN Test 96T 628.92 EUR

Estrone(Estrone) ELISA Kit

EKF57997-48T Biomatik Corporation 48T 396.9 EUR

Estrone(Estrone) ELISA Kit

EKF57997-5x96T Biomatik Corporation 5x96T 2693.25 EUR

Estrone(Estrone) ELISA Kit

EKF57997-96T Biomatik Corporation 96T 567 EUR

Rat Estrone(Estrone) ELISA Kit

ER1506 FN Test 96T 628.92 EUR

Estrone

AT185 Unibiotest 1mg 1336.8 EUR

Estrone

AG185 Unibiotest 1 mg 627.6 EUR

Estrone

A8426-5.1 ApexBio 10 mM (in 1mL DMSO) 135.6 EUR

Estrone

A8426-50 ApexBio 50 mg 157.2 EUR

Estrone

HY-B0234 MedChemExpress 10mM/1mL 135.6 EUR

Estrone

T1009-10mg TargetMol Chemicals 10mg Ask for price

Estrone

T1009-1g TargetMol Chemicals 1g Ask for price

Estrone

T1009-1mg TargetMol Chemicals 1mg Ask for price

Estrone

T1009-50mg TargetMol Chemicals 50mg Ask for price

Estrone

T1009-5mg TargetMol Chemicals 5mg Ask for price

Estrone

A8426-10000 ApexBio 10g 106 EUR

Estrone

A8426-5000 ApexBio 5g 77 EUR

Estrone

300149 MedKoo Biosciences 500.0mg 90 EUR

Estrone

TBZ2970 ChemNorm 25mg Ask for price

Estrone

E02400 Pfaltz & Bauer 400MG 398 EUR

Estrone

DE4174 Demeditec Diagnostics 96 146 EUR

Estrone ELISA Kit| Rat Estrone ELISA Kit

EF018156 Lifescience Market 96 Tests 826.8 EUR

Estrone ELISA Kit| General Estrone ELISA Kit

EF019603 Lifescience Market 96 Tests 826.8 EUR

Estrone-BSA

80-1448 Fitzgerald 1 mg 781.2 EUR

Estrone-OVA

80-1449 Fitzgerald 1 mg 781.2 EUR

Estrone-2,4,16,16-d4

GC2791-10 Glentham Life Sciences 10 242.4 EUR

Temporal compositional shifts in an activated sludge microbiome during estrone biodegradation

  • Microbial biodegradation is a key process for the removal of estrogens during wastewater treatment. At least four degradation pathways for natural estrogens have been proposed. However, major estrogen degraders and the occurrence of different estrogen biodegradation pathways in wastewater treatment plants have been rarely investigated. This study was conducted to elucidate estrone biodegradation pathway and to identify key estrone-degrading bacteria in activated sludge from a major wastewater treatment plant in Bahrain. The biodegradation experiments were performed in activated sludge microcosms supplemented with estrone. Sludge samples were retrieved at time intervals to analyze the biodegradation metabolites and the temporal shifts in the bacterial community composition.
  • Chemical analysis revealed the biodegradation of more than 90% of the added estrone within 6 days, and the compounds 4-hydroxyestrone and pyridinestrone acid, which are typical markers of the 4,5-seco pathway of aerobic estrone biodegradation, were detected. Temporal shifts in the relative abundance of bacteria were most prominent among members of Proteobacteria and Bacteroidetes. While the alphaproteobacterial genera Novosphingobium and Sphingoaurantiacus were significantly enriched (from ≤ 6% to an average of 31%) in the estrone-amended activated sludge after 2 days of incubation, the bacteroidete Pedobacter was uniquely detected in these microcosms at day 10. The relative abundance of Polyangia (Nannocyctis) increased to an average of 10 ± 0.4% in the estrone-amended activated sludge after 4 days of incubation.
  • Enrichment cultivation of bacteria from the activated sludge on estrone resulted in a mixed culture that was capable of degrading estrone. An estrone-degrading strain was isolated from this mixed culture and was affiliated with the known estrogen-degrading Alphaproteobacteria Sphingobium estrogenivorans. We conclude that estrone degradation in the activated sludge from the studied wastewater treatment plant proceeds via the 4,5-seco pathway and is most likely mediated by alphaproteobacterial taxa.

The Role of Estriol and Estrone in Keratoconic Stromal Sex Hormone Receptors

Keratoconus (KC) is a progressive corneal thinning disease that manifests in puberty and worsens during pregnancy. KC onset and progression are attributed to diverse factors that include: environmental, genetics, and hormonal imbalances; however, the pathobiology remains elusive. This study aims to determine the role of corneal stroma sex hormone receptors in KC and their interplay with estrone (E1) and estriol (E3) using our established 3D in vitro model. Healthy cornea stromal cells (HCFs) and KC cornea stromal cells (HKCs), both male and female, were stimulated with various concentrations of E1 and E3. Significant changes were observed between cell types, as well as between males and females in the sex hormone receptors tested; androgen receptor (AR), progesterone receptor (PR), estrogen receptor alpha (ERα), and estrogen receptor beta (ERβ) using Western blot analysis. E1 and E3 stimulations in HCF females showed AR, PR, and ERβ were significantly upregulated compared to HCF males.
In contrast, ERα and ERβ had significantly higher expression in HKC’s females than HKC’s males. Our data suggest that the human cornea is a sex-dependent, hormone-responsive tissue that is significantly influenced by E1 and E3. Therefore, it is plausible that E1, E3, and sex hormone receptors are involved in the KC pathobiology, warranting further investigation.

Compatibility of Estradiol, Estriol, Estrone, Progesterone, and Testosterone Single Formulation in Fitalite, Versatile, or HRT Supreme Cream Base

In this work, we focus on three ready-to-use vehicles: Fitalite, Versatile, and HRT Supreme Cream Base. Fitalite is a natural, light, hydrophilic gel-cream that contains vitamin E and oil bodies from plant sources (phytosomes), providing antioxidant and skinmoisturizing properties. Versatile is a vanishing oil-inwater cream base which retains its consistency with a broad range and high concentrations of active pharmaceutical ingredients, dermaceutical ingredients, and solvents. Finally, HRT Supreme Cream Base is a paraben-free, dye-free, fragrance-free O/W emulsion base, formulated with a complex of botanical oils to soothe and provide moisture to dry and sensitive skin. In the current study, we evaluated the beyond-use date of formulations containing estradiol, estriol, estrone, progesterone, and testosterone in combination, compounded with these three vehicles.
Validated, stability-indicating high-performance liquid chromatography methods were used throughout a 180-day period. A beyond-use date of 180 days was observed for all vehicles stored both at refrigerated and at room temperature. The combination of five ingredients represents a worst-case scenario since there are more possibilities of cross reactions. Therefore, we expect the same or greater stability as individual ingredients are removed from the tested formulation. The extended beyond-use dates provide convenience for both the compounding pharmacist and the patient.

A technical and clinical evaluation of the new ThermoFisher BRAHMS unconjugated estriol and inhibin-A assays and their use in second trimester Down syndrome screening

To evaluate second-trimester Down syndrome screening performance of the new ThermoFisher BRAHMS GOLD unconjugated estriol (uE3) and inhibin-A assays. Serum samples were analyzed for levels of uE3 and inhibin-A using the ThermoFisher BRAHMS GOLD immunoanalyzer and compared to other platforms. Levels were transformed to multiples of the median (MoM) in unaffected pregnancies. Log10 MoM distributions in unaffected and Down syndrome pregnancies were assessed for central tendency (mean) and dispersion (SD). Empirical and estimated screening performances were determined. Correlation between BRAHMS and AutoDELFIA® uE3 and inhibin-A were 0.63 and 0.97, respectively, the respective mean difference was 31.3% [95%CI 50.2% to -112.8%] and -23.3% [95%CI -41.9% to -4.7%]. Passing-Bablok indicated significant systematic (-2.78 [95%CI -3.57 to -2.04]) and proportional bias (1.30 [95%CI 1.15 to -1.47]) between uE3 assays and significant proportional bias (0.71[95%CI 0.65-0.78]) between inhibin-A assays.
The uE3 and inhibin-A log10 MoM distribution mean [SD] in unaffected and Down syndrome pregnancies were 0.0024 [SD = 0.2341] and -0.0001 [SD = 0.2078], and -0.2028 [SD = 0.2495] and 0.3645 [SD = 0.2576], respectively. The new BRAHMS uE3 and inhibin-A assays had an 81-83% detection rate for Trisomy21 for a 5% false-positive rate. The new BRAHMS assays achieved the expected screening performance provided the risk estimation model is adjusted to account for the higher BRAHMS uE3 MoM measurement distribution variance.

Estriol dissolving microneedle patches for protection against ionizing radiation-induced injury

Estriol can be used to treat radiation-induced leukopenia by increasing peripheral blood leukocytes and therefore it plays an important role in radiation protection. However, only high-dose injectable suspensions are available when estriol is used to combat against ionizing radiation-induced injury. Intramuscular (i.m.) administration of estriol is very painful and inconvenient, and the lack of timely self-administered formulation greatly limits the wide application of estriol. This will facilitate quick response under emergent conditions in complementary with the available estriol formulations. Herein, we prepared estriol microneedle (MNs) patches for the convenient and efficient treatment of radiation-induced injury.
A biocompatible polymer, polyvinylpyrrolidone K90, was dissolved in an estriol solution of methanol and cast into a mold to obtain conical-shaped MNs. N-vinyl pyrrolidone was poured on the base of the MNs and photocured to enhance the mechanical strength of estriol MNs (EMNs). EMNs were easily pierced 200 μm into the mouse skin. More importantly, the EMNs tips were dissolved very quickly within 5 min so that the drugs could permeate across skin. Mouse models of ionizing radiation-induced injury were established with 6.5 Gy radiation of 60Co γ ray. Moreover, EMNs increased peripheral blood leukocytes in irradiated mice, protected the bone marrow hematopoietic system, and improved the survival rate of the irradiated mice to 80 %. EMNs are a promising transdermal drug delivery system that allows for easy, rapid administration and protects the body from damage caused by ionizing radiation.

Estradiol

20-abx185851 Abbexa
  • 226.80 EUR
  • 427.20 EUR
  • 292.80 EUR
  • 1 g
  • 25 g
  • 5 g

?-Estradiol

B7201-5.1 ApexBio 10 mM (in 1mL EtOH) 129.6 EUR

?-Estradiol

B7201-50 ApexBio 50 mg 174 EUR

Estradiol

AT070 Unibiotest 1mg 1641.6 EUR

Estradiol

AG070 Unibiotest 1 mg 627.6 EUR

Estradiol

A8425-5.1 ApexBio 10 mM (in 1mL DMSO) 129.6 EUR

Estradiol

A8425-50 ApexBio 50 mg 157.2 EUR

Estradiol

E1KS1709 EnoGene 100 mg 296.4 EUR

Estradiol

HY-B0141 MedChemExpress 500mg 129.6 EUR

Estradiol

GP9683-10G Glentham Life Sciences 10 g 244.8 EUR

Estradiol

GP9683-1G Glentham Life Sciences 1 g 69.6 EUR

Estradiol

GP9683-25G Glentham Life Sciences 25 g 438 EUR

Estradiol

GP9683-5G Glentham Life Sciences 5 g 156 EUR

Estradiol

317788 MedKoo Biosciences 500.0mg 195 EUR

Estradiol

GP9683-1 Glentham Life Sciences 1 27.8 EUR

Estradiol

GP9683-10 Glentham Life Sciences 10 172.4 EUR

Estradiol

GP9683-25 Glentham Life Sciences 25 332.2 EUR

Estradiol

GP9683-5 Glentham Life Sciences 5 98.8 EUR

Estradiol

A8425-1000 ApexBio 1g 52 EUR

Estradiol

T1048-10mg TargetMol Chemicals 10mg Ask for price

Estradiol

T1048-1g TargetMol Chemicals 1g Ask for price

Estradiol

T1048-1mg TargetMol Chemicals 1mg Ask for price

Cortisol and estriol responses to awakening in the first pregnancy trimester: Associations with maternal stress and resilience factors

Background: Little is known about the maternal cortisol awakening response (CAR) in the first pregnancy trimester. Similarly unknown is how the CAR in early gestation relates to other steroid hormones, such as estriol. Maternal estriol in blood and urine is used to monitor fetal well-being since it is produced by the fetoplacental unit from fetal precursors. Low levels have been associated with maternal-fetal complications. We were recently able to show that estriol is measurable in maternal saliva from 6 weeks’ gestation onwards. However, its pattern following morning awakening and potential links with salivary cortisol in early gestation is relatively unknown. In this prospective study, we explored the cortisol and estriol responses to morning awakening in first-trimester pregnant women, the potential association of these endocrine variables with maternal stress and resilience factors, and their predictive value for the further pregnancy course.
Methods: Fifty-one women with an uncomplicated, singleton pregnancy responded to questionnaires measuring chronic and pregnancy-specific stress, emotional support, and daily uplifts at 6 weeks’ gestation. At 8 and 10 weeks, the women collected saliva samples immediately, 30, and 60 min after morning awakening. After 12 weeks, 40 women reported on the further pregnancy course, of whom 6 had developed complications.
Results: In response to morning awakening, cortisol levels increased significantly at 10 weeks (p = .04), while estriol levels decreased significantly at both 8 and 10 weeks (p < .001). A stronger cortisol increase was linked to a stronger estriol decrease at 8 (p = .03), but not at 10 weeks. Then, perceived emotional support at 6 weeks was negatively associated with cortisol baseline at 8 (p = .01) and positively with estriol baseline at 10 weeks (p = .03). Moreover, higher pregnancy-specific stress was related to a lower estriol baseline at 8 weeks (p = .047). Furthermore, compared to healthy women, those with complications at follow-up had already reported less emotional support (p = .03) and fewer daily uplifts (p = .03) at 6 weeks. These women also seemed to lack a significant estriol response to morning awakening at 8 weeks (p > .10).
Discussion: These findings advance our knowledge of cortisol and estriol secretion following morning awakening and encourage the investigation of E3 in addition to cortisol when researching prenatal stress and its consequences for maternal and fetal health.

Analytical performance evaluation of sensitive and old generation reagent in routine practical use: estradiol experience

Evaluation of the analytical performance of tests in medical laboratories is important. Total Error (TE) and sigma analysis have been used as a quantitative indicator of quality for many years. The aim of this study is to evaluate the analytical performance of Beckman Coulter Access Estradiol (E2) and Sensitive E2 reagents. Analytical performance of two reagents were evaluated with TE, six sigma and measurement uncertainty values. Two Beckman Coulter Unicel DxI-800 autoanalyzers (A1 and A2) included in the study. Quality control data between December 2017 and December 2019 were used. CLIA-2019 values were used for total allowable error (TEa) limits. Uncertainty values were calculated with ISO/TS 20914.
The median TE of the old generation and sensitive E2 reagent were 27.46% (between 13.49 and 48.88) and 11.16% (between 7.08 and 24.81), respectively (p < .005) The process sigma results were below 3 sigma in all months with the old reagent, whereas with the new reagents it was seen to be above 3 sigma in 11 of 12 months for both autoanalyzers. Uncertainty of old reagent is higher than new reagent. Imprecisions decrease as concentration increases with both reagents. The uncertainty values of low concentration levels are greater than high concentration levels. In conclusion, in both auto analyzers, Sensitive E2 reagent was found to have better performance than old reagent in terms of TE, process sigma and measurement uncertainty. We believe that the sensitive E2 reagent still needs further improvement for patients who have low E2 levels.

Prothymosin Alpha: A Novel Contributor to Estradiol Receptor Alpha-Mediated CD8 + T-Cell Pathogenic Responses and Recognition of Type 1 Collagen in Rheumatic Heart Valve Disease

Background: Rheumatic heart valve disease (RHVD) is a leading cause of cardiovascular death in low- and middle-income countries and affects predominantly women. The underlying mechanisms of chronic valvular damage remain unexplored and regulators of sex predisposition are unknown.
Methods: Proteomics analysis of human heart valves (nondiseased aortic valves, nondiseased mitral valves [NDMVs], valves from patients with rheumatic aortic valve disease, and valves from patients with rheumatic mitral valve disease; n=30) followed by system biology analysis identified ProTα (prothymosin alpha) as a protein associated with RHVD. Histology, multiparameter flow cytometry, and enzyme-linked immunosorbent assay confirmed the expression of ProTα. In vitro experiments using peripheral mononuclear cells and valvular interstitial cells were performed using multiparameter flow cytometry and quantitative polymerase chain reaction. In silico analysis of the RHVD and Streptococcus pyogenes proteomes were used to identify mimic epitopes.
Results: A comparison of NDMV and nondiseased aortic valve proteomes established the baseline differences between nondiseased aortic and mitral valves. Thirteen unique proteins were enriched in NDMVs. Comparison of NDMVs versus valves from patients with rheumatic mitral valve disease and nondiseased aortic valves versus valves from patients with rheumatic aortic valve disease identified 213 proteins enriched in rheumatic valves. The expression of the 13 NDMV-enriched proteins was evaluated across the 213 proteins enriched in diseased valves, resulting in the discovery of ProTα common to valves from patients with rheumatic mitral valve disease and valves from patients with rheumatic aortic valve disease. ProTα plasma levels were significantly higher in patients with RHVD than in healthy individuals. Immunoreactive ProTα colocalized with CD8+ T cells in RHVD. Expression of ProTα and estrogen receptor alpha correlated strongly in circulating CD8+ T cells from patients with RHVD. Recombinant ProTα induced expression of the lytic proteins perforin and granzyme B by CD8+ T cells as well as higher estrogen receptor alpha expression. In addition, recombinant ProTα increased human leukocyte antigen class I levels in valvular interstitial cells. Treatment of CD8+ T cells with specific estrogen receptor alpha antagonist reduced the cytotoxic potential promoted by ProTα. In silico analysis of RHVD and S pyogenes proteomes revealed molecular mimicry between human type 1 collagen epitope and bacterial collagen-like protein, which induced CD8+ T-cell activation in vitro.
Conclusions: ProTα-dependent CD8+ T-cell cytotoxicity was associated with estrogen receptor alpha activity, implicating ProTα as a potential regulator of sex predisposition in RHVD. ProTα facilitated recognition of type 1 collagen mimic epitopes by CD8+ T cells, suggesting mechanisms provoking autoimmunity.

Pharmacokinetic Interaction Between the MEK1/MEK2 Inhibitor Trametinib and Oral Contraceptives Containing Norethindrone and Ethinyl Estradiol in Female Patients With Solid Tumors

This phase 1 postapproval study assessed the effect of the mitogen-activated protein kinase kinase enzyme 1/enzyme 2 inhibitor trametinib (2 mg once daily, repeat dosing) on the pharmacokinetics of combined oral contraceptives (COCs) containing norethindrone (NE; 1 mg daily) and ethinyl estradiol (EE; 0.035 mg daily) in 19 female patients with solid tumors. Compared with NE/EE administered without trametinib, NE/EE administered with steady-state trametinib was associated with a clinically nonrelevant 20% increase in NE exposure (area under the curve [AUC]) and no effect on EE exposure (geometric mean ratio [geo-mean] of NE/EE + trametinib to NE/EE [90%CI]: NE AUC calculated to the end of a dosing interval at steady-state [AUCtau ] 1.20 [1.02-1.41]; NE AUC from time zero to the last measurable concentration sampling time [AUClast ] 1.2 [0.999-1.45]; EE AUCtau 1.06 [0.923-1.22]; EE AUClast 1.05 [0.883-1.25]).
Maximum serum concentration (Cmax ) of NE increased by 13% and Cmax of EE decreased by 8.5% when dosed with steady-state trametinib compared with COCs administered alone (geo-mean ratio [90%CI]: NE Cmax 1.13 [0.933-1.36]; EE Cmax 0.915 [0.803-1.04]). These results indicate that repeat-dose trametinib does not lower exposure to NE or EE and, hence, is unlikely to impact the contraceptive efficacy of COCs. The pharmacokinetic parameters of trametinib and its metabolite M5 were consistent with historic data of trametinib alone. Coadministration of trametinib and COCs was generally well tolerated in this study, with observed safety signals consistent with the known safety profile of trametinib and no new reported safety events. Overall, the findings indicate that hormonal COCs can be coadministered in female patients who receive trametinib monotherapy without compromising the contraceptive efficacy.

Estradiol

20-abx185851 Abbexa
  • 226.80 EUR
  • 427.20 EUR
  • 292.80 EUR
  • 1 g
  • 25 g
  • 5 g

?-Estradiol

B7201-5.1 ApexBio 10 mM (in 1mL EtOH) 129.6 EUR

?-Estradiol

B7201-50 ApexBio 50 mg 174 EUR

Estradiol

AT070 Unibiotest 1mg 1641.6 EUR

Estradiol

AG070 Unibiotest 1 mg 627.6 EUR

Estradiol

A8425-5.1 ApexBio 10 mM (in 1mL DMSO) 129.6 EUR

Estradiol

A8425-50 ApexBio 50 mg 157.2 EUR

Estradiol

E1KS1709 EnoGene 100 mg 296.4 EUR

Estradiol

HY-B0141 MedChemExpress 500mg 129.6 EUR

Estradiol

GP9683-10G Glentham Life Sciences 10 g 244.8 EUR

Estradiol

GP9683-1G Glentham Life Sciences 1 g 69.6 EUR

Estradiol

GP9683-25G Glentham Life Sciences 25 g 438 EUR

Estradiol

GP9683-5G Glentham Life Sciences 5 g 156 EUR

Estradiol

317788 MedKoo Biosciences 500.0mg 195 EUR

Estradiol

GP9683-1 Glentham Life Sciences 1 27.8 EUR

Estradiol

GP9683-10 Glentham Life Sciences 10 172.4 EUR

Estradiol

GP9683-25 Glentham Life Sciences 25 332.2 EUR

Estradiol

GP9683-5 Glentham Life Sciences 5 98.8 EUR

Estradiol

A8425-1000 ApexBio 1g 52 EUR

Estradiol

T1048-10mg TargetMol Chemicals 10mg Ask for price

Estradiol

T1048-1g TargetMol Chemicals 1g Ask for price

Estradiol

T1048-1mg TargetMol Chemicals 1mg Ask for price

Sucrose acetate isobutyrate (SAIB) as a delivery vehicle for estradiol and sulpiride: Evaluation of endocrine responses in geldings and ovarian response in seasonally anovulatory mares

Sulpiride in vegetable shortening (VS) stimulates prolactin in horses for up to 10 days. Although effective, a pharmaceutical grade vehicle is needed for clinical application of sulpiride in horses. Sucrose acetate isobutyrate (SAIB), a hydrophobic polymer, may be an alternative to VS. Four in vivo experiments assessed the efficacy of SAIB for delivery of sulpiride, estradiol cypionate (ECP), and estradiol benzoate (EB). The first three studies utilized geldings to compare prolactin and luteinizing hormone (LH) concentrations between sulpiride delivered in VS and SAIB, and ECP or EB delivered in SAIB. Sulpiride stimulated (P < .01) prolactin similarly between vehicles. Geldings pre-treated with EB had higher (P < .05) prolactin responses to sulpiride compared to ECP-treated geldings on days 5, 6 and 9.
Both estradiol-sulpiride treatments stimulated LH with no differences between ECP and EB. Experiment 3 compared a simultaneous injection of EB-sulpiride to a non-simultaneous injection (one day apart) of EB-sulpiride. Prolactin was stimulated (P < .05) in both treatment groups, but the response lasted 2 days longer in geldings treated a day apart. Plasma LH increased (P < .01) in both groups equally for 10 days. Experiment 4 applied simultaneous and non-simultaneous EB-sulpiride treatments to seasonally anovulatory mares to induce ovarian activity. Prolactin and LH were stimulated similarly between treatments; however, non-simultaneously treated mares tended (P = .07) to have an ovarian response earlier. In conclusion, SAIB was a suitable vehicle for administration of estradiol and sulpiride and could be an alternative to VS for sustained-release drug delivery.

EVALUATION OF EPIANDROSTERONE AS A LONG-TERM MARKER OF TESTOSTERONE USE

  • Identification and evaluation of long-term markers is crucial in prolonging the detection window for anabolic steroid abuse in sport. Recently, sulfoconjugated epiandrosterone was identified as a potential long-term marker for the abuse of certain endogenous anabolic agents, including testosterone, which continues to be widely used as a performance enhancing agent in sport. To evaluate the applicability of epiandrosterone sulfate as a marker for testosterone use, administration studies were conducted with multiple modes of testosterone administration – transdermal, intramuscular, and subcutaneous.
  • A modified sample preparation method was used to collect both glucuronidated and sulfoconjugated analytes of interest. Carbon isotope ratio measurements from the administration studies are presented here. Epiandrosterone was less effective than the conventionally used target compounds for detection of the low dose application (transdermal gel). With intramuscular administration, epiandrosterone was more diagnostic than with transdermal administration, but it did not prolong the detection window more than the conventional target compounds.
  • With subcutaneous administration, the doses administered to the subjects were varied and the effect in the epiandrosterone values was dependent on the magnitude of the dose administered. Epiandrosterone does not appear to be a useful marker in the detection of low dose testosterone administration. It is responsive to higher dose administration, but it does not provide extension of the detection window relative to conventional target compounds.

Development and validation of a fast gas chromatography combustion isotope ratio mass spectrometry method for the detection of epiandrosterone sulfate in urine.

In doping control, to confirm the exogenous origin of exogenously administered anabolic androgenic steroids (AAS), a gas chromatography combustion isotope ratio mass spectrometry (GC-C-IRMS) analysis is performed. Recently published work suggests epiandrosterone sulfate (EpiAS) as a promising IRMS target compound for the detection of AAS, capable of prolonging the detection window. However, EpiAS is only excreted in urine in its sulfoconjugated form while all other IRMS target compounds are excreted glucuronidated, meaning that EpiAS cannot be incorporated in the existing IRMS methods.
A separate extensive sample preparation needs to be performed on this compound with a different hydrolysis and extraction procedure and a different liquid chromatography (LC) clean-up. The current work presents a new, fast and easy to implement EpiAS IRMS method. The approach was based on the direct GC analysis of non-hydrolysed EpiAS, making the solid phase extraction, hydrolysis and acetylation step redundant.
Sample preparation consisted of a simple liquid liquid extraction, followed by LC fraction collection. A population study was performed to check the compliance with the criteria drafted by the World Anti-Doping Agency (WADA). To verify the applicability of the developed approach, the method was applied to the samples of four administration studies (i.e., dehydroepiandrosterone (DHEA), testosterone gel (T gel), androstenedione (ADION) and intramuscular testosterone undecanoate. In contrast to previously published data, the strength of EpiAS as target compound and the prolongation of the detection window in comparison with the conventional IRMS target compounds was less pronounced.

Synthesis and bioevaluation of novel steroidal isatin conjugates derived from epiandrosterone/androsterone.

Steroids are classes of natural products widely distributed in nature, which have been demonstrated to exhibit broad biological functions, and have also attracted increasing interest from bioorganic and pharmaceutical researches. In order to develop novel chemical entities as potential cytotoxic agents, a series of steroidal isatin conjugations derived from epiandrosterone and androsterone were efficiently prepared and characterized, and all these obtained compounds were screened for their potential cytotoxic activities.
The preliminary bioassay indicated that most of the newly synthesized compounds exhibited good cytotoxic activities against human gastric cancer (SGC-7901), melanoma (A875), and hepatocellular liver carcinoma (HepG2) cell lines compared with 5-fluorouracil (5-FU), which might be considered as promising scaffold for further development of potential anticancer agents.

The quantitation of 7beta-hydroxy-epiandrosterone in the plasma and seminal plasma of men with different degrees of fertility.

7beta-hydroxy-epiandrosterone (7beta-OH-EpiA) is an endogenous androgen metabolite that has been shown to exert neuroprotective, anti-inflammatory and anti-estrogenic effects. However, to the best of our knowledge no information is available about this androgen steroid in relation to sperm quality. We analyzed 7beta-OH-EpiA in plasma and seminal plasma using a newly developed isotope dilution ultra-high performance liquid chromatography – mass spectrometry method. Validation met the requirements of FDA guidelines. Levels of 7beta-OH-EpiA were measured in 191 men with different degrees of infertility. One-way analysis of variance followed by multiple comparison and correlation analysis adjusted for age, BMI and abstinence time were performed to evaluate the relationships between this steroid and sperm quality.
Concentrations of 7beta-OH-EpiA in seminal plasma were significantly higher in severely infertile men in comparison with healthy men and slightly infertile men. The same trend was found when blood plasma was evaluated. Furthermore, plasma 7beta-OH-EpiA negatively correlated with sperm concentration (-0.215; p<0.01) and total count (-0.15; p<0.05). Seminal 7beta-OH-EpiA was negatively associated with motility (-0.26; p<0.01), progressively motile spermatozoa (-0.233; p<0.01) and nonprogressively motile spermatozoa (-0.188; p<0.05). 7beta-OH-EpiA is associated with lower sperm quality and deserves more research in that respect.

Epiandrosterone sulfate prolongs the detectability of testosterone, 4-androstenedione, and dihydrotestosterone misuse by means of carbon isotope ratio mass spectrometry.

In the course of investigations into the metabolism of testosterone (T) by means of deuterated T and hydrogen isotope ratio mass spectrometry, a pronounced influence of the oral administration of T on sulfoconjugated steroid metabolites was observed. Especially in case of epiandrosterone sulfate (EPIA_S), the contribution of exogenous T to the urinary metabolite was traceable up to 8 days after a single oral dose of 40 mg of T. These findings initiated follow-up studies on the capability of EPIA_S to extend the detection of T and T analogue misuse by carbon isotope ratio (CIR) mass spectrometry in sports drug testing. Excretion study urine samples obtained after transdermal application of T and after oral administration of 4-androstenedione, dihydrotestosterone, and EPIA were investigated regarding urinary concentrations and CIR.
With each administered steroid, EPIA_S was significantly depleted and prolonged the detectability when compared to routinely used steroidal target compounds by a factor of 2 to 5. In order to simplify the sample preparation procedure for sulfoconjugated compounds, enzymatic cleavage by Pseudomonas aeruginosa arylsulfatase was tested and implemented into CIR measurements for the first time. Further simplification was achieved by employing multidimensional gas chromatography to ensure the required peak purity for CIR determinations, instead of sample purification strategies using liquid chromatographic fractionation. Taking into account these results that demonstrate the unique and broad applicability of EPIA_S for the detection of illicit administrations of T or T-related steroids, careful consideration of how this steroid can be implemented into routine doping control analysis appears warranted.

An omics investigation into chronic widespread musculoskeletal pain reveals epiandrosterone sulfate as a potential biomarker.

Chronic widespread musculoskeletal pain (CWP) is common, having a population prevalence of 10%. This study aimed to define the biological basis of the CWP/body mass association by using a systems biology approach. Adult female twins (n = 2444) from the TwinsUK registry who had extensive clinical, anthropometric, and “omic” data were included. Nontargeted metabolomics screening including 324 metabolites was carried out for CWP and body composition using dual-energy X-ray absorptiometry. The biological basis of these associations was explored through a genome-wide association study and replicated in an independent population sample (Cooperative Health Research in the Region of Augsburg [KORA] study, n = 2483). A causal role for the genetic variants identified was sought in CWP using a Mendelian randomisation study design.
Fat mass/height2 was the body composition variable most strongly associated with CWP (TwinsUK: P = 2.4 × 10(-15) and KORA: P = 1.59 × 10(-10)). Of 324 metabolites examined, epiandrosterone sulfate (EAS) was highly associated with both CWP (P = 1.05 × 10(-09) in TwinsUK and P = 3.70 × 10(-06) in KORA) and fat mass/height2. Genome-wide association study of EAS identified imputed single nucleotide polymorphism rs1581492 at 7q22.1 to be strikingly associated with EAS levels (P ≤ 2.49 × 10(-78)), and this result was replicated in KORA (P = 2.12 × 10(-9)). Mendelian randomization by rs1581492 genotype showed that EAS is unlikely to be causally related to CWP. Using an agnostic omics approach to focus on the association of CWP with body mass index, we have confirmed a steroid hormone association and identified a genetic variant upstream of the CYP genes, which likely controls this response. This study suggests that steroid hormone abnormalities result from pain rather than causing it, and EAS may provide a biomarker that identifies subgroups at risk of CWP.

Epiandrosterone

B1505-1000 ApexBio 1 g 115.2 EUR

Epiandrosterone

B1505-5.1 ApexBio 10 mM (in 1mL DMSO) 135.6 EUR

Epiandrosterone

B1505-S ApexBio Evaluation Sample 97.2 EUR

Epiandrosterone

HY-I0352 MedChemExpress 500mg 129.6 EUR

Epiandrosterone

GP6146-1G Glentham Life Sciences 1 g 74.4 EUR

Epiandrosterone

GP6146-1 Glentham Life Sciences 1 31.7 EUR

Epiandrosterone-HRP

80-1155 Fitzgerald 500 ul 970.8 EUR

Epiandrosterone Sulfate

T2195L-10mg TargetMol Chemicals 10mg Ask for price

Epiandrosterone Sulfate

T2195L-1g TargetMol Chemicals 1g Ask for price

Epiandrosterone Sulfate

T2195L-1mg TargetMol Chemicals 1mg Ask for price

Epiandrosterone Sulfate

T2195L-50mg TargetMol Chemicals 50mg Ask for price

Epiandrosterone Sulfate

T2195L-5mg TargetMol Chemicals 5mg Ask for price

Epiandrosterone antibody

20-1677 Fitzgerald 100 ul 1054.8 EUR

Epiandrosterone ELISA Kit

E4852-100 Biovision 96 assays 903.6 EUR

Epiandrosterone Standard, 125UL

C233-125UL Arbor Assays 125UL 85 EUR

Epiandrosterone Standard, 625UL

C233-625UL Arbor Assays 625UL 207 EUR

Epiandrosterone ELISA Kit (1 Plate)

K063-H1 Arbor Assays 1x96 well plate 454 EUR

Epiandrosterone ELISA Kit (5 Plate)

K063-H5 Arbor Assays 5x96 well plate 1746 EUR

DetectX® Epiandrosterone Conjugate, 3ML

C232-3ML Arbor Assays 3ML 289 EUR

OORB00092-500UL - Epiandrosterone(17)-HRP

OORB00092-500UL Aviva Systems Biology 0.5ml 759 EUR

DetectX® Epiandrosterone Conjugate, 13ML

C232-13ML Arbor Assays 13ML 1156 EUR

DetectX® Epiandrosterone EIA Antibody, 3ML

C231-3ML Arbor Assays 3ML 289 EUR

DetectX® Epiandrosterone EIA Antibody, 13ML

C231-13ML Arbor Assays 13ML 1156 EUR

OKAU00056-1PLATE - Epiandrosterone ELISA Kit

OKAU00056-1PLATE Aviva Systems Biology 1plate 450 EUR

OKAU00056-5PLATE - Epiandrosterone ELISA Kit

OKAU00056-5PLATE Aviva Systems Biology 5plate 1649 EUR

Epiandrosterone sheep polyclonal antibody, Ig Fraction

AP09712PU-L Origene Technologies GmbH 1 ml Ask for price

Epiandrosterone sheep polyclonal antibody, Ig Fraction

AP09712PU-N Origene Technologies GmbH 100 µl Ask for price

14-Epiandrographolide

T125901-10mg TargetMol Chemicals 10mg Ask for price

An omics investigation into chronic widespread musculoskeletal pain reveals epiandrosterone sulfate as a potential biomarker.

Chronic widespread musculoskeletal pain (CWP) is common, having a population prevalence of 10%. This study aimed to define the biological basis of the CWP/body mass association by using a systems biology approach. Adult female twins (n = 2444) from the TwinsUK registry who had extensive clinical, anthropometric, and “omic” data were included. Nontargeted metabolomics screening including 324 metabolites was carried out for CWP and body composition using dual-energy X-ray absorptiometry. The biological basis of these associations was explored through a genome-wide association study and replicated in an independent population sample (Cooperative Health Research in the Region of Augsburg [KORA] study, n = 2483). A causal role for the genetic variants identified was sought in CWP using a Mendelian randomisation study design.
Fat mass/height2 was the body composition variable most strongly associated with CWP (TwinsUK: P = 2.4 × 10(-15) and KORA: P = 1.59 × 10(-10)). Of 324 metabolites examined, epiandrosterone sulfate (EAS) was highly associated with both CWP (P = 1.05 × 10(-09) in TwinsUK and P = 3.70 × 10(-06) in KORA) and fat mass/height2. Genome-wide association study of EAS identified imputed single nucleotide polymorphism rs1581492 at 7q22.1 to be strikingly associated with EAS levels (P ≤ 2.49 × 10(-78)), and this result was replicated in KORA (P = 2.12 × 10(-9)). Mendelian randomization by rs1581492 genotype showed that EAS is unlikely to be causally related to CWP. Using an agnostic omics approach to focus on the association of CWP with body mass index, we have confirmed a steroid hormone association and identified a genetic variant upstream of the CYP genes, which likely controls this response. This study suggests that steroid hormone abnormalities result from pain rather than causing it, and EAS may provide a biomarker that identifies subgroups at risk of CWP.

Involvement of c-Jun N-terminal kinase 2 (JNK2) in Endothelin1 (ET1) Mediated Neurodegeneration of Retinal Ganglion Cells

Purpose: The goal of this study was to determine whether JNK2 played a causative role in endothelin-mediated loss of RGCs in mice.
Methods: JNK2-/- and wild type (C57BL/6) mice were intravitreally injected in one eye with 1 nmole of ET-1, whereas the contralateral eye was injected with the vehicle. At two time points (two hours and 24 hours) after the intravitreal injections, mice were euthanized, and phosphorylated c-Jun was assessed in retinal sections. In a separate set of experiments, JNK2-/- and wild type mice were intravitreally injected with either 1 nmole of ET-1 or its vehicle and euthanized seven days after injection. Retinal flat mounts were stained with antibodies to the RGC marker, Brn3a, and surviving RGCs were quantified. Axonal degeneration was assessed in paraphenylenediamine stained optic nerve sections.
Results: Intravitreal ET-1 administration produced a significant increase in immunostaining for phospho c-Jun in wild type mice, which was appreciably lower in the JNK2 -/- mice. A significant (P < 0.05) 26% loss of RGCs was found in wild type mice, seven days after injection with ET-1. JNK2-/- mice showed a significant protection from RGC loss following ET-1 administration, compared to wild type mice injected with ET-1. A significant decrease in axonal counts and an increase in the collapsed axons was found in ET-1 injected wild type mice eyes.
Conclusions: JNK2 appears to play a major role in ET-1 mediated loss of RGCs in mice. Neuroprotective effects in JNK2-/- mice following ET-1 administration occur mainly in the soma and not in the axons of RGCs.

The ring size of monocyclic <em>ET</em>-<em>1</em> controls selectivity and signaling efficiency at both <em>endothelin</em> receptor subtypes

Cardiovascular diseases (CVDs) like hypertension are a major cause for death worldwide. In the cardiovascular tissue, the endothelin system-consisting of the receptor subtypes A (ETA R) and B (ETB R) and the mixed agonist endothelin 1 (ET-1)-is a major key player in the regulation of vascular tone and blood pressure. Tight control of this system is required to maintain homeostasis; otherwise, the endothelin system can cause severe CVDs like pulmonary artery hypertension. The high sequence homology between both receptor subtypes limits the development of novel and selective ligands. Identification of small differences in receptor-ligand interactions and determination of selectivity constraints are crucial to fine-tune ligand properties and subsequent signaling events.
Here, we report on novel ET-1 analogs and their detailed pharmacological characterization. We generated simplified ET-1-derived monocyclic peptides to provide an accessible synthesis route. By detailed in vitro characterization, we demonstrated that both G protein signaling and the subsequent arrestin recruitment of activated ETB R remain intact, whereas activation of the ETA R depends on the intramolecular ring size. Increasing of the intramolecular ring structure reduces activity at the ETA R and shifts the peptide toward ETB R selectivity. All ET-1 analogs displayed efficient ETB R-mediated signaling by G protein activation and arrestin 3 recruitment. Our study provides in-depth characterization of the ET-1/ETA R and ET-1/ETB R interactions, which has the potential for future development of endothelin-based drugs for CVD treatment. By identification of Lys9 for selective labeling, novel analogs for peptide-mediated shuttling by ET-1 are proposed.

<em>Endothelin</em>-<em>1</em> Decreases the Expression of Ephrin-A and B Subtypes in Cultured Rat Astrocytes through <em>ET</em> <sub>B</sub> Receptors

Ephrin family proteins are cell surface molecules that regulate several cellular functions through cell-cell interactions. During nervous tissue repair after injury, the expression of ephrin subtypes in astrocytes is altered, affecting the axonal elongation and migration of neuronal precursors. However, the mechanism regulating the expression of ephrin subtypes in astrocytes has not been investigated. Herein, we studied the effects of endothelin-1 (ET-1) on the expression of ephrin subtypes in cultured rat astrocytes. Our results showed that ET-1 (100 nM) treatment for 1-24 h reduced the expression of ephrin-A2, -A4, -B2, and -B3 mRNA and protein in astrocytes, whereas the expression of ephrin-A1, -A3, -A5, and -B1 mRNA were not affected.
Sarafotoxin S6c, a selective ETB receptor agonist, decreased the expression of ephrin-A2, -A4, -B2, and -B3 in cultured astrocytes. The decrease in ephrin-A2, -A4, -B2, and -B3 expression by ET-1 treatment was reduced in the presence of BQ788, an ETB receptor antagonist, while FR139317, an ETA receptor antagonist, had no effects. These results suggest that ET-1 is a signaling molecule that downregulates ephrin-A2, -A4, -B2, and -B3 expression in astrocytes.

C-type natriuretic peptide (CNP)/Guanylate cyclase B (GC-B) system and <em>endothelin</em>-<em>1</em>(<em>ET</em>-<em>1</em>)/<em>ET</em> receptor A and B system in human vasculature.

In order to assess the physiological and clinical implications of C-type natriuretic peptide (CNP)/guanylyl cyclase B (GC-B) system in the human vasculature, we have examined gene expressions of CNP and its receptor, GC-B, in human vascular endothelial cells (ECs) and smooth muscle cells (SMCs) and have also compared endothelin-1(ET-1)/endothelin receptor-A (ETR-A) and endothelin receptor-B (ETR-B) system in human aortic ECs (HAECs) and vascular SMCs (HSMCs) in vitro. We also examined these gene expressions in human embryonic stem (ES)/induced pluripotent stem cell (iPS)-derived ECs and mural cells (MCs).
A little but significant amount of mRNA encoding CNP was detected in both human ES-derived ECs and HAECs. Substantial amount of GC-B was expressed in both ECs (iPS-derived ECs and HAECs) and SMCs (iPS-derived MCs and HSMCs). ET-1 was expressed solely in ECs. ETR-A was expressed in SMCs, while ETR-B was expressed in ECs. These results indicate the existence of vascular CNP/GC-B system in the human vascular wall, indicating the evidence for clinical implication of CNP/GC-B system in concert with ET-1/ETR-A and ETR-B system in the human vasculature.

Downregulation of endothelial nitric oxide synthase (eNOS) and <em>endothelin</em>-<em>1</em> (<em>ET</em>-<em>1</em>) in a co-culture system with human stimulated X-linked CGD neutrophils.

Phagocytes in patients with chronic granulomatous disease (CGD) do not generate reactive oxidative species (ROS), whereas nitric oxide (NO) production is increased in response to the calcium ionophore A23187 in CGD phagocytes compared with healthy phagocytes. Recently, patients with X-linked CGD (X-CGD) have been reported to show higher flow-mediated dilation, suggesting that endothelial cell function is affected by NO production from phagocytes. We studied NOS3 and EDN1 mRNA and protein expression in human umbilical vein endothelial cells (HUVECs) in a co-culture system with neutrophils from X-CGD patients. HUVECs were co-cultured for 30 minutes with human neutrophils from X-CGD or healthy participants in response to A23187 without cell-to-cell contact. The expression of NOS3 and EDN1 mRNA in HUVECs was quantified by real-time polymerase chain reaction.
Moreover, we demonstrated the protein expression of eNOS, ET-1, and NFκB p65, including phosphorylation at Ser1177 of eNOS and Ser536 of NFκB p65. Neutrophils from X-CGD patients showed significantly higher NO and lower H2O2 production in response to A23187 than healthy neutrophils in vitro. Compared with healthy neutrophils, X-CGD neutrophils under A23187 stimulation exhibited significantly increased NO and decreased H2O2, and promoted downregulated NOS3 and EDN1 expression in HUVECs. The total expression and phosphorylation at Ser1177 of eNOS and ET-1 expression were significantly decreased in HUVECs co-cultures with stimulated X-CGD neutrophils. Also, phosphorylation at Ser536 of NFκB p65 were significantly decreased. In conclusions, eNOS and ET-1 significantly down-regulated in co-culture with stimulated X-CGD neutrophils through their excessive NO and the lack of ROS production. These findings suggest that ROS generated from neutrophils may mediate arterial tone affecting eNOS and ET-1 expression via their NO and ROS production.

DHEA-S production capacity in relation to perceived prolonged stress

We and other research groups have previously described that levels of the anabolic hormone dehydroepiandrosterone sulfate (DHEA-S) are lowered in individuals who report prolonged stress. We have also shown that the DHEA-S production capacity during acute stress is attenuated in individuals reporting high prolonged stress. This study aimed to further investigate the DHEA and DHEA-S production capacity in relation to prolonged stress. Eighty-one healthy participants in the age 20-50 years old were included in the study and divided into a low stress (n = 45) and a high stress group (n = 36) according their response to a single question regarding perceived stress during the preceding month.
They underwent the Trier Social Stress Test while blood samples were drawn before, during and after the stress test. The concentration of DHEA, DHEA-S, cortisol and ACTH was measured. The results showed that the high stress group exhibited a significantly lower response of DHEA-S (40% lower) than the low stress group, while DHEA, cortisol and ACTH responses did not differ between the groups. Reduced DHEA-S production may constitute one of the links between stress and poor health.

Inter-individual differences in pain anticipation and pain perception in migraine: Neural correlates of migraine frequency and cortisol-to-dehydroepiandrosterone sulfate (DHEAS) ratio

Previous studies targeting inter-individual differences in pain processing in migraine mainly focused on the perception of pain. Our main aim was to disentangle pain anticipation and perception using a classical fear conditioning task, and investigate how migraine frequency and pre-scan cortisol-to-dehydroepiandrosterone sulfate (DHEA-S) ratio as an index of neurobiological stress response would relate to neural activation in these two phases. Functional Magnetic Resonance Imaging (fMRI) data of 23 participants (18 females; mean age: 27.61± 5.36) with episodic migraine without aura were analysed.
We found that migraine frequency was significantly associated with pain anticipation in brain regions comprising the midcingulate and caudate, whereas pre-scan cortisol-to DHEA-S ratio was related to pain perception in the pre-supplementary motor area (pre-SMA). Both results suggest exaggerated preparatory responses to pain or more general to stressors, which may contribute to the allostatic load caused by stressors and migraine attacks on the brain.

Circulating DHEAS levels and major cardiovascular outcomes in chronic Chagas cardiomyopathy: A prospective cohort study

Objective: To analyze the association of circulating dehydroepiandrosterone sulfate (DHEA-S) levels with cardiovascular outcomes in patients with chronic Chagas cardiomyopathy (CCM) diagnosis.
Background: DHEA-S is among the main endogenous steroid hormones. Some studies have suggested a relevant role of this hormone in infections and the setting of CCM. Nevertheless, no study has evaluated the prognostic role of DHEA-S in CCM patients.
Methods: Prospective cohort study. Patients with CCM and reduced ejection fraction were included. We explored the association of DHEA-S levels with NT-proBNP levels and echocardiographic variables using linear regression models. Next, by using Cox Proportional Hazard models, we examined whether levels of DHEA-S could predict a composite outcome (CO) including all-cause mortality, cardiac transplantation, and implantation of a left ventricular assist device (LVAD).
Results: Seventy-four patients were included (59% males, median age: 64 years). After adjustment for confounding factors, high DHEA-S levels were associated with better LVEF, lower left atrium volume, end-systolic volume of the left ventricle and lower NT-proBNP levels. 43% of patients experienced the CO during a median follow-up of 40 months. Increased levels of DHEA-S were associated with a lower risk of developing the CO (HR 0.43; 95%CI 0.21-0.86). Finally, adding DHEA-S to the multivariate model did not improve the prediction of the CO, but substituting NT-proBNP in the model with DHEA-S showed similar performance.
Conclusions: In patients with CCM, higher DHEA-S levels were associated with lower mortality, heart transplantation, and LVAD implantation. Further larger studies are required to confirm our results and assess causality.

Comparative Profiling of Salivary Cortisol and Salivary DHEAS Among Healthy Pregnant and Non-Pregnant Women

  • During pregnancy, circulatory cortisol levels increase, remaining steady over the second-third trimester. In contrast, profile of salivary cortisol during pregnancy is debatable, more influenced by factors like time of sample collection in the day. Circulatory DHEA-S decrease by at least 50% over the second-third trimester of pregnancy. However, profile of salivary DHEA-S is unclear. Objective was to determine changes in salivary cortisol and DHEA-S in healthy pregnant women, compared to non-pregnant women during late morning-early afternoon sampling to avoid fluctuations associated with other times.
  • Pregnant women in their second-third trimester prospectively (n=500) and non-pregnant women (n=133) were enrolled in study with informed consent. Live birth outcome with no pregnancy complications and≥2.5 Kg infant birth weight were included. Concentrations of salivary cortisol and DHEA-S were determined through ELISA assays. Compared to non-pregnant women, pregnant women demonstrated significant increases in salivary cortisol [median (interquartile range)=4.2 (5.1) nmol/l vs. 17.2 (13.9) nmol/l, p<0.001] and salivary DHEA-S median (interquartile range)=2.7 (2.9) nmol/l vs. 3.8 (3.2) nmol/l, p<0.001).
  • Consistently, quartile scores representing higher levels of salivary cortisol and DHEA-S concentrations demonstrated significant association with pregnancy. Quartile scores representing higher salivary cortisol/DHEA-S ratio demonstrated significant association with pregnancy. Study suggests the indicated time range of saliva sampling might best parallel the established profile of circulatory cortisol in pregnant women. However, unlike cortisol, study indicates that the salivary DHEA-S profile is distinct from the well-known profile of circulatory DHEA-S during pregnancy. A combinatorial approach involving both salivary and circulatory compartments could provide comprehensive picture of DHEA-S and hypothalamus-pituitary-adrenal axis during pregnancy.

DHEA-S

DE1562 Demeditec Diagnostics 96 95 EUR

DHEA-S ELISA

E22-HC9024 EnoGene 96T 495 EUR

DHEA-S Standard, 350UL

C201-350UL Arbor Assays 350UL 207 EUR

DHEA-S Standard, 70UL

C201-70UL Arbor Assays 70UL 85 EUR

DHEA-S (human) ELISA Kit

K7428-100 Biovision each 940.8 EUR

DHEA-S ELISA KIT|Human

EF006758 Lifescience Market 96 Tests 826.8 EUR

RealScreen DHEA-S ELISA Kit

EL102-096 GenDepot 96T 1161.6 EUR

DHEA-S ELISA Kit (1 Plate)

K054-H1 Arbor Assays 1x96 well plate 407 EUR

DHEA-S ELISA Kit (5 Plate)

K054-H5 Arbor Assays 5x96 well plate 1622 EUR

DetectX® DHEA-S Antibody, 3ML

C199-3ML Arbor Assays 3ML 218 EUR

DetectX® DHEA-S Antibody, 13ML

C199-13ML Arbor Assays 13ML 817 EUR

DetectX® DHEA-S Conjugate, 3ML

C200-3ML Arbor Assays 3ML 218 EUR

DetectX® DHEA-S Conjugate, 13ML

C200-13ML Arbor Assays 13ML 817 EUR

OKAU00048-1PLATE - DHEA-S ELISA Kit

OKAU00048-1PLATE Aviva Systems Biology 1plate 400 EUR

OKAU00048-5PLATE - DHEA-S ELISA Kit

OKAU00048-5PLATE Aviva Systems Biology 5plate 1529 EUR

DHEA

2172-100 Biovision each 130.8 EUR

DHEA

2172-500 Biovision each 301.2 EUR

DHEA

HY-14650 MedChemExpress 500mg 325.2 EUR

DHEA

DEH3344 Demeditec Diagnostics 96 107 EUR

Dehydroepiandrosterone Sulfate (DHEA-S) ELISA Kit

abx513009-96tests Abbexa 96 tests 801.6 EUR

DHEA-S(Dehydroepiandrosterone sulfate) ELISA Kit

ELK8370-48T ELK Biotech 48T Ask for price

DHEA-S(Dehydroepiandrosterone sulfate) ELISA Kit

ELK8370-96T ELK Biotech 96T Ask for price

Human DHEA-S ELISA Kit (Competitive EIA)

EK7047 BosterBio 96wells/kit, with removable strips. 573.6 EUR

DHEA [BSA]

DAGPY6646 Creative Diagnostics 500ug 1014 EUR

Rat Dehydroepiandrosterone Sulfate (DHEA-S) CLIA Kit

abx196899-96tests Abbexa 96 tests 990 EUR

Rat Dehydroepiandrosterone Sulfate (DHEA-S) ELISA Kit

abx256871-96tests Abbexa 96 tests 848.4 EUR

Rat Dehydroepiandrosterone sulfate,DHEA-S ELISA Kit

CN-01982R1 ChemNorm 96T 553.2 EUR

Rat Dehydroepiandrosterone sulfate,DHEA-S ELISA Kit

CN-01982R2 ChemNorm 48T 372 EUR

Rat Dehydroepiandrosterone sulfate, DHEA-S ELISA Kit

CSB-E05106r-24T Cusabio 1 plate of 24 wells 198 EUR

Rat Dehydroepiandrosterone sulfate, DHEA-S ELISA Kit

1-CSB-E05106r Cusabio
  • 1160.40 EUR
  • 7110.00 EUR
  • 3760.80 EUR
  • 1 plate of 96 wells
  • 10 plates of 96 wells each
  • 5 plates of 96 wells each

Comparative profiling of prenatal cortisol and DHEAS among pregnant women with poor birth outcome and pregnant women with normal birth outcome

Context: Cortisol and dehydroepiandrosterone-sulfate (DHEA-S) are indispensable hormones for normal pregnancy. It is unclear if these hormones, specifically DHEA-S can offer value for predicting poor birth outcome.
Objective: To compare prenatal cortisol and DHEA-S levels among pregnant women with normal or poor birth outcome.
Design-patients: Plasma and saliva were collected prospectively from women in second-third trimester of pregnancy. Women with normal birth outcome (NBO), (n=501) included live birth, no pregnancy complications and ≥ 2.5Kg infant birth weight. Women with poor birth outcome included adverse birth (ABO), (n=50) or low birth weight outcome (LBW), (n=147).
Measurements: ELISA was performed to measure hormone concentrations in plasma and saliva.
Results: Circulatory-DHEA-S levels in pregnant women with ABO were higher than women with NBO (p=0.043). Among ABO, only stillbirth cases demonstrated significant increase in circulatory-DHEA-S levels (p=0.006). Circulatory and salivary cortisol/DHEA-S ratio was lower among women with stillbirth (p=0.004) and ABO outcome (p=0.043) respectively compared to women with NBO. Consistently, increased odds of ABO were observed in pregnant women with highest circulatory-DHEA-S levels (odds ratio quartile score 1 vs 4, 2.79, p=0.027) and lowest salivary cortisol/DHEA-S ratio (score 4 vs 2, 2.83, p=0.025). Increased odds of stillbirth outcome were observed in pregnant women with highest circulatory-DHEA-S levels (odds ratio quartile score 1 vs 4, 8.47, p=0.046) and lowest circulatory cortisol/DHEA-S ratio (score 4 vs 1, 4.803, p=0.048). Associations remained significant after adjusting for confounders. Women with LBW did not demonstrate significant changes in cortisol or DHEA-S levels.
Conclusion: Prenatal measurement of DHEA-S or cortisol/DHEA-S ratio may offer significant value for predicting adverse birth, specifically stillbirth outcome.

Nitrate Is an Environmental Cue in the Gut for Salmonella enterica Serovar Typhimurium Biofilm Dispersal through Curli Repression and Flagellum Activation via Cyclic-di-GMP Signaling

Curli, a major component of the bacterial biofilms in the intestinal tract, activates pattern recognition receptors and triggers joint inflammation after infection with Salmonella enterica serovar Typhimurium. The factors that allow S. Typhimurium to disperse from biofilms and invade the epithelium to establish a successful infection during acute inflammation remain unknown. Here, we studied S. Typhimurium biofilms in vitro and in vivo to understand how the inflammatory environment regulates the switch between multicellular and motile S. Typhimurium in the gut. We discovered that nitrate generated by the host is an environmental cue that induces S. Typhimurium to disperse from the biofilm. Nitrate represses production of an important biofilm component, curli, and activates flagella via the modulation of intracellular cyclic-di-GMP levels. We conclude that nitrate plays a central role in pathogen fitness by regulating the sessile-to-motile lifestyle switch during infection.
IMPORTANCE Recent studies provided important insight into our understanding of the role of c-di-GMP signaling and the regulation of enteric biofilms. Despite an improved understanding of how c-di-GMP signaling regulates S. Typhimurium biofilms, the processes that affect the intracellular c-di-GMP levels and the formation of multicellular communities in vivo during infections remain unknown. Here, we show that nitrate generated in the intestinal lumen during infection with S. Typhimurium is an important regulator of biofilm formation in vivo.

Second Messenger 2’3′-cyclic GMP-AMP (2’3′-cGAMP):Synthesis, transmission, and degradation

Cyclic GMP-AMP synthase (cGAS) senses foreign DNA to produce 2’3′-cyclic GMP-AMP (2’3′-cGAMP). 2’3′-cGAMP is a second messenger that binds and activates the adaptor protein STING, which triggers the innate immune response. As a STING agonist, the small molecule 2’3′-cGAMP plays pivotal roles in antiviral defense and has adjuvant applications, and anti-tumor effects. 2’3′-cGAMP and its analogs are thus putative targets for immunotherapy and are currently being testedin clinical trials to treat solid tumors.
However, several barriers to further development have emerged from these studies, such as evidence of immune and inflammatory side-effects, poor pharmacokinetics, and undesirable biodistribution. Here, we review the status of 2’3′-cGAMP research and outline the role of 2’3′-cGAMP in immune signaling, adjuvant applications, and cancer immunotherapy, as well as various 2’3′-cGAMP detection methods.

A pGpG-specific phosphodiesterase regulates cyclic di-GMP signaling in Vibrio cholerae

The bacterial second messenger cyclic diguanylate monophosphate (c-di-GMP) controls various cellular processes, including motility, toxin production and biofilm formation. c-di-GMP is enzymatically synthesized by GGDEF domain-containing diguanylate cyclases and degraded by HD-GYP domain-containing phosphodiesterases (PDEs) to 2 GMP or by EAL domain-containing PDE-As to 5′-phosphoguanylyl-(3′,5′)-guanosine (pGpG). Since excess pGpG feedback inhibits PDE-A activity and thereby can lead to the uncontrolled accumulation of c-di-GMP, a PDE that degrades pGpG to 2 GMP (PDE-B) has been presumed to exist.
To date, the only enzyme known to hydrolyze pGpG is Oligoribonuclease Orn, which degrades all kinds of oligoribonucleotides. Here, we identified a pGpG-specific PDE, which we named PggH, using biochemical approaches in the gram-negative bacteria Vibrio cholerae. Biochemical experiments revealed that PggH exhibited specific PDE activity only toward pGpG, thus differing from the previously reported Orn. Furthermore, the high-resolution structure of PggH revealed the basis for its PDE activity and narrow substrate specificity. Finally, we propose that PggH could modulate the activities of PDE-As and the intracellular concentration of c-di-GMP, resulting in phenotypic changes including in biofilm formation.

The Campylobacter jejuni Response Regulator and Cyclic-Di-GMP Binding CbrR Is a Novel Regulator of Flagellar Motility

A leading cause of bacterial gastroenteritis, Campylobacter jejuni is also associated with broad sequelae, including extragastrointestinal conditions such as reactive arthritis and Guillain-Barré Syndrome (GBS). CbrR is a C. jejuni response regulator that is annotated as a diguanylate cyclase (DGC), an enzyme that catalyzes the synthesis of c-di-GMP, a universal bacterial second messenger, from GTP. In C. jejuni DRH212, we constructed an unmarked deletion mutant, cbrR, and complemented mutant, cbrR+. Motility assays indicated a hyper-motile phenotype associated with cbrR, whereas motility was deficient in cbrR+.
The overexpression of CbrR in cbrR+ was accompanied by a reduction in expression of FlaA, the major flagellin. Biofilm assays and scanning electron microscopy demonstrated similarities between DRH212 and cbrR; however, cbrR+ was unable to form significant biofilms. Transmission electron microscopy showed similar cell morphology between the three strains; however, cbrR+ cells lacked flagella. Differential radial capillary action of ligand assays (DRaCALA) showed that CbrR binds GTP and c-di-GMP. Liquid chromatography tandem mass spectrometry detected low levels of c-di-GMP in C. jejuni and in E. coli expressing CbrR. CbrR is therefore a negative regulator of FlaA expression and motility, a critical virulence factor in C. jejuni pathogenesis.

The Regulatory Network of Cyclic GMP-AMP Synthase-Stimulator of Interferon Genes Pathway in Viral Evasion

Virus infection has been consistently threatening public health. The cyclic GMP-AMP synthase (cGAS)-Stimulator of Interferon Genes (STING) pathway is a critical defender to sense various pathogens and trigger innate immunity of mammalian cells. cGAS recognizes the pathogenic DNA in the cytosol and then synthesizes 2’3′-cyclic GMP-AMP (2’3’cGAMP). As the second messenger, cGAMP activates STING and induces the following cascade to produce type I interferon (IFN-I) to protect against infections. However, viruses have evolved numerous strategies to hinder the cGAS-STING signal transduction, promoting their immune evasion.
Here we outline the current status of the viral evasion mechanism underlying the regulation of the cGAS-STING pathway, focusing on how post-transcriptional modifications, viral proteins, and non-coding RNAs involve innate immunity during viral infection, attempting to inspire new targets discovery and uncover potential clinical antiviral treatments.

Cyclic GMP Antibody

abx022640-02ml Abbexa 0.2 ml 1128 EUR

Cyclic GMP EIA Kit

SKT-211-96 Stressmarq 1 plate of 96 wells 568.8 EUR

Cyclic GMP Standard, 125UL

C080-125UL Arbor Assays 125UL 85 EUR

Cyclic GMP Standard, 350UL

C080-350UL Arbor Assays 350UL 207 EUR

Cyclic GMP Standard, 625UL

C080-625UL Arbor Assays 625UL 207 EUR

Cyclic GMP Standard, 70UL

C080-70UL Arbor Assays 70UL 85 EUR

ELISA kit for cGMP (Cyclic GMP)

E-EL-0083 Elabscience Biotech 1 plate of 96 wells 452.4 EUR

DetectX® Cyclic GMP Antibody, 3ML

C078-3ML Arbor Assays 3ML 218 EUR

DetectX® Cyclic GMP Antibody, 3ML

C237-3ML Arbor Assays 3ML 254 EUR

DetectX® Cyclic GMP Antibody, 13ML

C078-13ML Arbor Assays 13ML 1021 EUR

DetectX® Cyclic GMP Conjugate, 3ML

C079-3ML Arbor Assays 3ML 218 EUR

DetectX® Cyclic GMP Antibody, 13ML

C237-13ML Arbor Assays 13ML 1021 EUR

DetectX® Cyclic GMP Conjugate, 13ML

C079-13ML Arbor Assays 13ML 1021 EUR

Human Cyclic GMP-AMP synthase (MB21D1)

1-CSB-EP822726HU Cusabio
  • 456.00 EUR
  • 256.80 EUR
  • 1570.80 EUR
  • 672.00 EUR
  • 1047.60 EUR
  • 314.40 EUR
  • 100ug
  • 10ug
  • 1MG
  • 200ug
  • 500ug
  • 50ug

Cyclic GMP CLIA Kit (High-Sensitivity)

SKT-210-96 Stressmarq 1 plate of 96 wells 624 EUR

Cyclic di-GMP

B7839-.5 ApexBio 500 µg 217.2 EUR

Cyclic di-GMP

B7839-1 ApexBio 1 mg 362.4 EUR

Cyclic-di-GMP

B2045-1000 Biovision each 666 EUR

Cyclic-di-GMP

B2045-250 Biovision each 248.4 EUR

Cyclic-di-GMP

HY-107780 MedChemExpress 10mM/1mL 4454.4 EUR

Cyclic-di-GMP

T10909-10mg TargetMol Chemicals 10mg Ask for price

Cyclic-di-GMP

T10909-1g TargetMol Chemicals 1g Ask for price

Cyclic-di-GMP

T10909-1mg TargetMol Chemicals 1mg Ask for price

Cyclic-di-GMP

T10909-50mg TargetMol Chemicals 50mg Ask for price

Cyclic-di-GMP

T10909-5mg TargetMol Chemicals 5mg Ask for price

cyclic-di-GMP

NU-951L Jena Bioscience GmbH 5 x 1µmol 505.6 EUR

cyclic-di-GMP

NU-951S Jena Bioscience GmbH 1µmol 126.3 EUR

cyclic GMP sheep polyclonal antibody, Serum

AP05354SU-N Origene Technologies GmbH 2 ml Ask for price

BldD-based bimolecular fluorescence complementation for in vivo detection of the second messenger cyclic di-GMP

The widespread bacterial second messenger bis-(3′-5′)-cyclic diguanosine monophosphate (c-di-GMP) is an important regulator of biofilm formation, virulence and cell differentiation. C-di-GMP-specific biosensors that allow detection and visualization of c-di-GMP levels in living cells are key to our understanding of how c-di-GMP fluctuations drive cellular responses. Here, we describe a novel c-di-GMP biosensor, CensYBL, that is based on c-di-GMP-induced dimerization of the effector protein BldD from Streptomyces resulting in bimolecular fluorescence complementation of split-YPet fusion proteins.
As a proof-of-principle, we demonstrate that CensYBL is functional in detecting fluctuations in intracellular c-di-GMP levels in the Gram-negative model bacteria Escherichia coli and Salmonella enterica serovar Typhimurium. Using deletion mutants of c-di-GMP diguanylate cyclases and phosphodiesterases, we show that c-di-GMP dependent dimerization of CBldD-YPet results in fluorescence complementation reflecting intracellular c-di-GMP levels. Overall, we demonstrate that the CensYBL biosensor is a user-friendly and versatile tool that allows to investigate c-di-GMP variations using single-cell and population-wide experimental set-ups.

Genetic Dissection of Nitrogen Use Efficiency in Tropical Maize Through Genome-Wide Association and Genomic Prediction.

Genetic Dissection of Nitrogen Use Efficiency in Tropical Maize Through Genome-Wide Association and Genomic Prediction.
In sub-Saharan Africa, one of the foremost challenges to smallholder farmers is soil with low fertility and incapacity to use nitrogen fertilizer externally because of the value. Development of maize hybrids, which carry out higher in nitrogen depleted soils, is one of the promising options.
However, breeding maize for nitrogen use effectivity (NUE) is hindered by costly phenotypic evaluations and trait complexity beneath low N stress. Genome-wide affiliation research (GWAS) and genomic prediction (GP) are promising instruments to avoid this interference.
Here, we evaluated a mapping panel in various environments each beneath optimum and low N administration. The goal of this research was to establish SNPs considerably related to grain yield (GY) and different traits via GWAS and assess the potential of GP beneath low N and optimum situations. Testcross progenies of 411 inbred traces had been planted beneath optimum and low N situations in a number of places in Africa and Latin America.
In all places, low N fields had been beforehand depleted over a number of seasons, and no N fertilizer was utilized all through the rising season. All inbred traces had been genotyped with genotyping by sequencing. Genotypic and GxE interplay variances had been vital, and heritability estimates had been reasonable to excessive for all traits beneath each optimum and low N situations.
Genome-wide LD decay at r2 = 0.2 and r2 = 0.34 had been 0.24 and 0.19 Mbp, respectively. Chromosome-specific LD decays ranged from 0.13 to 0.34 Mbps with a median of 0.22 Mbp at r2 = 0.2. GWAS analyses revealed 38 and 45 vital SNPs beneath optimum and low N situations, respectively. Out of these 83 vital SNPs, three SNPs on chromosomes 1, 2, and 6 had been related both with completely different traits or the identical trait beneath completely different administration situations, suggesting pleiotropic results of genes.

Polyclonal Rabbit Anti Myc Antibody

20-abx137181
  • EUR 661.20
  • EUR 1045.20
  • EUR 2064.00
  • 100 ul
  • 200 ul
  • 500 ul

Anti-n-Myc/MYCN Antibody

PB9728 100ug/vial
EUR 352.8

Anti-Myc Antibody

A00112 100ul
EUR 476.4
Description: Rabbit Polyclonal Myc Antibody. Validated in IHC and tested in Human, Mouse.

Anti-MYC Antibody

STJ500591 100 µg
EUR 571.2

Anti-MYC Antibody

STJ500592 100 µg
EUR 571.2

Anti-MYC antibody

STJ113115 100 µl
EUR 332.4
Description: The protein encoded by this gene is a multifunctional, nuclear phosphoprotein that plays a role in cell cycle progression, apoptosis and cellular transformation. It functions as a transcription factor that regulates transcription of specific target genes. Mutations, overexpression, rearrangement and translocation of this gene have been associated with a variety of hematopoietic tumors, leukemias and lymphomas, including Burkitt lymphoma. There is evidence to show that alternative translation initiations from an upstream, in-frame non-AUG (CUG) and a downstream AUG start site result in the production of two isoforms with distinct N-termini. The synthesis of non-AUG initiated protein is suppressed in Burkitt's lymphomas, suggesting its importance in the normal function of this gene.

Anti-MYC antibody

STJ113455 50 µl
EUR 344.4
Description: The protein encoded by this gene is a multifunctional, nuclear phosphoprotein that plays a role in cell cycle progression, apoptosis and cellular transformation. It functions as a transcription factor that regulates transcription of specific target genes. Mutations, overexpression, rearrangement and translocation of this gene have been associated with a variety of hematopoietic tumors, leukemias and lymphomas, including Burkitt lymphoma. There is evidence to show that alternative translation initiations from an upstream, in-frame non-AUG (CUG) and a downstream AUG start site result in the production of two isoforms with distinct N-termini. The synthesis of non-AUG initiated protein is suppressed in Burkitt's lymphomas, suggesting its importance in the normal function of this gene.

Anti-myc antibody

STJ140011 150 µg
EUR 277.2
Description: Goat polyclonal antibody to myc epitope tag. c-Myc epitope tag is useful for the labelling and detection of proteins by immunoprecipitation, immunostaining and immunoblotting techniques. Because of its small size, it is unlikely to affect the tagged protein's biochemical properties.

Anti-MYC antibody

STJ111071 100 µl
EUR 332.4
Description: The protein encoded by this gene is a multifunctional, nuclear phosphoprotein that plays a role in cell cycle progression, apoptosis and cellular transformation. It functions as a transcription factor that regulates transcription of specific target genes. Mutations, overexpression, rearrangement and translocation of this gene have been associated with a variety of hematopoietic tumors, leukemias and lymphomas, including Burkitt lymphoma. There is evidence to show that alternative translation initiations from an upstream, in-frame non-AUG (CUG) and a downstream AUG start site result in the production of two isoforms with distinct N-termini. The synthesis of non-AUG initiated protein is suppressed in Burkitt's lymphomas, suggesting its importance in the normal function of this gene.

Anti-C-Myc Epitope (Myc) Tag Polyclonal Antibody

TAX162Ge01 100ul
EUR 279

Anti-N myc interactor/NMI Antibody

PB9340 100ug/vial
EUR 400.8

Rabbit anti Myc(pT58) Polyclonal Antibody

TA354813 100 µg Ask for price

Rabbit anti Myc(pT358) Polyclonal Antibody

TA354802 100 µg Ask for price

Rabbit anti Myc-Tag Polyclonal Antibody

TA354821 100 µg Ask for price

Anti-MYC Antibody (FITC)

STJ500594 100 µg
EUR 703.2

Anti-MYC Antibody (FITC)

STJ500596 100 µg
EUR 703.2

anti- c-MYC antibody

FNab01791 100µg
EUR 702
Description: Antibody raised against c-MYC

Anti-Myc Tag Antibody

R1208-1 100ul
EUR 189
Description: Myc gene encodes for a transcription factor that is believed to regulate expression of 15% of all genes through binding on Enhancer Box sequences (E-boxes) and recruiting histone acetyltransferases (HATs). c-Myc is commonly activated in a variety of tumor cells and plays an important role in cellular proliferation, differentiation, apoptosis and cell cycle progression. This Myc-Tag antibody detects Myc-tagged fusion proteins.

Anti-MYC Antibody (Biotin)

STJ500593 100 µg
EUR 703.2

Anti-MYC Antibody (Biotin)

STJ500595 100 µg
EUR 703.2

Anti-c-Myc Antibody

PB9092 100ug/vial
EUR 400.8

Anti-c-Myc Antibody

PA1555 100ug/vial
EUR 352.8

Anti-c-MYC antibody

PAab01791 100 ug
EUR 494.4

Anti-c-myc antibody

STJ180021 0.1 ml
EUR 282

Anti-C-myc antibody

STJ160092 7 mL P
EUR 834

Anti-c-Myc antibody

STJ119460 100 µl
EUR 332.4
Description: The protein encoded by this gene is a multifunctional, nuclear phosphoprotein that plays a role in cell cycle progression, apoptosis and cellular transformation. It functions as a transcription factor that regulates transcription of specific target genes. Mutations, overexpression, rearrangement and translocation of this gene have been associated with a variety of hematopoietic tumors, leukemias and lymphomas, including Burkitt lymphoma. There is evidence to show that alternative translation initiations from an upstream, in-frame non-AUG (CUG) and a downstream AUG start site result in the production of two isoforms with distinct N-termini. The synthesis of non-AUG initiated protein is suppressed in Burkitt's lymphomas, suggesting its importance in the normal function of this gene.

Anti-c-Myc antibody

STJ97127 200 µl
EUR 236.4
Description: Rabbit polyclonal to c-Myc.

Anti-c-Myc antibody

STJ97962 100 µl
EUR 280.8
Description: Mouse monoclonal to c-Myc.

Anti-c-Myc antibody

STJ92355 200 µl
EUR 236.4
Description: Rabbit polyclonal to c-Myc.

Anti-c-Myc antibody

STJ92356 200 µl
EUR 236.4
Description: c-Myc is a protein encoded by the MYC gene which is approximately 48,8 kDa. c-Myc is localised to the nucleus. It is involved in signalling by NOTCH1, CDK-mediated phosphorylation and removal of Cdc6 and ERK signalling. It functions as a transcription factor that regulates transcription of specific target genes. It plays a role in cell cycle progression, apoptosis and cellular transformation. c-Myc is expressed in the nervous system, intestine, blood, liver and bone marrow. Mutations in the MYC gene may result in Burkitt lymphoma. STJ92356 was affinity-purified from rabbit antiserum by affinity-chromatography using epitope-specific immunogen. This polyclonal antibody detects endogenous levels of c-Myc protein.

Anti-c-Myc antibody

STJ92357 200 µl
EUR 236.4
Description: Rabbit polyclonal to c-Myc.

Anti-c-Myc antibody

STJ92358 200 µl
EUR 236.4
Description: Rabbit polyclonal to c-Myc.

Anti-c-Myc antibody

STJ92359 200 µl
EUR 236.4
Description: Rabbit polyclonal to c-Myc.

Anti-C-myc Antibody

0912-2 100ul
EUR 189
Description: Myc is a family of regulator genes and proto-oncogenes that code for transcription factors. The Myc family consists of three related human genes: c-myc (MYC), l-myc (MYCL), and n-myc (MYCN). c-myc (also sometimes referred to as MYC) was the first gene to be discovered in this family, due to homology with the viral gene v-myc. In cancer, c-myc is often constitutively (persistently) expressed. This leads to the increased expression of many genes, some of which are involved in cell proliferation, contributing to the formation of cancer. A common human translocation involving c-myc is critical to the development of most cases of Burkitt lymphoma. Constitutive upregulation of Myc genes have also been observed in carcinoma of the cervix, colon, breast, lung and stomach. Myc is thus viewed as a promising target for anti-cancer drugs. Unfortunately, Myc possesses several features that render it undruggable such that any anti-cancer drugs for Myc dysregulation will require acting on the protein indirectly, i.e. targeting the mRNA for the protein rather than a small molecule that targets the protein itself. In the human genome, C-myc is located on chromosome 8 and is believed to regulate expression of 15% of all genes through binding on enhancer box sequences (E-boxes). In addition to its role as a classical transcription factor, N-myc may recruit histone acetyltransferases (HATs). This allows it to regulate global chromatin structure via histone acetylation.

Anti-N-Myc Antibody

Y058042 100 µl
EUR 145

Anti-C-MYC Antibody

Y058202 100 µl
EUR 145

Anti-C-MYC Antibody

Y080045 100 µl
EUR 125

Anti-c-Myc Antibody

Y123314 100 µl
EUR 275

Anti-N-Myc Antibody

39222 100ul
EUR 479

Anti-MYC-tag antibody

PAab05462 100 ug
EUR 426

Anti-Myc-Tag antibody

STJ96904 200 µl
EUR 236.4
Description: Mouse monoclonal to Myc-Tag.

Anti-Myc-Tag antibody

STJ96926 200 µl
EUR 236.4
Description: Mouse monoclonal to Myc-Tag.

Anti-Myc-Tag antibody

STJ96929 200 µl
EUR 236.4
Description: Mouse monoclonal to Myc-Tag.

Anti-Myc-Tag antibody

STJ97044 200 µl
EUR 236.4
Description: Mouse monoclonal to Myc-Tag.

Anti-Myc-Tag antibody

STJ97078 200 µl
EUR 236.4
Description: Rabbit polyclonal to Myc-Tag.

Mouse Anti-Human MYC Monoclonal Antibody

CAB-1950MH 0.2mg
EUR 639.6

Anti-Myc Tag (Myc.A7 / M19) Monoclonal Antibody

ABP-MAB-MT005 100 ug Ask for price

Anti-Myc (Ab-58) Antibody

Y021034 100 µg
EUR 285

Anti-Myc (Ab-358) Antibody

Y021035 100 µg
EUR 285

Anti-Myc (Ab-373) Antibody

Y021036 100 µg
EUR 285

Anti-Myc-tag antibody (KLH)

STJ90105 200 µl
EUR 236.4
Description: Rabbit polyclonal to Myc-tag.

Anti-Myc-tag Antibody [A3C8]

EM1902-38 100ul
EUR 210
Description: Transcription factor that binds DNA in a non-specific manner, yet also specifically recognizes the core sequence 5'-CAC[GA]TG-3'. Activates the transcription of growth-related genes. Binds to the VEGFA promoter, promoting VEGFA production and subsequent sprouting angiogenesis . Regulator of somatic reprogramming, controls self-renewal of embryonic stem cells. Functions with TAF6L to activate target gene expression through RNA polymerase II pause release (By similarity).Myc proteins are transcription factors that activate expression of many pro-proliferative genes through binding enhancer box sequences (E-boxes) and recruiting histone acetyltransferases (HATs). Myc is thought to function by upregulating transcript elongation of actively transcribed genes through the recruitment of elongation factors.[8] It can also act as a transcriptional repressor. By binding Miz-1 transcription factor and displacing the p300 co-activator, it inhibits expression of Miz-1 target genes. In addition, myc has a direct role in the control of DNA replication.[9] This activity could contribute to DNA amplification in cancer cells.

Mouse anti-Myc-tag Antibody

YLD8522-100ul 100 ul
EUR 320
Description: Mouse monoclonal antibody to Myc-tag

Mouse anti-Myc-tag Antibody

YLD8522-50ul 50 ul
EUR 200
Description: Mouse monoclonal antibody to Myc-tag

Mouse anti-Myc-tag Antibody

DL95409A-100ul 100 ul
EUR 375

Mouse anti-Myc-tag Antibody

DL95409A-50ul 50 ul
EUR 262.5

Rabbit anti-Myc-tag Antibody

YLD5270-100ul 100 ul
EUR 320
Description: Rabbit polyclonal antibody to Myc-tag

Rabbit anti-Myc-tag Antibody

YLD5270-50ul 50 ul
EUR 200
Description: Rabbit polyclonal antibody to Myc-tag

Rabbit anti-Myc-tag Antibody

YLD5271-100ul 100 ul
EUR 320
Description: Rabbit polyclonal antibody to Myc-tag

Rabbit anti-Myc-tag Antibody

YLD5271-50ul 50 ul
EUR 200
Description: Rabbit polyclonal antibody to Myc-tag

Rabbit anti-Myc-tag Antibody

DL95375A-100ul 100 ul
EUR 350
Description: c Myc; c Myc Epitope Tag; c Myc Tag; Myc Epitope Tag; Myc proto-oncogene protein; Transcription factor p64

Rabbit anti-Myc-tag Antibody

DL95375A-50ul 50 ul
EUR 245
Description: c Myc; c Myc Epitope Tag; c Myc Tag; Myc Epitope Tag; Myc proto-oncogene protein; Transcription factor p64

Rabbit anti-Myc-tag Antibody

DL95435A-100ul 100 ul
EUR 350

Rabbit anti-Myc-tag Antibody

DL95435A-50ul 50 ul
EUR 245

Rabbit anti-c-Myc Antibody

YLD2001-100ul 100 ul
EUR 320
Description: Rabbit polyclonal antibody to c-Myc

Rabbit anti-c-Myc Antibody

YLD2001-50ul 50 ul
EUR 200
Description: Rabbit polyclonal antibody to c-Myc

Rabbit anti-c-Myc Antibody

YLD2002-100ul 100 ul
EUR 320
Description: Rabbit polyclonal antibody to c-Myc

Rabbit anti-c-Myc Antibody

YLD2002-50ul 50 ul
EUR 200
Description: Rabbit polyclonal antibody to c-Myc

Rabbit anti-c-Myc Antibody

YLD2003-100ul 100 ul
EUR 320
Description: Rabbit polyclonal antibody to c-Myc

Rabbit anti-c-Myc Antibody

YLD2003-50ul 50 ul
EUR 200
Description: Rabbit polyclonal antibody to c-Myc

Rabbit anti-c-Myc Antibody

YLD2004-100ul 100 ul
EUR 320
Description: Rabbit polyclonal antibody to c-Myc

Rabbit anti-c-Myc Antibody

YLD2004-50ul 50 ul
EUR 200
Description: Rabbit polyclonal antibody to c-Myc

Rabbit anti-c-Myc Antibody

YLD2005-100ul 100 ul
EUR 320
Description: Rabbit polyclonal antibody to c-Myc

Rabbit anti-c-Myc Antibody

YLD2005-50ul 50 ul
EUR 200
Description: Rabbit polyclonal antibody to c-Myc

Rabbit anti-c-Myc Antibody

YLD2006-100ul 100 ul
EUR 320
Description: Rabbit polyclonal antibody to c-Myc

Rabbit anti-c-Myc Antibody

YLD2006-50ul 50 ul
EUR 200
Description: Rabbit polyclonal antibody to c-Myc

Rabbit anti-N-myc Antibody

YLD5575-100ul 100 ul
EUR 320
Description: Rabbit polyclonal antibody to N-myc

Rabbit anti-N-myc Antibody

YLD5575-50ul 50 ul
EUR 200
Description: Rabbit polyclonal antibody to N-myc

Rabbit anti-c-Myc Antibody

DL93746A-100ul 100 ul
EUR 316
Description: BHLHE39; Myc proto-oncogene protein; Class E basic helix-loop-helix protein 39; bHLHe39; Proto-oncogene c-Myc; Transcription factor p64

Rabbit anti-c-Myc Antibody

DL93746A-50ul 50 ul
EUR 221.2
Description: BHLHE39; Myc proto-oncogene protein; Class E basic helix-loop-helix protein 39; bHLHe39; Proto-oncogene c-Myc; Transcription factor p64

Rabbit anti-c-Myc Antibody

DL93748A-100ul 100 ul
EUR 342
Description: BHLHE39; Myc proto-oncogene protein; Class E basic helix-loop-helix protein 39; bHLHe39; Proto-oncogene c-Myc; Transcription factor p64

Rabbit anti-c-Myc Antibody

DL93748A-50ul 50 ul
EUR 239.4
Description: BHLHE39; Myc proto-oncogene protein; Class E basic helix-loop-helix protein 39; bHLHe39; Proto-oncogene c-Myc; Transcription factor p64

Rabbit anti-N-myc Antibody

DL97202A-100ul 100 ul
EUR 325
Description: BHLHE37; NMYC; N-myc proto-oncogene protein; Class E basic helix-loop-helix protein 37; bHLHe37

Rabbit anti-N-myc Antibody

DL97202A-50ul 50 ul
EUR 227.5
Description: BHLHE37; NMYC; N-myc proto-oncogene protein; Class E basic helix-loop-helix protein 37; bHLHe37

Rabbit anti-c-Myc Antibody

DL95608A-100ul 100 ul
EUR 270
Description: BHLHE39; Myc proto-oncogene protein; Class E basic helix-loop-helix protein 39; bHLHe39; Proto-oncogene c-Myc; Transcription factor p64

Rabbit anti-c-Myc Antibody

DL95608A-50ul 50 ul
EUR 189
Description: BHLHE39; Myc proto-oncogene protein; Class E basic helix-loop-helix protein 39; bHLHe39; Proto-oncogene c-Myc; Transcription factor p64

Rabbit anti-c-Myc Antibody

DL90777A-100ul 100 ul
EUR 342
Description: BHLHE39; Myc proto-oncogene protein; Class E basic helix-loop-helix protein 39; bHLHe39; Proto-oncogene c-Myc; Transcription factor p64

Rabbit anti-c-Myc Antibody

DL90777A-50ul 50 ul
EUR 239.4
Description: BHLHE39; Myc proto-oncogene protein; Class E basic helix-loop-helix protein 39; bHLHe39; Proto-oncogene c-Myc; Transcription factor p64

Rabbit anti-c-Myc Antibody

DL90778A-100ul 100 ul
EUR 316
Description: BHLHE39; Myc proto-oncogene protein; Class E basic helix-loop-helix protein 39; bHLHe39; Proto-oncogene c-Myc; Transcription factor p64

Rabbit anti-c-Myc Antibody

DL90778A-50ul 50 ul
EUR 221.2
Description: BHLHE39; Myc proto-oncogene protein; Class E basic helix-loop-helix protein 39; bHLHe39; Proto-oncogene c-Myc; Transcription factor p64

Rabbit anti-c-Myc Antibody

DL93474A-100ul 100 ul
EUR 334
Description: BHLHE39; Myc proto-oncogene protein; Class E basic helix-loop-helix protein 39; bHLHe39; Proto-oncogene c-Myc; Transcription factor p64

Rabbit anti-c-Myc Antibody

DL93474A-50ul 50 ul
EUR 233.8
Description: BHLHE39; Myc proto-oncogene protein; Class E basic helix-loop-helix protein 39; bHLHe39; Proto-oncogene c-Myc; Transcription factor p64

Myc Antibody

abx242911-100ul 100 ul
EUR 477.6

Myc antibody

10R-10451 100 ug
EUR 522
Description: Mouse monoclonal Myc antibody

MYC antibody

10R-10606 100 ug
EUR 418.8
Description: Mouse monoclonal MYC antibody

MYC antibody

10R-1757 100 ug
EUR 614.4
Description: Mouse monoclonal MYC antibody

Myc antibody

10R-4914 100 ul
EUR 871.2
Description: Mouse monoclonal Myc antibody

Myc antibody

10R-4915 100 ul
EUR 829.2
Description: Mouse monoclonal Myc antibody

Myc antibody

10R-4916 100 ul
EUR 829.2
Description: Mouse monoclonal Myc antibody

Myc antibody

10R-7246 50 ug
EUR 337.2
Description: Mouse monoclonal Myc antibody

Myc antibody

20R-1901 50 ug
EUR 337.2
Description: Rabbit polyclonal Myc antibody

Myc antibody

20R-1902 50 ug
EUR 337.2
Description: Rabbit polyclonal Myc antibody

Myc antibody

20R-1903 50 ug
EUR 337.2
Description: Rabbit polyclonal Myc antibody

Myc antibody

20R-2131 50 ug
EUR 337.2
Description: Rabbit polyclonal Myc antibody

Myc antibody

20R-2218 50 ug
EUR 337.2
Description: Rabbit polyclonal Myc antibody

Myc antibody

20R-2219 50 ug
EUR 337.2
Description: Rabbit polyclonal Myc antibody

Myc antibody

20R-2220 50 ug
EUR 337.2
Description: Rabbit polyclonal Myc antibody

Myc antibody

70R-30593 100 ug
EUR 392.4
Description: Rabbit polyclonal Myc antibody

MYC Antibody

BF0467 200ul
EUR 540

MYC antibody

70R-18694 50 ul
EUR 522
Description: Rabbit polyclonal MYC antibody

Myc antibody

70R-31557 100 ug
EUR 392.4
Description: Rabbit polyclonal Myc antibody

MYC antibody

70R-33161 100 ug
EUR 522
Description: Rabbit polyclonal MYC antibody

Myc antibody

70R-37474 100 ug
EUR 327.6
Description: Rabbit Polyclonal Myc antibody

Myc antibody

70R-37475 100 ug
EUR 327.6
Description: Rabbit Polyclonal Myc antibody

Myc antibody

70R-37476 100 ug
EUR 327.6
Description: Rabbit Polyclonal Myc antibody

Myc antibody

70R-35535 100 ug
EUR 392.4
Description: Purified Rabbit polyclonal Myc antibody

Myc Antibody

33647-100ul 100ul
EUR 302.4

Myc Antibody

33647-50ul 50ul
EUR 224.4

Myc Antibody

34647-100ul 100ul
EUR 302.4

Myc Antibody

34647-50ul 50ul
EUR 224.4

MYC Antibody

ABF0358 100 ug
EUR 525.6

MYC Antibody

ABF6054 100 ug
EUR 525.6

MYC Antibody

ABF6055 100 ug
EUR 525.6

MYC Antibody

CSB-PA153029- each
EUR 402
Description: A polyclonal antibody against MYC. Recognizes MYC from Human, Mouse, Rat. This antibody is Unconjugated. Tested in the following application: ELISA, WB, IHC;WB:1:500-1:3000, IHC:1:50-1:100

MYC Antibody

CSB-PA153029-100ul 100ul
EUR 379.2
Description: A polyclonal antibody against MYC. Recognizes MYC from Human, Mouse, Rat. This antibody is Unconjugated. Tested in the following application: ELISA, WB, IHC;WB:1:500-1:3000, IHC:1:50-1:100

MYC Antibody

1-CSB-PA02589A0Rb
  • EUR 380.40
  • EUR 402.00
  • 100ug
  • 50ug
Description: A polyclonal antibody against MYC. Recognizes MYC from Human, Mouse. This antibody is Unconjugated. Tested in the following application: ELISA, WB, IHC; Recommended dilution: WB:1:500-1:5000, IHC:1:20-1:200

Myc Antibody

1-CSB-PA015270DA01MO
  • EUR 380.40
  • EUR 402.00
  • 100ug
  • 50ug
Description: A polyclonal antibody against Myc. Recognizes Myc from Mouse. This antibody is Unconjugated. Tested in the following application: ELISA

MYC Antibody

1-CSB-PA015270GA01HU
  • EUR 716.40
  • EUR 399.60
  • 150ul
  • 50ul
Description: A polyclonal antibody against MYC. Recognizes MYC from Human, Mouse, Rat. This antibody is Unconjugated. Tested in the following application: ELISA

MYC Antibody

1-CSB-PA407491
  • EUR 380.40
  • EUR 292.80
  • 100ul
  • 50ul
Description: A polyclonal antibody against MYC. Recognizes MYC from Human, Rat. This antibody is Unconjugated. Tested in the following application: ELISA, WB, IHC;ELISA:1:1000-1:10000, WB:1:1000-1:5000, IHC:1:15-1:50

MYC Antibody

1-CSB-PA000389
  • EUR 266.40
  • EUR 234.00
  • 100ug
  • 50ug
Description: A polyclonal antibody against MYC. Recognizes MYC from Human. This antibody is Unconjugated. Tested in the following application: WB;WB:1:1000

MYC Antibody

1-CSB-PA001729
  • EUR 266.40
  • EUR 234.00
  • 100ug
  • 50ug
Description: A polyclonal antibody against MYC. Recognizes MYC from Human, Mouse, Rat. This antibody is Unconjugated. Tested in the following application: WB, IHC, ELISA;WB:1/500-1/2000.IHC:1/100-1/300.ELISA:1/20000

Myc Antibody

F47611-0.08ML 0.08 ml
EUR 140.25
Description: MYC is a multifunctional, nuclear phosphoprotein that plays a role in cell cycle progression, apoptosis and cellular transformation. It functions as a transcription factor that regulates transcription of specific target genes. Mutations, overexpression, rearrangement and translocation of the gene encoding MYC have been associated with a variety of hematopoietic tumors, leukemias and lymphomas, including Burkitt lymphoma.

Myc Antibody

F47611-0.4ML 0.4 ml
EUR 322.15
Description: MYC is a multifunctional, nuclear phosphoprotein that plays a role in cell cycle progression, apoptosis and cellular transformation. It functions as a transcription factor that regulates transcription of specific target genes. Mutations, overexpression, rearrangement and translocation of the gene encoding MYC have been associated with a variety of hematopoietic tumors, leukemias and lymphomas, including Burkitt lymphoma.

Myc Antibody

F47612-0.08ML 0.08 ml
EUR 140.25
Description: MYC is a multifunctional, nuclear phosphoprotein that plays a role in cell cycle progression, apoptosis and cellular transformation. It functions as a transcription factor that regulates transcription of specific target genes. Mutations, overexpression, rearrangement and translocation of the gene encoding MYC have been associated with a variety of hematopoietic tumors, leukemias and lymphomas, including Burkitt lymphoma. There is evidence to show that alternative translation initiations from an upstream, in-frame non-AUG (CUG) and a downstream AUG start site result in the production of two isoforms with distinct N-termini. The synthesis of non-AUG initiated protein is suppressed in Burkitt's lymphomas, suggesting its importance in the normal function of this gene.

Myc Antibody

F47612-0.4ML 0.4 ml
EUR 322.15
Description: MYC is a multifunctional, nuclear phosphoprotein that plays a role in cell cycle progression, apoptosis and cellular transformation. It functions as a transcription factor that regulates transcription of specific target genes. Mutations, overexpression, rearrangement and translocation of the gene encoding MYC have been associated with a variety of hematopoietic tumors, leukemias and lymphomas, including Burkitt lymphoma. There is evidence to show that alternative translation initiations from an upstream, in-frame non-AUG (CUG) and a downstream AUG start site result in the production of two isoforms with distinct N-termini. The synthesis of non-AUG initiated protein is suppressed in Burkitt's lymphomas, suggesting its importance in the normal function of this gene.

MYC Antibody

E10-30209 100μg/100μl
EUR 225
Description: Available in various conjugation types.

MYC Antibody

E11-10262C 100μg
EUR 225
Description: Available in various conjugation types.

Myc Antibody

E11-15409C 100μg
EUR 225
Description: Available in various conjugation types.

Myc Antibody

E033647 100μg/100μl
EUR 255
Description: Available in various conjugation types.

Myc Antibody

E034647 100μg/100μl
EUR 255
Description: Available in various conjugation types.

MYC Antibody

E18-0358-1 50μg/50μl
EUR 145
Description: Available in various conjugation types.

MYC Antibody

E18-0358-2 100μg/100μl
EUR 225
Description: Available in various conjugation types.

MYC Antibody

E18-6054-1 50μg/50μl
EUR 145
Description: Available in various conjugation types.

MYC Antibody

E18-6054-2 100μg/100μl
EUR 225
Description: Available in various conjugation types.

MYC Antibody

E18-6055-1 50μg/50μl
EUR 145
Description: Available in various conjugation types.

MYC Antibody

E18-6055-2 100μg/100μl
EUR 225
Description: Available in various conjugation types.

MYC Antibody

E315137 100ug/200ul
EUR 295
Description: Available in various conjugation types.

MYC Antibody

8C10262 50ug
EUR 368
Description: MYC Antibody

MYC Antibody

E911394 100ul
EUR 255
Description: Available in various conjugation types.

MYC Antibody

E561029-A-SE 100ug
EUR 295
Description: Available in various conjugation types.

Myc Antibody

34647 100ul
EUR 319

Myc Antibody

33647 100ul
EUR 319

Goat Polyclonal Anti-myc Antibody

AB0127-200 600 µg Ask for price

9E10, Anti-Myc Monoclonal Antibody

TA150121 100 µl Ask for price

9E10, Anti-Myc Monoclonal Antibody

TA150121-1 1 ml Ask for price

Anti-Myc (Phospho-Ser62) Antibody

Y011311 100 µg
EUR 285

Anti-Myc (Phospho-Thr58) Antibody

Y011034 100 µg
EUR 285

Anti-Phospho-MYC-(T58) antibody

STJ22298 100 µl
EUR 471.6
Description: The protein encoded by this gene is a multifunctional, nuclear phosphoprotein that plays a role in cell cycle progression, apoptosis and cellular transformation. It functions as a transcription factor that regulates transcription of specific target genes. Mutations, overexpression, rearrangement and translocation of this gene have been associated with a variety of hematopoietic tumors, leukemias and lymphomas, including Burkitt lymphoma. There is evidence to show that alternative translation initiations from an upstream, in-frame non-AUG (CUG) and a downstream AUG start site result in the production of two isoforms with distinct N-termini. The synthesis of non-AUG initiated protein is suppressed in Burkitt's lymphomas, suggesting its importance in the normal function of this gene.

Anti-Phospho-MYC-(S62) antibody

STJ22299 100 µl
EUR 471.6
Description: The protein encoded by this gene is a multifunctional, nuclear phosphoprotein that plays a role in cell cycle progression, apoptosis and cellular transformation. It functions as a transcription factor that regulates transcription of specific target genes. Mutations, overexpression, rearrangement and translocation of this gene have been associated with a variety of hematopoietic tumors, leukemias and lymphomas, including Burkitt lymphoma. There is evidence to show that alternative translation initiations from an upstream, in-frame non-AUG (CUG) and a downstream AUG start site result in the production of two isoforms with distinct N-termini. The synthesis of non-AUG initiated protein is suppressed in Burkitt's lymphomas, suggesting its importance in the normal function of this gene.

Anti-Phospho-MYC-(T58) antibody

STJ22300 100 µl
EUR 471.6
Description: The protein encoded by this gene is a multifunctional, nuclear phosphoprotein that plays a role in cell cycle progression, apoptosis and cellular transformation. It functions as a transcription factor that regulates transcription of specific target genes. Mutations, overexpression, rearrangement and translocation of this gene have been associated with a variety of hematopoietic tumors, leukemias and lymphomas, including Burkitt lymphoma. There is evidence to show that alternative translation initiations from an upstream, in-frame non-AUG (CUG) and a downstream AUG start site result in the production of two isoforms with distinct N-termini. The synthesis of non-AUG initiated protein is suppressed in Burkitt's lymphomas, suggesting its importance in the normal function of this gene.

Anti-Phospho-MYC-(S62) antibody

STJ22302 100 µl
EUR 471.6
Description: The protein encoded by this gene is a multifunctional, nuclear phosphoprotein that plays a role in cell cycle progression, apoptosis and cellular transformation. It functions as a transcription factor that regulates transcription of specific target genes. Mutations, overexpression, rearrangement and translocation of this gene have been associated with a variety of hematopoietic tumors, leukemias and lymphomas, including Burkitt lymphoma. There is evidence to show that alternative translation initiations from an upstream, in-frame non-AUG (CUG) and a downstream AUG start site result in the production of two isoforms with distinct N-termini. The synthesis of non-AUG initiated protein is suppressed in Burkitt's lymphomas, suggesting its importance in the normal function of this gene.

Rabbit Polyclonal Anti-MYC Antibody

TA347557 100 µg Ask for price

Anti-Myc (Phospho-Thr358) Antibody

Y011035 100 µg
EUR 285

Anti-Myc (Phospho-Ser373) Antibody

Y011036 100 µg
EUR 285

Anti-c-Myc Monoclonal Antibody

M00026-1 100ug
EUR 476.4
Description: Rabbit Monoclonal c-Myc Antibody. Validated in WB and tested in Human, Mouse, Rat.

Anti-Phospho-MYC-(S373) antibody

STJ22301 100 µl
EUR 471.6
Description: The protein encoded by this gene is a multifunctional, nuclear phosphoprotein that plays a role in cell cycle progression, apoptosis and cellular transformation. It functions as a transcription factor that regulates transcription of specific target genes. Mutations, overexpression, rearrangement and translocation of this gene have been associated with a variety of hematopoietic tumors, leukemias and lymphomas, including Burkitt lymphoma. There is evidence to show that alternative translation initiations from an upstream, in-frame non-AUG (CUG) and a downstream AUG start site result in the production of two isoforms with distinct N-termini. The synthesis of non-AUG initiated protein is suppressed in Burkitt's lymphomas, suggesting its importance in the normal function of this gene.

Anti-Phospho-MYC-(T358) antibody

STJ22303 100 µl
EUR 471.6
Description: The protein encoded by this gene is a multifunctional, nuclear phosphoprotein that plays a role in cell cycle progression, apoptosis and cellular transformation. It functions as a transcription factor that regulates transcription of specific target genes. Mutations, overexpression, rearrangement and translocation of this gene have been associated with a variety of hematopoietic tumors, leukemias and lymphomas, including Burkitt lymphoma. There is evidence to show that alternative translation initiations from an upstream, in-frame non-AUG (CUG) and a downstream AUG start site result in the production of two isoforms with distinct N-termini. The synthesis of non-AUG initiated protein is suppressed in Burkitt's lymphomas, suggesting its importance in the normal function of this gene.

Rabbit Anti-Human MYC Polyclonal Antibody, aa.56-60

CPB-949RH 100 ul
EUR 552

Rabbit Anti-Human MYC Polyclonal Antibody, aa.356-360

CPB-950RH 100 ul
EUR 552

Rabbit Anti-Human MYC Polyclonal Antibody, aa.371-375

CPB-951RH 100 ul
EUR 552

Anti-Myc Tag Antibody [A3-B4]

EM31105 100ul
EUR 210
Description: Myc gene encodes for a transcription factor that is believed to regulate expression of 15% of all genes through binding on Enhancer Box sequences (E-boxes) and recruiting histone acetyltransferases (HATs). c-Myc is commonly activated in a variety of tumor cells and plays an important role in cellular proliferation, differentiation, apoptosis and cell cycle progression. This Myc-Tag antibody detects Myc-tagged fusion proteins.

c-Myc Epitope (Myc) Antibody

20-abx132269
  • EUR 526.80
  • EUR 159.60
  • EUR 1513.20
  • EUR 727.20
  • EUR 410.40
  • 100 ug
  • 10 ug
  • 1 mg
  • 200 ug
  • 50 ug

c-Myc Epitope (Myc) Antibody

20-abx130438
  • EUR 376.80
  • EUR 910.80
  • EUR 493.20
  • EUR 184.80
  • EUR 292.80
  • 100 ug
  • 1 mg
  • 200 ug
  • 20 ug
  • 50 ug

c Myc antibody

10R-8403 100 ul
EUR 471.6
Description: Mouse monoclonal c Myc antibody

N Myc Antibody

ABF5204 100 ug
EUR 525.6

N Myc Antibody

E18-5204-1 50μg/50μl
EUR 145
Description: Available in various conjugation types.

N Myc Antibody

E18-5204-2 100μg/100μl
EUR 225
Description: Available in various conjugation types.

Anti-c-Myc Oncoprotein Antibody Clone MYC275, Unconjugated-100ug

4609-MSM3-P1 100ug
EUR 513.6

Anti-c-Myc Oncoprotein Antibody Clone MYC909, Unconjugated-100ug

4609-MSM5-P1 100ug
EUR 513.6

Anti-c-Myc Antibody [PS00-11]

HA721182 100ul
EUR 231
Description: The proto-oncogene c-MYC is located on chromosome 8q24. It encodes a nuclear posphoprotein that acts as a growth promotor and transcription factor regulating a variety of cellular functions such as cell growth, differentiation and apoptosis. c-MYC is involved in the regulation of 10-15% of all human genes and is estimated to be involved in 20% of all human cancers. c-MYC is essential for early B-cell development in the bone marrow and the unregulated expression of c-MYC in germinal center B-cells increases the chances of oncogentic events for the development of B-cell lymphomas. Mutations, amplification, rearrangement, and translocation of the c-MyC gene have been associated with various hematopoietic tumors, leukemias, and lymphomas as well as a variety of carcinomas (e.g. thyroid, breast, endometrium) and gliomas. IHC for c-MYC overexpression (>40%) is used to screen and predict c-MYC rearrangements and distinguish diffuse large B-cell lymphoma (DLBCL) NOS from high grade B-cell lymphoma with c-MYC, BCL2 and/or BCL6 rearrangements or so-called “double or triple hit lymphomas” who tend to have aggressive behavior and poor outcome when treated with standard therapy. c-MYC protein is overexpressed in 90% of Burkitt lymphomas (BL) and caused by c-Myc gene translocation. tonsil and colon are recommended as positive and negative tissue controls for c-MYC. In the tonsil, protocols must be calibrated to provide a moderate to strong, distinct nuclear staining reaction in approximately 10% of lymphocytes scattered both in the interfollicular zones and in the reactive germinal centers of the tonsil. A weak, distinct nuclear staining reaction of mantle zone B-cells (app. 10-20%) should be seen. In colon, a weak to moderate nuclear staining reaction should be displayed in scattered epithelial cells in the basal crypts, whereas the luminal epithelial cells and smooth muscle cells of the tunica muscularis should be unstained.

Anti-C-Myc Antibody | CMYC-45A

CMYC-45A 1.0 mg
EUR 1142
Description:

Anti-C-Myc Antibody ; CMYC-45A ; Immunology Consultants Laboratory

Host: Chicken

Format: Unconjugated AP

Product Type: Primary Antibody

Antibody Clonality: Polyclonal

Anti-C-Myc Antibody | CMYC-45B

CMYC-45B 1.0 mg
EUR 1157
Description:

Anti-C-Myc Antibody ; CMYC-45B ; Immunology Consultants Laboratory

Host: Chicken

Format: Biotin Conjugated

Product Type: Primary Antibody

Antibody Clonality: Polyclonal

Anti-C-Myc Antibody | CMYC-45F

CMYC-45F 1.0 mg
EUR 1157
Description:

Anti-C-Myc Antibody ; CMYC-45F ; Immunology Consultants Laboratory

Host: Chicken

Format: FITC Conjugated

Product Type: Primary Antibody

Antibody Clonality: Polyclonal

Anti-C-Myc Antibody | CMYC-45P

CMYC-45P 1.0 mg
EUR 1173
Description:

Anti-C-Myc Antibody ; CMYC-45P ; Immunology Consultants Laboratory

Host: Chicken

Format: HRP Conjugated

Product Type: Primary Antibody

Antibody Clonality: Polyclonal

Anti-C-Myc Antibody | GMYC-45A

GMYC-45A 0.1 mg
EUR 1142
Description:

Anti-C-Myc Antibody ; GMYC-45A ; Immunology Consultants Laboratory

Host: Goat

Format: Unconjugated AP

Product Type: Primary Antibody

Antibody Clonality: Polyclonal

Anti-C-Myc Antibody | RMYC-45A

RMYC-45A 1.0 mg
EUR 1142
Description:

Anti-C-Myc Antibody ; RMYC-45A ; Immunology Consultants Laboratory

Host: Rabbit

Format: Unconjugated AP

Product Type: Primary Antibody

Antibody Clonality: Polyclonal

Anti-C-Myc Antibody | RMYC-45F

RMYC-45F 1.0 mg
EUR 1157
Description:

Anti-C-Myc Antibody ; RMYC-45F ; Immunology Consultants Laboratory

Host: Rabbit

Format: FITC Conjugated

Product Type: Primary Antibody

Antibody Clonality: Polyclonal

Anti-C-Myc Antibody | RMYC-45P

RMYC-45P 1.0 mg
EUR 1173
Description:

Anti-C-Myc Antibody ; RMYC-45P ; Immunology Consultants Laboratory

Host: Rabbit

Format: HRP Conjugated

Product Type: Primary Antibody

Antibody Clonality: Polyclonal

A7, Anti-Myc tag monoclonal antibody

TA100010 100 µl Ask for price

Rabbit anti-c-Myc (pS62) Antibody

YLD1998-100ul 100 ul
EUR 320
Description: Rabbit polyclonal antibody to c-Myc (pS62)

Rabbit anti-c-Myc (pS62) Antibody

YLD1998-50ul 50 ul
EUR 200
Description: Rabbit polyclonal antibody to c-Myc (pS62)

Rabbit anti-c-Myc (pT58) Antibody

YLD2000-100ul 100 ul
EUR 320
Description: Rabbit polyclonal antibody to c-Myc (pT58)
A complete of 136 putative candidate genes had been related to the numerous SNPs, of which seven SNPs had been linked with 4 recognized genes. Prediction accuracies had been reasonable to excessive for all traits beneath each optimum and low N situations. These outcomes can be utilized as helpful sources for additional purposes to develop hybrids or traces with higher efficiency beneath low N situations.
Genetic Dissection of Nitrogen Use Efficiency in Tropical Maize Through Genome-Wide Association and Genomic Prediction.
Genetic Dissection of Nitrogen Use Efficiency in Tropical Maize Through Genome-Wide Association and Genomic Prediction.

Genetic and genomic analyses for predicted methane-related traits in Japanese Black steers.

The aims of this research had been to estimate genetic parameters and to carry out a genome-wide affiliation research (GWAS) for predicted methane-related traits in Japanese Black steers.

The methane manufacturing and yield traits had been predicted utilizing on-farm measurable traits, corresponding to dry matter consumption and common each day acquire. A complete of 4,578 Japanese Black steers, which had been progenies of 362 sires genotyped with imputed 551,995 single nucleotide polymorphisms (SNPs), had phenotypes of predicted methane-related traits throughout the complete fattening interval (52 weeks).

For the estimation of genetic parameters, the estimated heritabilities had been reasonable (ranged from 0.57 to 0.60). In addition, the estimated genetic correlations of methane manufacturing traits with most of carcass traits and feed-efficiency traits had been unfavorable, however these of methane yield traits had been favorable or low. For the GWAS, no genome-wide vital SNP was detected, however a complete of 4 quantitative trait locus (QTL) areas that defined greater than 5.0% of genetic variance had been localized on the genome, and some candidate genes related to progress and feed-efficiency traits had been situated on the areas.

Our outcomes counsel that the expected methane-related traits are heritable and some QTL areas for the traits are localized on the genome in Japanese Black steers.