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Anti-Mullerian hormone is a member of the transforming growth factor-beta gene family which mediates male sexual differentiation. Additionally we are shipping AMH Antibodies (111) and AMH Kits (65) and many more products for this protein.
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nuclear receptor subfamily 5, group A, member 1b is a new candidate for sex determination and differentiation in a way similar to steroidogenic factor 1 (show NR5A1 Proteins), possibly involving AMH
zebrafish Anti-Mullerian hormone (Amh) is regulated by sox9a, sox9b, and cyp19a1a during gonad development
amh is a candidate gene down-regulating cyp19a1a, leading to "juvenile ovary-to-testis" transformation.
It was shown that the male-to-female sex reversal phenotype in hotei medaka mutants is not a direct consequence of anti-Mullerian hormone signaling in supporting cells, but is instead mediated by germ cells.
Data from a longitudinal, observational study suggest that, among women with type 1 diabetes, AMH levels in serum decline in manner similar to that previously reported in women without diabetes; thus, it is possible that AMH may be used to risk-stratify women with type 1 diabetes at risk for diminished ovarian reserve and poor reproductive outcomes in a similar manner as used in healthy women.
Ile(49)Ser (show SIGLEC1 Proteins) genotype not associated with estradiol levels, ovarian parameters, menstrual cycle length, or pregnancy outcomes in healthy Singapore women
High serum Anti-Mullerian Hormone levels are associated with Polycystic Ovary Syndrome.
Women with systemic lupus erythematosus demonstrated similar AMH levels as healthy controls, suggesting preserved ovarian reserve in this population.
These findings contribute in clarifying the relationship between hormones regulating the early phase of steroidogenesis confirming that AMH is playing a suppressive role on CYP19A1 (show CYP19A1 Proteins) expression stimulated by gonadotropin in hGCs. Furthermore, a similar inhibitory effect for AMH was observed on P450scc (show CYP11A1 Proteins) gene expression when activated by gonadotropin treatment.
The AMH and AMHRII gene polymorphisms were not found a significant difference in non-IR-PCOS and normal groups. To IR-PCOS women, genotypes of AMH were closely related to the serum levels of LH (P = 0.000), testosterone (P = 0.000) and HOMA-IR (P = 0.038), while in the non-IR-PCOS and normal groups, no relationship was found
Plasma AMH levels were lower in chronic kidney disease stages 1-4 by 30% and by 70% in CKD stage 5 compared with controls.
The Sertoli cell hormones inhibin-B and anti Mullerian hormone have different patterns of secretion in prepubertal cryptorchid boys.
SNPs at the AMH gene locus that strongly predict serum AMH levels in males.
unilateral ovarian endometriosis had a moderately negative and nonsignificant effect on AMH-based ovarian reserve evaluated prior to surgery, irrespective of age
AMH increases GnRH-dependent LH pulsatility and secretion, supporting a central action of AMH on GnRH neurons.
AMH and FOXL2 (show FOXL2 Proteins) collaboratively work to reserve ovarian follicles. AMH is an endogenous target gene of FOXL2 (show FOXL2 Proteins).
Up-regulation of SOX9 (show SOX9 Proteins) in sertoli cells from testiculopathic patients accounts for increasing anti-mullerian hormone expression via impaired androgen receptor (show AR Proteins) signaling.
Male mice require AMH to undergo normal social development.
Data show that Purkinje cells express receptors for Mullerian inhibiting substance (MIS), and that MIS(-/-) male mice have female-like numbers of Purkinje cells and a female-like size to other parts of their cerebellum.
MIS may be involved in anterograde rather than autocrine or retrograde regulation of neurons.
FSH (show BRD2 Proteins) and cAMP stimulate AMH transcription by granulosa cells. FSH (show BRD2 Proteins) and LH have an additive effect, which may be important in polycystic ovary syndrome.
This suggests that MIS is one of the determinants of "boy"-specific behavior.
Role of anti-Mullerian hormone (AMH) as a regulator and marker of ovarian function.
Administration of MIS to male mice induced IEX-1S mRNA in the prostate in vivo, suggesting that MIS may function as an endogenous hormonal regulator of NF-kappaB (show NFKB1 Proteins) signaling and growth in the prostate gland.
These findings indicate the followings: AMH mRNA levels decrease in both dominant and secondary follicles during follicular deviation; granulosa cells from heathy follicles express more AMH mRNA compared to subordinate follicles undergoing atresia and FSH (show BRD2 Proteins) stimulates AMH and AMHR2 (show AMHR2 Proteins) mRNA expression in granulosa cells of co-dominant follicles.
Measurement of AMH concentration in the plasma of cows can help to predict their capacity for embryo production in response to gonadotrophin treatment.
In first study to investigate the blood profile and immunohuistochemistry of anti-Mullerian hormone in bovine granulosa-theca cell tumors, the findings indicated that anti-Mullerian hormone is a novel biomarker for granulosa-theca cell tumors in cattle.
Regulation of anti-Mullerian hormone production in the cow.
Intrafollicular AMH was not a marker of cystic development in the cow, but low AMH concentrations in cysts were associated with luteinization.
AMH expression is modulated by androgens in bovine granulosa cells from small follicles.
Anti-Mullerian hormone is a member of the transforming growth factor-beta gene family which mediates male sexual differentiation. Anti-Mullerian hormone causes the regression of Mullerian ducts which would otherwise differentiate into the uterus and fallopian tubes. Some mutations in the anti-Mullerian hormone result in persistent Mullerian duct syndrome.
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