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Human AMH Protein expressed in HEK-293 Cells - ABIN2714759
Signorile, Petraglia, Baldi: Anti-mullerian hormone is expressed by endometriosis tissues and induces cell cycle arrest and apoptosis in endometriosis cells. in Journal of experimental & clinical cancer research : CR 2014
Gdf9 significantly suppressed the expression of amh while increased that of activin beta subunits (inhbaa and inhbb) in vitro.
These data suggest that an important aspect of Fsh bioactivity in stimulating spermatogenesis is implemented by restricting the different inhibitory effects of Amh and by counterbalancing them with stimulatory signals, such as Igf3.
amh controls the balance between proliferation and differentiation of male germ cells.
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, 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.
Moderate elevations in AMH levels can severely restrict reproductive output and the number of developing follicles in the ovary. This evidence suggests that early antral follicles are a target for AMH signaling, which may regulate early follicle survival.
AMH levels were found to be increased in polycystic ovary syndrome patients compared to controls.
Pregnant women with polycystic ovary syndrome present with elevated AMH and androgen levels even at term, suggesting a hormonal imbalance during PCOS pregnancy.
AMH expression was confirmed in 23 patients with well differentiated endometrioid adenocarcinoma (G1), moderately differentiated endometrioid adenocarcinoma (G2), clear cell carcinoma (CCA) and nonatypical hyperplasia. AMH was not found in endometrial cancer tissues in regularly menstruating women.
In premenopausal patients with HR+ eBC, prechemotherapy AMH concentration was associated with the patient's 2-year amenorrhea status, independent of age. The nomogram model based on age and pretreatment AMH and FSH levels accurately predicted the 2-year amenorrhea status.
Serum AMH levels may reflect the primordial follicle stockpile and may predict outcomes of in vitro maturation and ovarian tissue cryopreservation when performed for fertility preservation.
Higher luteinizing hormone levels are associated with antimullerian hormone in postmenarchal daughters of women with polycystic ovary syndrome.
These findings highlight a critical role for excess prenatal AMH exposure and subsequent aberrant GnRH receptor signaling in the neuroendocrine dysfunctions of polycystic ovary syndrome.
AMH [anti-Mullerian hormone] has no predictive value of clinical pregnancy outcomes for patients with in vitro fertilization and embryo transfer treatment, while age has certain predictive value of pregnancy outcomes. AMH level may have indictive value for the evaluation of ovarian reserve.
Serum AMH concentrations decreased in endometrioma patients, at 6 and 12 months following cystectomy.
Women with higher testosterone and AMH had more frequent anovulatory cycles but there were marginal impacts on time to pregnancy or pregnancy loss.
These findings indicate a pregnancy-associated AMH-decline independent of pre-pregnancy elevated AMH levels.
serum AMH levels were negatively correlated with age. AMH concentrations approximately 31.1% depended on age and descended by an average of 6.2% per year. Around 25, 35 and 40 years, the decrease of AMH values accelerated.
AMH is a poor independent predictor of live birth outcome in either fresh or frozen embryo transfer.
AMH, IGF1 and leptin levels in follicular fluid have no relation to the fertility disorders caused by endometriosis or fallopian tube damage, though they are biomarkers for anovulatory fertility disorders.
serum levels between women with insulin resistance and without insulin resistance in polycystic ovary syndrome were not significantly different
Data suggest that serum levels of AMH are down-regulated during second half of gestation in (1) women with gestational diabetes, (2) pregnant women with type 2 diabetes, and (3) control pregnant women. A positive association between AMH and testosterone levels was observed in all groups. Also, serum AMH levels are negatively associated with maternal age in the population studied.
Data confirm that serum levels of AMH decline as function of age (not menstrual cycle) in women ages 20-50; here, results of ELISA assays of serum levels of AMH vary according to kit used. These studies were conducted at a fertility clinic in Poland; serum AMH is proposed as biomarker for ovarian reserve.
AMH single nucleotide polymorphism is associated with Endometriosis-associated infertility.
This study demonstrated the existence of an AMH-FOXL2 relationship in hGCs. AMH is capable of increasing both gene and protein expression of FOXL2. Because FOXL2 induces AMH transcription, these ovarian factors could be finely regulated by a positive feedback loop mechanism to preserve the ovarian follicle reserve.
These results suggest that AMH acts on the Mullerian duct in male mice by exuding into the interstitium surrounding the testis cord and infiltrating through the cranial region from the testis to the mesonephros.
Surface plasmon resonance analysis showed no significant association between FS288 and AMHC , suggesting that FS288 indirectly regulates AMH signaling. Activin A, a direct target of FS288, did not itself induce reporter activity in P19 cells, but did prevent the FS288-induced increase in AMH signaling. Hence, local concentrations of FS288 and Activin A may influence the response of some cell types to AMH.
AMH increases GnRH-dependent LH pulsatility and secretion, supporting a central action of AMH on GnRH neurons.
AMH and FOXL2 collaboratively work to reserve ovarian follicles. AMH is an endogenous target gene of FOXL2.
Up-regulation of SOX9 in sertoli cells from testiculopathic patients accounts for increasing anti-mullerian hormone expression via impaired androgen receptor 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 and cAMP stimulate AMH transcription by granulosa cells. FSH 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 signaling and growth in the prostate gland.
cAMP induces expression of Cyp17 by a PKA-mediated mechanism which is inhibited by MIS signal transduction
prepubertal testicular AMH production is increased by follicle-stimulating hormone stimulation through Sertoli cell proliferation and an enhancement of anti-Mullerian hormone gene transcription.
In postnatal ovary, granulosa cells of growing follicles express FOG-2, partially overlapping with the expression of MIS.
the AMH promoter in mice is activated by SOX8 during testis differentiation
Mullerian inhibiting substance regulates gonadotropin gene expression
stage-specific oocyte regulation of antimullerian hormone expression may play a role in intra- and inter-follicular coordination of follicle development
steroidogenic capacity appears to be mediated by a direct loss of MIS action in Leydig cells as well as by indirect effects via the hypothalamic-pituitary-gonadal axis in knockout mice
By avoiding premature exhaustion of the ovarian follicular reserve, AMH may contribute to optimization of reproductive performance in female pigs.
Anti-Mullerian hormone inhibits activation and growth of bovine ovarian follicles in vitro and is localized to growing follicles.
This study showed that antral follicle counts (AFC) and AMH levels were repeatable when determined at an unknown stage of follicular growth and expected day of follicular wave emergence, but repeatability was greater for AMH than AFC.
The effects of castration and other surgical intervention on the blood levels of anti-Muellerian hormone, inhibin A, gonadotropins, and gonadotropin receptors in bull calves are reported.
Results from these studies indicate that AMH signaling plays a role in both regulating granulosa cell proliferation and preventing granulosa cells from 5- to 8-mm follicles from undergoing premature differentiation before follicle selection.
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 stimulates AMH and AMHR2 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.
, anti-Mullerian hormone
, anti-mullerian hormone
, Mullerian inhibiting factor
, Mullerian inhibiting substance
, anti-Muellerian hormone
, muellerian-inhibiting substance
, Mullerian inhibitory substance
, Anti - Mullerian hormone (Mulerian inhibiting substance)