AMHR2

The anti-Müllerian hormone receptor type II (AMHR2) is a transmembrane serine/threonine kinase receptor that mediates the biological effects of anti-Müllerian hormone (AMH) in gonadal development and folliculogenesis^[1][2]. Mechanistically, AMHR2 forms a heteromeric complex with type I receptors to initiate SMAD1/5/8 phosphorylation, regulating granulosa cell differentiation, proliferation, and follicle selection^[1]. In vertebrate models, loss of AMHR2 function leads to male-to-female sex reversal in teleosts and affects ovarian follicle growth, indicating its critical role in sex differentiation and reproductive function^[2][3]. Compared with related type II receptors in the TGF-β superfamily, AMHR2 exhibits restricted expression in granulosa cells and fetal reproductive tissues, which underpins its specificity in AMH signaling^[1]. Polymorphisms in AMHR2, such as the -482 A>G variant, are associated with altered luteinizing hormone levels and polycystic ovary syndrome risk, highlighting its clinical relevance in human reproductive endocrinology^[4]. For experimental applications, synthetic agonists and antagonistic peptides, including AMHR2BP, can modulate granulosa cell proliferation, oocyte maturation, and protein expression of FSH-R, BMP15, and GDF9, thus providing tools for studying folliculogenesis and potential fertility interventions^[3]. Collectively, AMHR2 serves as a selective mediator of AMH-dependent reproductive signaling, with isoform-specific expression and function that can be leveraged for both mechanistic studies and translational research.