Inhibin subunit alpha (INHA)

Inhibin subunit alpha is a glycoprotein produced primarily in the gonads and is an obligate partner in inhibin A and B heterodimers, which are members of the TGF-beta superfamily[1][2][4]. These heterodimers (alpha with either beta-A or beta-B subunits) act as endocrine hormones antagonizing activin signaling and serving as key negative feedback regulators of follicle-stimulating hormone (FSH) secretion from the pituitary gland[1][2]. Inhibin thereby coordinates reproductive function in both sexes, regulates gonadal hormone secretion, germ cell development, and impacts additional physiological processes such as apoptosis, immune responses, and cell proliferation[2][3]. Alterations in INHA function or expression are strongly implicated in reproductive disorders such as premature ovarian failure, male infertility, and several endocrine-related cancers[2][4]. Experimental data further highlight the unique role of the INHA N-terminal region in mediating direct antagonism of activin signaling, specifically through binding to the activin type I receptor (ALK4), disrupting activin receptor complex formation at the pituitary[1]. Inhibin A and B (which require INHA) are clinically used as serological biomarkers for ovarian and testicular neoplasms, and in fertility diagnostics[2][3].

Other names

Inhibin alpha chainA-inhibin subunitInhibin alpha subunitINHA

Experimental anti-inhibin antibodies: neutralization of inhibin's antagonism of activin, thereby increasing FSH (primarily studied in animal models)[1]. Inhibin antagonism of activin: Binds activin type II receptor and betaglycan to block activin signaling[1][2]. Modulation of pituitary feedback on FSH.