Receptor for follicle-stimulating hormone. The activity of this receptor is mediated by G proteins which activate adenylate cyclase.
Sertoli cells and ovarian granulosa cells.
Defects in FSHR are a cause of ovarian dysgenesis type 1 (ODG1) [MIM:233300]; also known as premature ovarian failure or gonadal dysgenesis XX type or XX gonadal dysgenesis (XXGD) or hereditary hypergonadotropic ovarian failure or hypergonadotropic ovarian dysgenesis with normal karyotype. ODG1 is an autosomal recessive disease characterized by primary amenorrhea, variable development of secondary sex characteristics, and high serum levels of follicle-stimulating hormone (FSH) and luteinizing hormone (LH). Defects in FSHR are a cause of ovarian hyperstimulation syndrome (OHSS) [MIM:608115]. OHSS is a disorder which occurs either spontaneously or most often as an iatrogenic complication of ovarian stimulation treatments for in vitro fertilization. The clinical manifestations vary from abdominal distention and discomfort to potentially life-threatening, massive ovarian enlargement and capillary leak with fluid sequestration. Pathologic features of this syndrome include the presence of multiple serous and hemorrhagic follicular cysts lined by luteinized cells, a condition called hyperreactio luteinalis.
Belongs to the G-protein coupled receptor 1 family. FSH/LSH/TSH subfamily. Contains 9 LRR (leucine-rich) repeats. Contains 1 LRRNT domain.
N-glycosylated; indirectly required for FSH-binding, possibly via a conformational change that allows high affinity binding of hormone.
Li X et al. Follicular Stimulating Hormone Accelerates Atherogenesis by Increasing Endothelial VCAM-1 Expression. Theranostics7:4671-4688 (2017).
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Sen A et al. Androgens regulate ovarian follicular development by increasing follicle stimulating hormone receptor and microRNA-125b expression. Proc Natl Acad Sci U S A111:3008-13 (2014).
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