Gene Information
Gene Symbol
Entrez Gene ID
Gene Name
Inhibin, beta B
Chromosomal Location
The inhibin beta B subunit joins the alpha subunit to form a pituitary FSH secretion inhibitor. Inhibin has been shown to regulate gonadal stromal cell proliferation negatively and to have tumour-suppressor activity. In addition, serum levels of inhibin have been shown to reflect the size of granulosa-cell tumors and can therefore be used as a marker for primary as well as recurrent disease. Because expression in gonadal and various extragonadal tissues may vary severalfold in a tissue-specific fashion, it is proposed that inhibin may be both a growth/differentiation factor and a hormone. Furthermore, the beta B subunit forms a homodimer, activin B, and also joins with the beta A subunit to form a heterodimer, activin AB, both of which stimulate FSH secretion. (provided by RefSeq, Jul 2008)
GeneCards ID
RefSeq mRNA

Gene Ontology (GO)

GO ID Ontology Definition Evidence Reference
GO:0001541 Biological process Ovarian follicle development NAS 12790766
GO:0006952 Biological process Defense response TAS 3122219
GO:0009612 Biological process Response to mechanical stimulus IDA 10320815
GO:0030154 Biological process Cell differentiation NAS 10320815
GO:0032924 Biological process Activin receptor signaling pathway IDA 16650820
Protein Information
Protein Name
Inhibin beta B chain
Inhibins and activins inhibit and activate, respectively, the secretion of follitropin by the pituitary gland. Inhibins/activins are involved in regulating a number of diverse functions such as hypothalamic and pituitary hormone secretion, gonadal hormone secretion, germ cell development and maturation, erythroid differentiation, insulin secretion, nerve cell survival, embryonic axial development or bone growth, depending on their subunit composition. Inhibins appear to oppose the functions of activins
Refseq Proteins
Pfam Accession Pfam ID
PF00019 TGF_beta Transforming growth factor beta like domain
PF00688 TGFb_propeptide TGF-beta propeptide

Associated Diseases

Diseases References
Follicle arrest 9666869
Hyperandrogenism 20630504
Hypogonadotropic amenorrhea 8528356
Insulin resistance 20630504
Ovarian dysfunction 19240152

Comparison of follicle-stimulating-hormone-stimulated dimeric inhibin and estradiol responses as indicators of granulosa cell function in polycystic ovary syndrome and normal women.

Wachs Deborah S, Coffler Mickey S, Malcom Pamela J, Chang R Jeffrey
Department of Reproductive Medicine, School of Medicine, University of California-San Diego, 9500 Gilman Drive, La Jolla, CA 92093-0633, USA.
J Clin Endocrinol Metab. 2006 Aug;91(8):2920-5. Epub 2006 May 23.
Supporting Literature:
PubMed ID Associated gene/s Associated condition Genetic Mutation Diagnostic Criteria Association with PCOS Ethnicity Conclusion
Activin and follistatin 
Follicle development 
 PCOS patients were otherwise healthy, between the ages of 18–40 yr, had fewer than nine menses per yr, had been taking no medication for 3 months, and had biochemical and/or clinical evidence of hyperandrogenism. Each patient had at least two pelvic u 
These results suggest that insufficient production of inhibin alpha and possibly beta(A)-subunits, but not follistatin, is associated with follicular arrest in polycystic ovary syndrome follicles. 
Inhibin A 
Follicle development 
Rotterdam criteria 
These data demonstrate that inhibin A and inhibin B concentrations are significantly reduced in the follicular fluid of women with PCOS compared with those in the follicular fluid of size-matched follicles from normal women, consistent with the decreased inhibin subunit mRNA expression in previous studies.  
Adams et al. 
Italy and New York-46 PCOS and 25 controls 
Measurements of MIS reflect ovarian findings in PCOS better than levels of inhibin B and are more frequently elevated. However, MIS lacks sensitivity for use as a diagnostic tool in PCOS. 
Follicle development 
In PCOS women, the 24-h production of inhibin B and E(2) after FSH was significantly greater than that of normal controls. 
Either oligomenorrheic or amenorrheic, and all exhibited clinical and biochemical evidence of hyperandrogenism.Each PCOS subject exhibited ultrasound evidence of bilaterally enlarged polycystic ovaries and greater than 12 follicles per ovary.  
After FSH injection, PCOS women demonstrated enhanced production of 17-OHP, A, DHEA, and Inh B, whereas in normal women no increases were observed. T levels declined slightly in both groups. 


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