INHBB

Gene Information
 
Gene Symbol
INHBB
 
Aliases
-
 
Entrez Gene ID
 
Gene Name
Inhibin subunit beta B
 
Chromosomal Location
2q14.2
 
HGNC ID
 
Summary
This gene encodes a member of the TGF-beta (transforming growth factor-beta) superfamily of proteins. The encoded preproprotein is proteolytically processed to generate a subunit of the dimeric activin and inhibin protein complexes. These complexes activate and inhibit, respectively, follicle stimulating hormone secretion from the pituitary gland. Polymorphisms near this gene are associated with pre-eclampsia in female human patients. [provided by RefSeq, Aug 2016]
  e!Ensembl
Gene
Transcript  
Protein

Gene Ontology (GO)

GO ID Ontology Function Evidence Reference
GO:0001541 Biological process Ovarian follicle development NAS 12790766
GO:0006952 Biological process Defense response TAS 3122219
GO:0009611 Biological process Response to wounding IEP 10320815
GO:0010862 Biological process Positive regulation of pathway-restricted SMAD protein phosphorylation IBA 21873635
GO:0030154 Biological process Cell differentiation NAS 10320815
Protein Information
 
Protein Name
Inhibin beta B chain, Inhibin, beta-2, activin AB beta polypeptide, activin beta-B chain, inhibin beta B subunit
 
Function
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
 
UniProt
 
Pfam
Pfam Accession Pfam ID
PF00019 TGF_beta
PF00688 TGFb_propeptide
Pathways
 
KEGG
 
Reactome
 

Cytokine-cytokine receptor interaction
TGF-beta signaling pathway
Signaling pathways regulating pluripotency of stem cells

 

Signaling by Activin
Glycoprotein hormones
Antagonism of Activin by Follistatin

Interactions
 
STRING MINT IntAct
ENSP00000369927 P42330
    View interactions
     

Associated Diseases

Disease groupDisease NameReferences
Endocrine System Diseases
Familial Testotoxicosis
PCOS
References
 
 
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 1840 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 ultr 
Related 
 
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 
Related 
 
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. 
E(2) 
 
 
Adams et al. 
Related 
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. 
E(2) 
Follicle development 
 
 
Related 
 
In PCOS women, the 24-h production of inhibin B and E(2) after FSH was significantly greater than that of normal controls. 
DHEA 
 
 
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.  
Related 
 
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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