Activin and inhibin are two closely related protein complexes that have almost directly opposite biological effects.
Identified in 1986,[1][2] activin enhances FSH biosynthesis and secretion, and participates in the regulation of the menstrual cycle.
[10] In addition, both complexes are derived from the same family of related genes and proteins but differ in their subunit composition.
[13] Activin is produced in the gonads, pituitary gland, placenta, and other organs: In both females and males, inhibin inhibits FSH production.
[16][17] However, the overall mechanism differs between the sexes: Inhibin is produced in the gonads, pituitary gland, placenta, corpus luteum and other organs.
Smad3 then translocates to the nucleus and interacts with SMAD4 through multimerization, resulting in their modulation as transcription factor complexes responsible for the expression of a large variety of genes.
[21] This condition is characterized by the formation of an extra skeleton that produces immobilization and eventually death by suffocation.
[21] On 2 September 2015, Regeneron Pharmaceuticals announced that they had developed an antibody for activin A that effectively cures the disease in an animal model of the condition.
[27] Quantification of inhibin A is part of the prenatal quad screen that can be administered during pregnancy at a gestational age of 16–18 weeks.
[31] In men with azoospermia, a positive test for inhibin B slightly raises the chances for successfully achieving pregnancy through testicular sperm extraction (TESE), although the association is not very substantial, having a sensitivity of 0.65 (95% confidence interval [CI]: 0.56–0.74) and a specificity of 0.83 (CI: 0.64–0.93) for prediction the presence of sperm in the testes in non-obstructive azoospermia.