Predicted to enable cytokine activity. Predicted to be involved in BMP signaling pathway; SMAD protein signal transduction; and positive regulation of pathway-restricted SMAD protein phosphorylation. Predicted to be active in extracellular space. Orthologous to human INHBC (inhibin subunit beta C); PARTICIPATES IN transforming growth factor-beta superfamily mediated signaling pathway; INTERACTS WITH (+)-schisandrin B; 1-naphthyl isothiocyanate; 4,4'-diaminodiphenylmethane.
[INS protein co-treated with Dexamethasone co-treated with 1-Methyl-3-isobutylxanthine co-treated with Indomethacin co-treated with bisphenol A] results in decreased expression of INHBC mRNA
[bisphenol A co-treated with Fulvestrant] results in increased methylation of INHBC gene, [INS protein co-treated with Dexamethasone co-treated with 1-Methyl-3-isobutylxanthine co-treated with Indomethacin co-treated with bisphenol A] results in decreased expression of INHBC mRNA
[Tetradecanoylphorbol Acetate co-treated with Calcimycin] results in increased expression of INHBC mRNA, fulvic acid inhibits the reaction [[Tetradecanoylphorbol Acetate co-treated with Calcimycin] results in increased expression of INHBC mRNA]
[INS protein co-treated with Dexamethasone co-treated with 1-Methyl-3-isobutylxanthine co-treated with Indomethacin co-treated with bisphenol A] results in decreased expression of INHBC mRNA
[INS protein co-treated with Dexamethasone co-treated with 1-Methyl-3-isobutylxanthine co-treated with Indomethacin co-treated with bisphenol A] results in decreased expression of INHBC mRNA
[Tetradecanoylphorbol Acetate co-treated with Calcimycin] results in increased expression of INHBC mRNA, fulvic acid inhibits the reaction [[Tetradecanoylphorbol Acetate co-treated with Calcimycin] results in increased expression of INHBC mRNA]