Enables cAMP-dependent protein kinase inhibitor activity. Predicted to act upstream of or within negative regulation of protein import into nucleus; negative regulation of protein kinase activity; and negative regulation of transcription by RNA polymerase II. Predicted to be active in cytoplasm and nucleus. Orthologous to human PKIG (cAMP-dependent protein kinase inhibitor gamma); INTERACTS WITH 2,3,7,8-tetrachlorodibenzodioxine; bisphenol A; dibutyl phthalate.
[Tetrachlorodibenzodioxin co-treated with Ethinyl Estradiol] results in increased expression of PKIG mRNA and Tetrachlorodibenzodioxin inhibits the reaction [EGF protein results in increased expression of PKIG mRNA]
[Benzo(a)pyrene co-treated with benz(a)anthracene co-treated with benzo(b)fluoranthene co-treated with chrysene] results in increased expression of PKIG mRNA
[Benzo(a)pyrene co-treated with benz(a)anthracene co-treated with benzo(b)fluoranthene co-treated with chrysene] results in increased expression of PKIG mRNA
[Benzo(a)pyrene co-treated with benz(a)anthracene co-treated with benzo(b)fluoranthene co-treated with chrysene] results in increased expression of PKIG mRNA
[Benzo(a)pyrene co-treated with benz(a)anthracene co-treated with benzo(b)fluoranthene co-treated with chrysene] results in increased expression of PKIG mRNA
Endogenous protein kinase inhibitor gamma terminates immediate-early gene expression induced by cAMP-dependent protein kinase (PKA) signaling: termination depends on PKA inactivation rather than PKA export from the nucleus.