protein kinase cAMP-dependent type I regulatory subunit alpha
RGD ID:
3391
Description:
Enables cAMP binding activity and cAMP-dependent protein kinase regulator activity. Involved in female meiotic nuclear division and negative regulation of meiotic nuclear division. Part of cAMP-dependent protein kinase complex. Human ortholog(s) of this gene implicated in Carney complex; acrodysostosis; and primary pigmented nodular adrenocortical disease. Orthologous to human PRKAR1A (protein kinase cAMP-dependent type I regulatory subunit alpha); PARTICIPATES IN acebutolol pharmacodynamics pathway; adrenergic beta receptor agonist and beta-blocker pharmacodynamics pathway; amiodarone pharmacodynamics pathway; INTERACTS WITH 17alpha-ethynylestradiol; 17beta-estradiol 3-benzoate; 2,3,7,8-tetrachlorodibenzodioxine.
cAMP-dependent protein kinase type I-alpha regulatory subunit; Protein kinase cAMP dependent regulatory type 1; protein kinase cAMP-dependent type 1 regulatory subunit alpha; protein kinase, cAMP dependent regulatory, type I, alpha; Protein kinase, cAMP dependent, regulatory, type 1; protein kinase, cAMP-dependent, regulatory subunit type I alpha; protein kinase, cAMP-dependent, regulatory, type I, alpha; RIIA
Note: On NCBI's build 4.2, GeneID 25725 (Prkar1a) was annotated incorrectly on chromosome X of the reference assembly but annotated correctly on chromosome 10 of the alternate Celera assembly. The chromosome X location appears to be a Prkar1a pseudogene now represented by GeneID 100510791 and the Reference Sequence NG_027837. [17 Jun 2014]
Dihydrotestosterone inhibits the reaction [[Androgens deficiency affects the activity of PRKAR1A gene mutant form] which results in increased secretion of Corticosterone] more ...
[PRKACB protein mutant form affects the susceptibility to Cyclic AMP] results in decreased stability of [PRKACB protein mutant form binds to PRKAR1A protein]
[PRKACB protein mutant form results in increased susceptibility to [Colforsin co-treated with 1-Methyl-3-isobutylxanthine]] results in decreased stability of [PRKACB protein mutant form binds to PRKAR1A protein]
[PRKACB protein mutant form results in increased susceptibility to 8-Bromo Cyclic Adenosine Monophosphate analog] results in decreased stability of [PRKACB protein mutant form binds to PRKAR1A protein]
[Acrolein co-treated with methacrylaldehyde co-treated with alpha-pinene co-treated with Ozone] results in decreased expression of and results in increased oxidation of PRKAR1A mRNA, [Air Pollutants results in increased abundance of [Acrolein co-treated with methacrylaldehyde co-treated with alpha-pinene co-treated with Ozone]] which results in decreased expression of and results in increased oxidation of PRKAR1A mRNA
[Acrolein co-treated with methacrylaldehyde co-treated with alpha-pinene co-treated with Ozone] results in decreased expression of and results in increased oxidation of PRKAR1A mRNA, [Air Pollutants results in increased abundance of [Acrolein co-treated with methacrylaldehyde co-treated with alpha-pinene co-treated with Ozone]] which results in decreased expression of and results in increased oxidation of PRKAR1A mRNA
[PRKACB protein mutant form results in increased susceptibility to [Colforsin co-treated with 1-Methyl-3-isobutylxanthine]] results in decreased stability of [PRKACB protein mutant form binds to PRKAR1A protein]
Dexamethasone inhibits the reaction [[PRKAR1A gene mutant form results in increased susceptibility to Androgens deficiency] which results in increased secretion of Corticosterone] more ...
[NOG protein co-treated with trichostatin A co-treated with dorsomorphin co-treated with 4-(5-benzo(1, 3)dioxol-5-yl-4-pyridin-2-yl-1H-imidazol-2-yl)benzamide] results in increased expression of PRKAR1A mRNA
[Acrolein co-treated with methacrylaldehyde co-treated with alpha-pinene co-treated with Ozone] results in decreased expression of and results in increased oxidation of PRKAR1A mRNA more ...
[perfluorooctane sulfonic acid co-treated with Cellulose] results in decreased expression of PRKAR1A mRNA, [perfluorooctane sulfonic acid co-treated with Inulin] results in decreased expression of PRKAR1A mRNA
[NOG protein co-treated with trichostatin A co-treated with dorsomorphin co-treated with 4-(5-benzo(1, 3)dioxol-5-yl-4-pyridin-2-yl-1H-imidazol-2-yl)benzamide] results in increased expression of PRKAR1A mRNA
[NOG protein co-treated with trichostatin A co-treated with dorsomorphin co-treated with 4-(5-benzo(1, 3)dioxol-5-yl-4-pyridin-2-yl-1H-imidazol-2-yl)benzamide] results in increased expression of PRKAR1A mRNA
Differential effects of haloperidol and clozapine on cAMP binding, protein kinase A (PKA) activity, and mRNA and protein expression of selective regulatory and catalytic subunit isoforms of PKA in rat brain.
The conformationally dynamic C helix of the RIalpha subunit of protein kinase A mediates isoform-specific domain reorganization upon C subunit binding.
