Enables identical protein binding activity and mitogen-activated protein kinase p38 binding activity. Involved in several processes, including cell growth involved in cardiac muscle cell development; regulation of cellular biosynthetic process; and regulation of ion transport. Located in several cellular components, including Golgi apparatus; acrosomal vesicle; and nucleoplasm. Colocalizes with sarcolemma. Biomarker of allergic rhinitis; hypertension; hypogonadism; impotence; and obesity. Human ortholog(s) of this gene implicated in thoracic aortic aneurysm. Orthologous to human PRKG1 (protein kinase cGMP-dependent 1); PARTICIPATES IN eicosanoid signaling pathway; long term depression; INTERACTS WITH 1H-[1,2,4]oxadiazolo[4,3-a]quinoxalin-1-one; 3,4-methylenedioxymethamphetamine; 4-Hydroxy-TEMPO.
cAMP-dependent protein kinase catalytic subunit PRKX-like; cGk1; cGMP dependent protein kinase type 1; cGMP dependent protein kinase type1; cGMP-dependent protein kinase 1; LOC100912084; LOC365449; Pkgi; Prkg1_mapped; protein kinase, cGMP-dependent, type 1; protein kinase, cGMP-dependent, type 1 (mapped); Protein kinase, cGMP-dependent, type I
[INS protein co-treated with Dexamethasone co-treated with 1-Methyl-3-isobutylxanthine co-treated with Indomethacin co-treated with bis(4-hydroxyphenyl)sulfone] results in increased expression of PRKG1 mRNA more ...
[INS protein co-treated with Dexamethasone co-treated with 1-Methyl-3-isobutylxanthine co-treated with Indomethacin co-treated with bis(4-hydroxyphenyl)sulfone] results in increased expression of PRKG1 mRNA
[8-((4-chlorophenyl)thio)cyclic-3', 5'-GMP co-treated with PRKG1 protein alternative form] inhibits the reaction [Phenylephrine results in increased expression of NPPA mRNA]
[bisphenol A co-treated with Fulvestrant] results in increased methylation of PRKG1 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 increased expression of PRKG1 mRNA
[INS protein co-treated with Dexamethasone co-treated with 1-Methyl-3-isobutylxanthine co-treated with Indomethacin co-treated with bisphenol F] results in increased expression of PRKG1 mRNA
[calyculin A co-treated with Okadaic Acid] inhibits the reaction [2-methyl-1-((4-methyl-5-isoquinolinyl)sulfonyl)homopiperazine inhibits the reaction [[8-((4-chlorophenyl)thio)cyclic-3', 5'-GMP co-treated with PRKG1 protein] results in increased activity of ARHGEF17 protein]]
[Phenylephrine co-treated with Copper] results in increased activity of PRKG1 protein, VIM mutant form inhibits the reaction [[Copper co-treated with Phenylephrine] results in increased activity of PRKG1 protein]
[Phenylephrine co-treated with Copper] results in increased activity of PRKG1 protein, VIM mutant form inhibits the reaction [[Copper co-treated with Phenylephrine] results in increased activity of PRKG1 protein]
Phenylephrine inhibits the reaction [Cyclosporine results in increased expression of PRKG1 mRNA], Phenylephrine inhibits the reaction [Cyclosporine results in increased expression of PRKG1 protein]
[INS protein co-treated with Dexamethasone co-treated with 1-Methyl-3-isobutylxanthine co-treated with Indomethacin co-treated with bis(4-hydroxyphenyl)sulfone] results in increased expression of PRKG1 mRNA more ...
[NOG protein co-treated with Phenylmercuric Acetate 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 decreased expression of PRKG1 mRNA
[INS protein co-treated with Dexamethasone co-treated with 1-Methyl-3-isobutylxanthine co-treated with Indomethacin co-treated with bis(4-hydroxyphenyl)sulfone] results in increased expression of PRKG1 mRNA more ...
[calyculin A co-treated with Okadaic Acid] inhibits the reaction [2-methyl-1-((4-methyl-5-isoquinolinyl)sulfonyl)homopiperazine inhibits the reaction [[8-((4-chlorophenyl)thio)cyclic-3', 5'-GMP co-treated with PRKG1 protein] results in increased activity of ARHGEF17 protein]]
[NOG protein co-treated with Phenylmercuric Acetate 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 decreased expression of PRKG1 mRNA
Resveratrol promotes the reaction [Vitamin K 3 results in increased oxidation of PRKG1 protein], Resveratrol results in increased oxidation of and results in increased activity of PRKG1 protein
[S-Nitroso-N-Acetylpenicillamine co-treated with PRKG1 protein alternative form] inhibits the reaction [Phenylephrine results in increased expression of NPPA mRNA]
[NOG protein co-treated with Phenylmercuric Acetate 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 decreased expression of PRKG1 mRNA
PRKG1 protein promotes the reaction [Sildenafil Citrate inhibits the reaction [AGT protein modified form results in increased expression of CCN2 mRNA]] more ...
5-Methoxypsoralen inhibits the reaction [Streptozocin results in decreased expression of PRKG1 protein], Tadalafil inhibits the reaction [Streptozocin results in decreased expression of PRKG1 protein]
[Tadalafil co-treated with Thioacetamide] results in increased expression of PRKG1 protein, Tadalafil inhibits the reaction [Streptozocin results in decreased expression of PRKG1 protein]
testosterone enanthate promotes the reaction [Triptorelin Pamoate results in decreased expression of PRKG1 mRNA], testosterone enanthate promotes the reaction [Triptorelin Pamoate results in decreased expression of PRKG1 protein]
testosterone enanthate promotes the reaction [Triptorelin Pamoate results in decreased expression of PRKG1 mRNA], testosterone enanthate promotes the reaction [Triptorelin Pamoate results in decreased expression of PRKG1 protein]
Y 27632 inhibits the reaction [[8-((4-chlorophenyl)thio)cyclic-3', 5'-GMP co-treated with PRKG1 protein] results in increased activity of ARHGEF17 protein]
expressed at high levels in cerebellar Purkinje cells and human platelets, moderately in vascular smooth muscle cells, and at a lower levels in cardiac myocytes
lowers intracellular Ca2+, and inhibits vascular smooth muscle contraction, platelet activation and endothelial cell permeability, thereby opposing events leading to hypertension, thrombosis, and atherosclerosis
