Enables cyclic-nucleotide phosphodiesterase activity. Involved in negative regulation of cAMP-mediated signaling and negative regulation of cGMP-mediated signaling. Located in perikaryon. Is active in glutamatergic synapse. Is extrinsic component of postsynaptic density membrane. Biomarker of traumatic brain injury. Orthologous to human PDE10A (phosphodiesterase 10A); PARTICIPATES IN adenine phoshoribosyltransferase deficiency pathway; adenosine monophosphate deaminase deficiency pathway; adenylosuccinate lyase deficiency pathway; INTERACTS WITH 17alpha-ethynylestradiol; 17beta-estradiol; 2,2',4,4'-Tetrabromodiphenyl ether.
[NOG protein co-treated with belinostat co-treated with dorsomorphin co-treated with 4-(5-benzo(1 and 3)dioxol-5-yl-4-pyridin-2-yl-1H-imidazol-2-yl)benzamide] results in decreased expression of PDE10A mRNA
[bisphenol A co-treated with Estradiol] results in increased expression of PDE10A mRNA and [bisphenol A co-treated with Testosterone] results in increased expression of PDE10A mRNA
Dipyridamole inhibits the reaction [PDE10A protein results in increased hydrolysis of Cyclic AMP] and Dipyridamole inhibits the reaction [PDE10A protein results in increased hydrolysis of Cyclic GMP]
[NOG protein co-treated with entinostat co-treated with dorsomorphin co-treated with 4-(5-benzo(1 and 3)dioxol-5-yl-4-pyridin-2-yl-1H-imidazol-2-yl)benzamide] results in decreased expression of PDE10A mRNA
[NOG protein co-treated with mercuric bromide co-treated with dorsomorphin co-treated with 4-(5-benzo(1 and 3)dioxol-5-yl-4-pyridin-2-yl-1H-imidazol-2-yl)benzamide] results in decreased expression of PDE10A mRNA
[NOG protein co-treated with p-Chloromercuribenzoic Acid co-treated with dorsomorphin co-treated with 4-(5-benzo(1 and 3)dioxol-5-yl-4-pyridin-2-yl-1H-imidazol-2-yl)benzamide] results in decreased expression of PDE10A mRNA
[NOG protein co-treated with Panobinostat co-treated with dorsomorphin co-treated with 4-(5-benzo(1 and 3)dioxol-5-yl-4-pyridin-2-yl-1H-imidazol-2-yl)benzamide] results in decreased expression of PDE10A mRNA
[NOG protein co-treated with Phenylmercuric Acetate co-treated with dorsomorphin co-treated with 4-(5-benzo(1 and 3)dioxol-5-yl-4-pyridin-2-yl-1H-imidazol-2-yl)benzamide] results in decreased expression of PDE10A mRNA
[NOG protein co-treated with trichostatin A co-treated with dorsomorphin co-treated with 4-(5-benzo(1 and 3)dioxol-5-yl-4-pyridin-2-yl-1H-imidazol-2-yl)benzamide] results in decreased expression of PDE10A mRNA
[NOG protein co-treated with Valproic Acid co-treated with dorsomorphin co-treated with 4-(5-benzo(1 and 3)dioxol-5-yl-4-pyridin-2-yl-1H-imidazol-2-yl)benzamide] results in decreased expression of PDE10A mRNA
[NOG protein co-treated with Vorinostat co-treated with dorsomorphin co-treated with 4-(5-benzo(1 and 3)dioxol-5-yl-4-pyridin-2-yl-1H-imidazol-2-yl)benzamide] results in decreased expression of PDE10A mRNA
Subcellular localization of cyclic nucleotide phosphodiesterase type 10A variants, and alteration of the localization by cAMP-dependent protein kinase-dependent phosphorylation.