Enables diacylglycerol kinase activity. Involved in diacylglycerol metabolic process; lipid phosphorylation; and phosphatidic acid biosynthetic process. Located in several cellular components, including postsynaptic density; presynaptic active zone; and synaptic membrane. Is active in glutamatergic synapse and synaptic vesicle. Is extrinsic component of postsynaptic density membrane and extrinsic component of presynaptic active zone membrane. Orthologous to human DGKI (diacylglycerol kinase iota); PARTICIPATES IN glycerolipid metabolic pathway; glycerophospholipid metabolic pathway; phosphatidylinositol 3-kinase signaling pathway; INTERACTS WITH 17alpha-ethynylestradiol; 2,3,7,8-tetrachlorodibenzodioxine; 2,3,7,8-Tetrachlorodibenzofuran.
[NOG protein co-treated with belinostat 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 DGKI mRNA
[NOG protein co-treated with mercuric bromide 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 DGKI mRNA
[Diethylnitrosamine co-treated with Phenobarbital] results in decreased methylation of DGKI promoter, [Diethylnitrosamine co-treated with Phenobarbital] results in increased expression of DGKI mRNA
[NOG protein co-treated with p-Chloromercuribenzoic Acid 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 DGKI mRNA
[Diethylnitrosamine co-treated with Phenobarbital] results in decreased methylation of DGKI promoter, [Diethylnitrosamine co-treated with Phenobarbital] results in increased expression of DGKI 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 DGKI mRNA
in Northern blot analysis, a major transcript of 3.3 kb was detected exclusively in brain and eye out of 11 tissues tested; testis showed only a shorter trascript (1.2 kb) of unknown origin
in brain, in situ hybridization showed strong signals in the hippocampus, cerebellar cortex, olfactory bulb and olfactory tubercle, and moderate signals in cerebral cortex, caudate putamen and thalamus
tanscript varient 1 codes for the full length Dgki protein; transcript varients 2 and 3 code for proteins which lack the C-terminal ankyrin repeats and varient 3 also lacks a portion of the DGK catalytic domain
enzymatic activity of the protein encoded by transcript varient 2 is approximately half that of varient 1; activity of the varient 3 protein is essentially background
three transcript varients have been characterized in the brain; varients 2 and 3 contain 19 bp and 71 bp inserts, respectively, resulting in frameshift mutations which give rise to premature stop codons