Predicted to enable acid sphingomyelin phosphodiesterase activity and zinc ion binding activity. Involved in several processes, including ceramide biosynthetic process; positive regulation of apoptotic process; and response to cocaine. Located in extracellular space and lamellar body. Used to study Wilson disease. Human ortholog(s) of this gene implicated in Niemann-Pick disease; Niemann-Pick disease type A; and Niemann-Pick disease type B. Orthologous to human SMPD1 (sphingomyelin phosphodiesterase 1); PARTICIPATES IN ceramide signaling pathway; FasL mediated signaling pathway; Trail mediated signaling pathway; INTERACTS WITH 17alpha-ethynylestradiol; 2,3,7,8-tetrachlorodibenzodioxine; 3,3',4,4',5-pentachlorobiphenyl.
[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 SMPD1 mRNA
[Amitriptyline results in decreased expression of and results in decreased activity of SMPD1 protein] which results in decreased abundance of Ceramides and Amitriptyline results in decreased expression of and results in decreased activity of SMPD1 protein
[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 SMPD1 mRNA
[S-allylcysteine co-treated with Clotrimazole] inhibits the reaction [lead acetate results in increased activity of SMPD1 protein] and Clotrimazole inhibits the reaction [lead acetate results in increased activity of SMPD1 protein]
[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 SMPD1 mRNA
[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 SMPD1 mRNA
[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 SMPD1 mRNA
[Fluoxetine results in decreased expression of and results in decreased activity of SMPD1 protein] which results in decreased abundance of Ceramides and Fluoxetine results in decreased expression of and results in decreased activity of SMPD1 protein
[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 SMPD1 mRNA
Morphine affects the reaction [SMPD1 protein affects the abundance of Ceramides] and Naloxone inhibits the reaction [Morphine results in increased expression of SMPD1 protein]
SMPD1 mutant form inhibits the reaction [Tetradecanoylphorbol Acetate results in increased expression of and results in increased stability of IL6 mRNA] and SMPD1 mutant form inhibits the reaction [Tetradecanoylphorbol Acetate results in increased expression of IL6 protein]
[S-allylcysteine co-treated with Clotrimazole] inhibits the reaction [lead acetate results in increased activity of SMPD1 protein] and S-allylcysteine inhibits the reaction [lead acetate results in increased activity of SMPD1 protein]
[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 SMPD1 mRNA
[vorinostat co-treated with sorafenib] promotes the reaction [SMPD1 protein results in increased abundance of Ceramides] and SMPD1 protein promotes the reaction [[vorinostat co-treated with sorafenib] affects the localization of FAS protein]
[vorinostat co-treated with sorafenib] promotes the reaction [SMPD1 protein results in increased abundance of Ceramides] and SMPD1 protein promotes the reaction [[vorinostat co-treated with sorafenib] affects the localization of FAS protein]
Oxidized phospholipids in minimally modified low density lipoprotein induce apoptotic signaling via activation of acid sphingomyelinase in arterial smooth muscle cells.
