EC Number |
General Information |
Reference |
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3.2.2.6 | malfunction |
ablation of the CD38 gene in mice causes multiple physiological defects, including impaired oxytocin release, that result in altered social behavior |
731296 |
3.2.2.6 | physiological function |
CD38 is an ectoenzyme that consumes NAD+ to produce cyclic ADP-ribose, a potent agonist of ryanodine receptors. Basal CD38/cyclic ADP-ribose-dependent signaling plays a key role in ATP release, which mediates basal survival of microglia, overview |
731882 |
3.2.2.6 | physiological function |
CD38 is an NAD+-metabolizing enzyme in mammals, a type II transmembrane protein that converts NAD+ primarily to adenosine diphosphate ribose and a small amount of cyclic adenosine diphosphate ribose. The major enzymatic function of the enzyme is to hydrolyze extracellular rather than intracellular NAD+ |
731987 |
3.2.2.6 | malfunction |
CD38 knockout mice manifest multiple defects relating to Ca2+ signaling, including that of insulin secretion, hormonal signaling in pancreatic acinar cells, migration of dendritic cell precursors, bone resorption, airway responsiveness, alpha-adrenoceptor signaling in aorta, cardiac hypertrophy, susceptibility to bacterial infection, as well as social behavior in mice through modulation of oxytocin secretion |
716910 |
3.2.2.6 | malfunction |
CD38 reductions lead to microglial apoptosis. inhibition of CD38/cADPR-dependent signaling by CD38 silencing or 8-bromo-cADPR, a ryanodine receptor antagonist, produced significant ATP release from BV2 microglia. Cx43 small interfering RNA and Cx43 hemichannel blocker 18-alpha-glycyrrhetinic acid completely prevented the CD38 silencing or 8-bromo-cADPR-induced ATP release. Prevention of the ATP release might also be due to P2X7 receptor antagonists. Key role of ATP release in the microglial apoptosis induced by decreased CD38/cADPR-dependent signaling, overview |
731882 |
3.2.2.6 | more |
D226/Q226 and K129 residues of the two CD38 enzyme are the ADP-ribosylation sites. 6-Alkyne-F-araNAD, 6-alkyne-NAD, and Rh-N3 are used in the labeling reactions of CD38 wild-type and mutants, overview |
731119 |
3.2.2.6 | physiological function |
in cultured macrophages, lipopolysaccharide LPS can upregulate CD38 expression in time- and dose-dependent manner. Knocking down or blockade of CD38 in macrophages inhibits LPS-induced macrophage M1 polarization accompanied by diminished NF-kappaB signaling activation. In a mouse model with LPS-induced acute kidney injury, blocking CD38 with quercetin significantly relieves kidney dysfunction, kidney pathological changes as well as inflammatory cell accumulation |
750282 |
3.2.2.6 | more |
invariant glutamate 218 identified is the catalytic residue of the enzyme, Structure homology modelling, overview |
732691 |
3.2.2.6 | physiological function |
leukocyte antigen CD38 expression is an early marker of all-trans retinoic acid-stimulated differentiation in the leukemic cell line HL-60 where CD38 promotes induced myeloid maturation when overexpressed. The ability of CD38 to propel all-trans retinoic acid-induced myeloid differentiation and G1/0 arrest is unimpaired by loss of its ectoenzymeactivity |
714921 |
3.2.2.6 | physiological function |
senescent cells do not have high expression of CD38. The senescent associated secretory phenotype factors secreted by senescent cells induce CD38 mRNA and protein expression and increase CD38-NADase activity in non-senescent cells such as endothelial cells or bone marrow derived macrophages |
749830 |