EC Number |
General Information |
Reference |
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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 | 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 |
3.2.2.6 | physiological function |
the enzyme is a signaling enzyme responsible for catalyzing the synthesis of cyclic ADP ribose (cADPR) and nicotinic acid adenine dinucleotide phosphate, both are universal Ca2+ messenger molecules |
731296 |
3.2.2.6 | physiological function |
the enzyme is CD38-cADPR signaling system in frog cells |
732501 |