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Mobilization of intracellular Ca2+ stores is involved inmany diverse cell functions, including: cell proliferation;differentiation; fertilization; muscle contraction; secre-tion of neurotransmitters, hormones and enzymes;and lymphocyte activation and proliferation. Cyclic ad-enosine diphosphate ribose(cADPR) is an endogenousCa2+ mobilizing nucleotide present in many cell typesand species, from plants to animals. cADPR is formedby ADP-ribosyl cyclases from nicotinamide adenine di-nucleotide. The main ADP-ribosyl cyclase in mammalsis CD38, a multi-functional enzyme and a type Ⅱ mem-brane protein. It has been shown that many extracel-lular stimuli can induce cADPR production that leadsto calcium release or influx, establishing cADPR as asecond messenger. cADPR has been linked to a widevariety of cellular processes, but the molecular mecha-nisms regarding cADPR signaling remain elusive. Theaim of this review is to summarize the CD38/cADPR/Ca2+ signaling pathway, focusing on the recent advanc-es involving the mechanism and physiological functionsof cADPR-mediated Ca2+ mobilization.
Mobilization of intracellular Ca2 + stores is involved inmany diverse cell functions, including: cell proliferation; differentiation; muscle contraction; secrection of neurotransmitters, hormones and enzymes; and lymphocyte activation and proliferation. Cyclic ad-enosine diphosphate ribose (cADPR) an endogenous Ca2 + mobilizing nucleotide present in many cell types and species, from plants to animals. cADPR is formedby ADP-ribosyl cyclases from nicotinamide adenine di-nucleotide. The main ADP-ribosyl cyclase in mammals CD38, a multi-functional enzyme and a type II mem It has been shown that many extracel-lular stimuli can induce cADPR production that lead to calcium release or influx, establishing cADPR as a second messenger. cADPR has been linked to a wide variety of cellular processes, but the molecular mecha-nisms regarding cADPR signaling remain elusive. Theaim of this review is to summarize the CD38 / cADPR / Ca2 + signaling pathway, focusing on the recent ad vanc-es involving the mechanism and physiological functions of cADPR-mediated Ca2 + mobilization.