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Citation Information: J Clin Invest. 1998;102(2):395-401. https://doi.org/10.1172/JCI1656.
Abstract
Cyclic ADP-ribose (cADPR) has been shown to be a mediator for intracellular Ca2+ mobilization for insulin secretion by glucose in pancreatic beta cells, and CD38 shows both ADP-ribosyl cyclase to synthesize cADPR from NAD+ and cADPR hydrolase to hydrolyze cADPR to ADP-ribose. We show here that 13.8% of Japanese non-insulin-dependent diabetes (NIDDM) patients examined have autoantibodies against CD38 and that the sera containing anti-CD38 autoantibodies inhibit the ADP-ribosyl cyclase activity of CD38 (P
Authors
F Ikehata, J Satoh, K Nata, A Tohgo, T Nakazawa, I Kato, S Kobayashi, T Akiyama, S Takasawa, T Toyota, H Okamoto
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