Autoantibodies against CD38 (ADP-ribosyl cyclase/cyclic ADP-ribose hydrolase) that impair glucose-induced insulin secretion in noninsulin- dependent diabetes patients.
AUTOR(ES)
Ikehata, F
RESUMO
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
ACESSO AO ARTIGO
http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=508898Documentos Relacionados
- Bringing the Ends Together♦: Mechanism of Cyclizing NAD to Cyclic ADP-ribose by ADP-ribosyl Cyclase and CD38
- Mechanism of Cyclizing NAD to Cyclic ADP-ribose by ADP-ribosyl Cyclase and CD38*♦
- Abscisic acid-induced stomatal closure mediated by cyclic ADP-ribose
- Defense gene induction in tobacco by nitric oxide, cyclic GMP, and cyclic ADP-ribose
- Comparison of Ca2+ mobilizing activities of cyclic ADP-ribose and inositol trisphosphate.
