Title : Okamoto model for necrosis and its expansions, CD38-cyclic ADP-ribose signal system for intracellular Ca2+ mobilization and Reg (Regenerating gene protein)-Reg receptor system for cell regeneration.

Pub. Date : 2021

PMID : 34629354






3 Functional Relationships(s)
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1 The diabetogenic agents, alloxan and streptozotocin, caused DNA strand breaks, which in turn activated poly(ADP-ribose) polymerase/synthetase (PARP) to deplete NAD+, thereby inhibiting islet beta-cell functions such as proinsulin synthesis and ultimately leading to beta-cell necrosis. NAD poly(ADP-ribose) polymerase 1 Homo sapiens
2 The diabetogenic agents, alloxan and streptozotocin, caused DNA strand breaks, which in turn activated poly(ADP-ribose) polymerase/synthetase (PARP) to deplete NAD+, thereby inhibiting islet beta-cell functions such as proinsulin synthesis and ultimately leading to beta-cell necrosis. NAD poly(ADP-ribose) polymerase 1 Homo sapiens
3 Inhibitors of PARP prevented the NAD+ depletion, inhibition of proinsulin synthesis and beta-cell death. NAD poly(ADP-ribose) polymerase 1 Homo sapiens