NDLI: Regulatory roles for nm23/nucleoside diphosphate kinase-like enzymes in insulin secretion from the pancreatic islet beta cell

Content Provider	Springer Nature Link
Author	Kowluru, Anjaneyulu Veluthakal, Rajakrishnan Kaetzel, David M.
Copyright Year	2006
Abstract	Recent studies from multiple laboratories, including our own, provided fresh insights into the contributory roles for GTP-binding proteins (G-proteins) in glucose-stimulated insulin secretion (GSIS) from the islet β cell. However, the precise mechanisms underlying the activation of this class of signaling proteins by insulin secretagogues remain only partially understood. We recently proposed that nm23/nucleoside diphosphate kinase (NDPK) catalyzes an alternate, non-receptor-dependent activation of islet endogenous G-proteins. In further support of this proposal, we report, herein, that overexpression of wild type (WT) nm23-H1 mutant in INS cells markedly potentiated GSIS. However, an inactive mutant of nm23-H1(H118F), which is deficient in histidine kinase and NDPK activities, was considerably less effective in potentiating GSIS from these cells, suggesting that both of these activities may be relevant for the potentiating effects of nm23-H1. Potential significance of these findings in relation to contributory roles for nm23/NDPK-like enzymes in the stimulus-secretion coupling of GSIS is discussed.
Starting Page	227
Ending Page	232
Page Count	6
File Format	PDF
ISSN	0145479X
Journal	Journal of Bioenergetics and Biomembranes
Volume Number	38
Issue Number	3-4
e-ISSN	15736881
Language	English
Publisher	Springer-Verlag
Publisher Date	2006-09-08
Publisher Place	New York
Access Restriction	One Nation One Subscription (ONOS)
Subject Keyword	nm23-H1 Nucleoside diphosphate kinase Histidine kinase Pancreatic islet β cell Insulin secretion G-proteins Bioorganic Chemistry Biochemistry Animal Anatomy / Morphology / Histology Animal Biochemistry Organic Chemistry
Content Type	Text
Resource Type	Article
Subject	Cell Biology Physiology

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