ArticleCellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology2013
Nm23-H1 regulates glucose-stimulated insulin secretion in pancreatic β-cells via Arf6-Rac1 signaling axis.
Article in Cellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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10 citing papers in PubMed, 13 citations in OpenAlex.
- The Potential Target Value of ADP-Ribosylation Factor 6 in Insulin Secretion Regulation and the Treatment of Metabolic Disorders.Metabolites · 2026Review
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- HeterozygousGenes · 2021Article
- Identification of Urinary Biomarkers for Exercise-Induced Immunosuppression by iTRAQ Proteomics.BioMed research international · 2020Article
- Cdc42: A Novel Regulator of Insulin Secretion and Diabetes-Associated Diseases.International journal of molecular sciences · 2019Review
- Small molecule activator of Nm23/NDPK as an inhibitor of metastasis.Scientific reports · 2018Article
- Modulation of small GTPase activity by NME proteins.Laboratory investigation; a journal of technical methods and pathology · 2018Review
- Dual functions of NME1 in suppression of cell motility and enhancement of genomic stability in melanoma.Naunyn-Schmiedeberg's archives of pharmacology · 2015Article
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3 authors at 2 institutions in 1 country.
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Abstract
backgroundA growing body of evidence implicates novel roles for nm23-like proteins in the regulation of cellular functions. However, roles of these proteins in islet function and glucose-stimulated insulin secretion (GSIS) remain largely unknown.
methodssiRNA-nm23-H1 and nucleoside diphosphate kinase and histidine kinase-deficient mutants of nm23-H1 (K12Q and H118F) were used to assess roles of nm23-H1 in GSIS.
resultssiRNA-mediated knockdown of the expression of nm23-H1 markedly inhibited GSIS in INS-1 832/13 cells. Nm23-H1 knockdown also resulted in significant inhibition of glucose-mediated activation of Arf6, a small G-protein, which has been implicated in GSIS. Expression of K12Q and H118F mutants of nm23-H1 in INS-1 832/13 cells led to inhibition of glucose-induced translocation and membrane association of Rac1, another small G-protein, which is downstream to Arf6 in the signaling events leading to GSIS. A significant inhibition of GSIS was also seen in these cells expressing K12Q and H118F.
conclusionsWe conclude that the nm23-H1 activation step is upstream of Arf6 activation in signaling events leading to GSIS. NDP kinase and histidine kinase functions of nm23-H1 are necessary for glucose-induced membrane association of Rac1 and ensuing insulin secretion. We present the first evidence for regulation of GSIS by nm23-H1 in pancreatic β-cells.
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