ArticleThe Biochemical journal1994
Stimulation by prostaglandin E2 of a high-affinity GTPase in the secretory granules of normal rat and human pancreatic islets.
Article in The Biochemical journal, 1994. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 42 citations in OpenAlex.
- GPCRs, G Proteins, and Their Impact on β-cell Function.Comprehensive Physiology · 2020Review
- EHT 1864, a small molecule inhibitor of Ras-related C3 botulinum toxin substrate 1 (Rac1), attenuates glucose-stimulated insulin secretion in pancreatic β-cells.Cellular signalling · 2015Article
- Article
- A farnesylated G-protein suppresses Akt phosphorylation in INS 832/13 cells and normal rat islets: regulation by pertussis toxin and PGE₂.Biochemical pharmacology · 2011Article
- Phagocyte-like NADPH oxidase generates ROS in INS 832/13 cells and rat islets: role of protein prenylation.American journal of physiology. Regulatory, integrative and comparative physiology · 2011Article
- An intracellular role for ABCG1-mediated cholesterol transport in the regulated secretory pathway of mouse pancreatic beta cells.The Journal of clinical investigation · 2010Article
- Small G proteins in islet beta-cell function.Endocrine reviews · 2010Review
- Regulatory roles for Tiam1, a guanine nucleotide exchange factor for Rac1, in glucose-stimulated insulin secretion in pancreatic beta-cells.Biochemical pharmacology · 2009Article
- Emerging roles for protein histidine phosphorylation in cellular signal transduction: lessons from the islet beta-cell.Journal of cellular and molecular medicine · 2008Review
- Article
- Aspects of novel sites of regulation of the insulin stimulus-secretion coupling in normal and diabetic pancreatic islets.Endocrine · 1998Review
- Basal expression of cyclooxygenase-2 and nuclear factor-interleukin 6 are dominant and coordinately regulated by interleukin 1 in the pancreatic islet.Proceedings of the National Academy of Sciences of the United States of America · 1998Article
- Glucose activates the carboxyl methylation of gamma subunits of trimeric GTP-binding proteins in pancreatic beta cells. Modulation in vivo by calcium, GTP, and pertussis toxin.The Journal of clinical investigation · 1997Article
- Glucose- and GTP-dependent stimulation of the carboxyl methylation of CDC42 in rodent and human pancreatic islets and pure beta cells. Evidence for an essential role of GTP-binding proteins in nutrient-induced insulin secretion.The Journal of clinical investigation · 1996Article
- Characterization of prenylcysteine methyltransferase in insulin-secreting cells.The Biochemical journal · 1996Article
- A novel regulatory mechanism for trimeric GTP-binding proteins in the membrane and secretory granule fractions of human and rodent beta cells.The Biochemical journal · 1996Article
- Protein prenylation in glucose-induced insulin secretion from the pancreatic islet beta cell: a perspective.Journal of cellular and molecular medicineReview
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Recent reports of a pertussis-toxin (Ptx)-sensitive inhibition of glucose-induced insulin release by prostaglandin E2 (PGE2) in transformed beta-cells prompted us to look for the presence of prostaglandin-regulatable GTP-binding proteins (G-proteins) on the secretory granules of normal pancreatic islets. PGE2 (but not PGF2 alpha, PGA2, PGB2 or PGD2) stimulated in a concentration-dependent manner a high-affinity GTPase activity in the secretory-granule-enriched fractions of both normal rat and human islets. Similar results were found after sucrose-density-gradient-centrifugation-based isolation of secretory granules to those after a differential-centrifugation procedure. Half-maximal stimulation occurred at 800 nM PGE2, a concentration known to inhibit both phases of glucose-induced insulin secretion from pure beta-cell lines. The GTPase stimulatory effect of PGE2 was blocked virtually totally by Ptx pretreatment; it was not due to an effect on substrate binding since no measurable effect of PGE2 on binding of guanosine 5'-[gamma-[35S]thio]triphosphate was observed in cognate fractions. Other Ptx-sensitive inhibitors of insulin secretion (such as adrenaline or clonidine) also stimulated GTPase activity, suggesting that one (or more) inhibitory exocytotic G-proteins (i.e. a putative GEi) is located on the secretory granules. These studies demonstrate, for the first time in an endocrine gland, the presence of a regulatable G-protein, strategically located on the secretory granules where it might regulate the exocytotic cascade distal to both plasma-membrane events and the generation of soluble mediators of insulin secretion.
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