158 results on '"Nenquin, Myriam"'
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2. In vitro insulin secretion by pancreatic tissue from infants with diazoxide-resistant congenital hyperinsulinism deviates from model predictions
3. Activators of PKA and Epac Distinctly Influence Insulin Secretion and Cytosolic Ca2+ in Female Mouse Islets Stimulated by Glucose and Tolbutamide
4. Glucose Stimulates Ca2+ Influx and Insulin Secretion in 2-Week-old β-Cells Lacking ATP-sensitive K+ Channels
5. Congenital Hyperinsulinism Caused by Hexokinase I Expression or Glucokinase-Activating Mutation in a Subset of β-Cells
6. cAMP-Mediated and Metabolic Amplification of Insulin Secretion Are Distinct Pathways Sharing Independence of β-Cell Microfilaments
7. Glucose Controls Cytosolic Ca2+ and Insulin Secretion in Mouse Islets Lacking Adenosine Triphosphate-Sensitive K+ Channels Owing to a Knockout of the Pore-Forming Subunit Kir6.2
8. Nutrient Control of Insulin Secretion in Isolated Normal Human Islets
9. In Vivo and In Vitro Glucose-Induced Biphasic Insulin Secretion in the Mouse: Pattern and Role of Cytoplasmic Ca2+ and Amplification Signals in β-Cells
10. SERCA3 Ablation Does Not Impair Insulin Secretion but Suggests Distinct Roles of Different Sarcoendoplasmic Reticulum Ca2+ Pumps for Ca2+ Homeostasis in Pancreatic β-cells
11. Signals and Pools Underlying Biphasic Insulin Secretion
12. Inhibition of Protein Synthesis Sequentially Impairs Distinct Steps of Stimulus-secretion Coupling in Pancreatic β Cells*
13. Insulin secretion in response to high extracellular calcium is not a pathognomonic feature of insulinoma cells.
14. Immaturity of insulin secretion by pancreatic islets isolated from one human neonate
15. Dynamics and Regulation of Insulin Secretion in Pancreatic Islets from Normal Young Children
16. Immaturity of insulin secretion by pancreatic islets isolated from one human neonate.
17. Disruption and stabilization of β-cell actin microfilaments differently influence insulin secretion triggered by intracellular Ca 2+ mobilization or store-operated Ca 2+ entry
18. Dynamics of glucose-induced insulin secretion in normal human islets
19. Activators of PKA and epac distinctly influence insulin secretion and cytosolic Ca2+in female mouse islets stimulated by glucose and tolbutamide
20. Inhibition of protein synthesis sequentially impairs distinct steps of stimulus-secretion coupling in pancreatic beta cells
21. Pharmacological stimulation and inhibition of insulin secretion in mouse islets lacking ATP-sensitive K(+) channels.
22. Metabolic amplifying pathway increases both phases of insulin secretion independently of beta-cell actin microfilaments
23. Glucose controls cytosolic Ca2+ and insulin secretion in mouse islets lacking ATP-sensitive K+ channels owing to a knockout of the pore-forming subunit Kir6.2
24. Insulin secretion in islets from mice with a double knockout for the dense core vesicle proteins islet antigen-2 (IA-2) and IA-2beta.
25. Glucose-induced cytosolic pH changes in beta-cells and insulin secretion are not causally related: studies in islets lacking the Na+/H+ exchangeR NHE1.
26. Overnight culture unmasks glucose-induced insulin secretion in mouse islets lacking ATP-sensitive K+ channels by improving the triggering Ca2+ signal.
27. Nutrient control of insulin secretion in perifused adult pig islets.
28. Glucose stimulates Ca2+ influx and insulin secretion in 2-week-old beta-cells lacking ATP-sensitive K+ channels.
29. Both triggering and amplifying pathways contribute to fuel-induced insulin secretion in the absence of sulfonylurea receptor-1 in pancreatic beta-cells.
30. Disruption and stabilization of β‐cell actin microfilaments differently influence insulin secretion triggered by intracellular Ca2+ mobilization or store‐operated Ca2+ entry
31. Metabolic amplification of insulin secretion by glucose is independent of β-cell microtubules
32. Hierarchy of the beta-cell signals controlling insulin secretion
33. Metabolic amplifying pathway increases both phases of insulin secretion independently of β-cell actin microfilaments
34. SERCA3 ablation does not impair insulin secretion but suggests distinct roles of different sarcoendoplasmic reticulum Ca(2+) pumps for Ca(2+) homeostasis in pancreatic beta-cells
35. Signals and pools underlying biphasic insulin secretion.
36. The elevation of glutamate content and the amplification of insulin secretion in glucose-stimulated pancreatic islets are not causally related.
37. Inhibition of protein synthesis sequentially impairs distinct steps of stimulus-secretion coupling in pancreatic beta cells
38. Glucose Controls Cytosolic Ca2+ and Insulin Secretion in Mouse Islets Lacking Adenosine Triphosphate-Sensitive K+ Channels Owing to a Knockout of the Pore-Forming Subunit Kir6.2
39. The oscillatory behavior of pancreatic islets from mice with mitochondrial glycerol-3-phosphate dehydrogenase knockout.
40. Glucose-induced Cytosolic pH Changes in β-Cells and Insulin Secretion Are Not Causally Related
41. Overnight Culture Unmasks Glucose-induced Insulin Secretion in Mouse Islets Lacking ATP-sensitive K+ Channels by Improving the Triggering Ca2+ Signal
42. Unbound rather than total concentration and saturation rather than unsaturation determine the potency of fatty acids on insulin secretion.
43. Both Triggering and Amplifying Pathways Contribute to Fuel-induced Insulin Secretion in the Absence of Sulfonylurea Receptor-1 in Pancreatic β-Cells
44. Relative contribution of Ca2+-dependent and Ca2+-independent mechanisms to the regulation of insulin secretion by glucose.
45. Physiological relevance of a Ca2+-independent pathway of regulation of insulin secretion by glucose
46. Do sulfonylureas and diazoxide influence insulin secretion by modulating the action of Ca2+ in pancreatic beta cells?
47. The Elevation of Glutamate Content and the Amplification of Insulin Secretion in Glucose-stimulated Pancreatic Islets Are Not Causally Related
48. No evidence for a role of reverse Na(+)-Ca2+ exchange in insulin release from mouse pancreatic islets
49. Multiple effects and stimulation of insulin secretion by the tyrosine kinase inhibitor genistein in normal mouse islets
50. Muscarinic stimulation exerts both stimulatory and inhibitory effects on the concentration of cytoplasmic Ca2+ in the electrically excitable pancreatic B-cell
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