ArticleThe Journal of physiology2001
The endoplasmic reticulum is a glucose-modulated high-affinity sink for Ca2+ in mouse pancreatic beta-cells.
Article in The Journal of physiology, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 57 citations in OpenAlex.
- Article
- High-resolution analysis of the cytosolic CaAmerican journal of physiology. Endocrinology and metabolism · 2023Article
- Physiological levels of adrenaline fail to stop pancreatic beta cell activity at unphysiologically high glucose levels.Frontiers in endocrinology · 2022Article
- Postnatal maturation of calcium signaling in islets of Langerhans from neonatal mice.Cell calcium · 2021Article
- GPR40 activation initiates store-operated CaScientific reports · 2019Article
- TALK-1 channels control β cell endoplasmic reticulum CaScience signaling · 2017Article
- Stress-induced dissociations between intracellular calcium signaling and insulin secretion in pancreatic islets.Cell calcium · 2015Article
- Glucose Evokes Rapid Ca2+ and Cyclic AMP Signals by Activating the Cell-Surface Glucose-Sensing Receptor in Pancreatic β-Cells.PloS one · 2015Article
- Article
- cAMP induces stromal interaction molecule 1 (STIM1) puncta but neither Orai1 protein clustering nor store-operated Ca2+ entry (SOCE) in islet cells.The Journal of biological chemistry · 2012Article
- The central role of calcium in the effects of cytokines on beta-cell function: implications for type 1 and type 2 diabetes.Cell calcium · 2011Review
- Article
- Ionic mechanisms and Ca2+ dynamics underlying the glucose response of pancreatic β cells: a simulation study.The Journal of general physiology · 2011Article
- PERK activation at low glucose concentration is mediated by SERCA pump inhibition and confers preemptive cytoprotection to pancreatic β-cells.Molecular endocrinology (Baltimore, Md.) · 2011Article
- Bursting and calcium oscillations in pancreatic beta-cells: specific pacemakers for specific mechanisms.American journal of physiology. Endocrinology and metabolism · 2010Review
- Bax inhibitor 1 increases cell adhesion through actin polymerization: involvement of calcium and actin binding.Molecular and cellular biology · 2010Article
- Evidence of diminished glucose stimulation and endoplasmic reticulum function in nonoscillatory pancreatic islets.Endocrinology · 2009Article
- Insulin secretion from beta-cells is affected by deletion of nicotinamide nucleotide transhydrogenase.Methods in enzymology · 2009Article
- Filtering of calcium transients by the endoplasmic reticulum in pancreatic beta-cells.Biophysical journal · 2004Article
- Ligand-induced recruitment of Na+/H+-exchanger regulatory factor to the PDGF (platelet-derived growth factor) receptor regulates actin cytoskeleton reorganization by PDGF.The Biochemical journal · 2003Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The regulation of organelle free Ca2+ was analysed in individual mouse pancreatic beta-cells loaded with the fluorescent low-affinity indicator furaptra. Removal of the cytoplasmic indicator by controlled digitonin permeabilization of the plasma membrane resulted in a sudden increase of the 340 nm/380 nm fluorescence excitation ratio followed by a gradual decay, reflecting the emptying of Ca2+ from organelle pools. Subsequent introduction of 3 mM ATP caused rapid refilling of a Ca2+ pool, which represented the endoplasmic reticulum (ER) in being mobilized with inositol 1,4,5-trisphosphate (IP3) and the sarco(endo)plasmic reticulum Ca2+-ATPase inhibitor thapsigargin. The concentration of Ca2+ in the ER observed immediately after permeabilization depended on the glucose concentration in a hyperbolic fashion with half-maximal filling at about 6 mM of the sugar. Glucose promotion of Ca2+ sequestration in the ER involved a high-affinity mechanism not requiring but accelerated by a rise of the cytoplasmic Ca2+ concentration. Glucose also exerted a long-term action on the ER storage of Ca2+, maintaining the set-point for its maximal concentration and preserving the response to IP3. The results indicate that the ER has an important role in the glucose-stimulated beta-cell by serving as a high-affinity sink for Ca2+, irrespective of the prevailing concentration of cytoplasmic Ca2+.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.