| 1. |
- Islam, M. Shahidul, et al.
(författare)
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Ca(2+)-induced Ca2+ release in insulin-secreting cells
- 1992
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Ingår i: FEBS Letters. - : Wiley. - 0014-5793 .- 1873-3468. ; 296:3, s. 287-291
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Tidskriftsartikel (refereegranskat)abstract
- The sulphydryl reagent thimerosal (50 microM) released Ca2+ from a non-mitochondrial intracellular Ca2+ pool in a dose-dependent manner in permeabilized insulin-secreting RINm5F cells. This release was reversed after addition of the reducing agent dithiothreitol. Ca2+ was released from an Ins(1,4,5)P3-insensitive pool, since release was observed even after depletion of the Ins(1,4,5)P3-sensitive pool by a supramaximal dose of Ins(2,4,5)P3 or thapsigargin. The Ins(1,4,5)P3-sensitive pool remained essentially unaltered by thimerosal. Thimerosal-induced Ca2+ release was potentiated by caffeine. These findings suggest the existence of Ca(2+)-induced Ca2+ release also in insulin-secreting cells.
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| 2. |
- Islam, M. Shahidul, et al.
(författare)
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Interaction with the inositol 1,4,5-trisphosphate receptor promotes Ca2+ sequestration in permeabilised insulin-secreting cells
- 1991
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Ingår i: FEBS Letters. - 0014-5793 .- 1873-3468. ; 288:1-2, s. 27-29
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Tidskriftsartikel (refereegranskat)abstract
- Electropermeabilised insulin-secreting RINm5F cells sequestered Ca2+, resulting in a steady-state level of the ambient free Ca2+ concentration corresponding to 723 +/- 127 nM (mean +/- SEM, n = 10), as monitored by a Ca(2+)-selective minielectrode. Inositol 1,4,5-trisphosphate (Ins(1,4,5)P3) promoted a rapid and pronounced release of Ca2+. This Ca2+ was resequestered and a new steady-state Ca2+ level was attained, which was always lower (460 +/- 102 nM, n = 10, P less than 0.001) than the steady-state Ca2+ level maintained before the addition of Ins(1,4,5)P3. Whereas the initial reuptake of Ca2+ subsequent to Ins(1,4,5)P3 stimulation was relatively slow, the later part of reuptake was fast as compared to the reuptake phases of a pulse addition of extraneous Ca2+. In the latter case the uptake of Ca2+ resulted in a steady-state level similar to that found in the absence of Ins(1,4,5)P3. Addition of Ins(1,4,5)P3 under this condition resulted in a further Ca2+ uptake and thus a lower steady-state Ca2+ level. Heparin, which binds to the Ins(1,4,5)P3 receptor, also lowered the steady-state free Ca2+ concentration. In contrast to Ins(1,4,5)P3, inositol 1,3,4,5-tetrakisphosphate was without effect on Ca2+ sequestration. These findings are consistent with the presence of a high-affinity Ins(1,4,5)P3 receptor promoting continuous release of Ca2+ under basal conditions and/or the Ins(1,4,5)P3 receptor being actively involved in Ca2+ sequestration.
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| 3. |
- Rorsman, Patrik, et al.
(författare)
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Ion channels, electrical activity and insulin secretion
- 1994
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Ingår i: Diabete & metabolisme. - 0338-1684. ; 20:2, s. 138-145
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Tidskriftsartikel (refereegranskat)abstract
- The insulin-secreting pancreatic beta cell is electrically excitable and changes in the membrane potential play an important role in coupling the metabolism of glucose (and other nutrient secretagogues) to the discharge of the insulin-containing granule. The application of the patch-clamp technique, which permits the recordings of the minute currents associated with the opening of individual ion channels, to pancreatic islet cells has revolutionized our understanding of the beta cell electrophysiology. Here we review some of the recent progress in the field. The properties of functionally important ion channels are described and their possible roles are discussed.
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