Abstract
Calmidazolium, a calmodulin inhibitor, suppressed influx of Ca2+ through voltage-gated Ca2+ channels in mouse pancreatic β-cells. Despite this fact, calmidazolium stimulated insulin release from β-cells at basal glucose concentration. This effect was not mediated by protein kinase C (PKC), since it persisted in PKC-depleted cells. RpcAMPS significantly attenuated tha calmidazolium-stimulated insulin secretion, indicating that calmidazolium acts, at least partly, through PKA. The compound also stimulated insulin secretion from electropermeabilized β-cells, indicating effects on distal steps in the stimulus-secretion coupling. The use of calmidazolium offers possibilities to investigate the mechanisms activating exocytosis under conditions where the cytoplasmic-free Ca2+ concentration does not increase.
| Original language | English |
|---|---|
| Pages (from-to) | 315-320 |
| Number of pages | 6 |
| Journal | FEBS Letters |
| Volume | 369 |
| Issue number | 2-3 |
| DOIs | |
| State | Published - Aug 7 1995 |
| Externally published | Yes |
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Keywords
- Calmidazolium
- Insulin secretion
- Protein kinase A
- Voltage-gated Ca channel
ASJC Scopus subject areas
- Biochemistry
- Biophysics
- Cell Biology
- Genetics
- Molecular Biology
- Structural Biology
Cite this
Dissociation between exocytosis and Ca2+-channel activity in mouse pancreatic β-cells stimulated with calmidazolium (compound R24571). / Kindmark, Henrik; Köhler, Martin; Larsson, Olof; Khan, Akhtar; Berggren, Per Olof.
In: FEBS Letters, Vol. 369, No. 2-3, 07.08.1995, p. 315-320.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Dissociation between exocytosis and Ca2+-channel activity in mouse pancreatic β-cells stimulated with calmidazolium (compound R24571)
AU - Kindmark, Henrik
AU - Köhler, Martin
AU - Larsson, Olof
AU - Khan, Akhtar
AU - Berggren, Per Olof
PY - 1995/8/7
Y1 - 1995/8/7
N2 - Calmidazolium, a calmodulin inhibitor, suppressed influx of Ca2+ through voltage-gated Ca2+ channels in mouse pancreatic β-cells. Despite this fact, calmidazolium stimulated insulin release from β-cells at basal glucose concentration. This effect was not mediated by protein kinase C (PKC), since it persisted in PKC-depleted cells. RpcAMPS significantly attenuated tha calmidazolium-stimulated insulin secretion, indicating that calmidazolium acts, at least partly, through PKA. The compound also stimulated insulin secretion from electropermeabilized β-cells, indicating effects on distal steps in the stimulus-secretion coupling. The use of calmidazolium offers possibilities to investigate the mechanisms activating exocytosis under conditions where the cytoplasmic-free Ca2+ concentration does not increase.
AB - Calmidazolium, a calmodulin inhibitor, suppressed influx of Ca2+ through voltage-gated Ca2+ channels in mouse pancreatic β-cells. Despite this fact, calmidazolium stimulated insulin release from β-cells at basal glucose concentration. This effect was not mediated by protein kinase C (PKC), since it persisted in PKC-depleted cells. RpcAMPS significantly attenuated tha calmidazolium-stimulated insulin secretion, indicating that calmidazolium acts, at least partly, through PKA. The compound also stimulated insulin secretion from electropermeabilized β-cells, indicating effects on distal steps in the stimulus-secretion coupling. The use of calmidazolium offers possibilities to investigate the mechanisms activating exocytosis under conditions where the cytoplasmic-free Ca2+ concentration does not increase.
KW - Calmidazolium
KW - Insulin secretion
KW - Protein kinase A
KW - Voltage-gated Ca channel
UR - http://www.scopus.com/inward/record.url?scp=0028984185&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=0028984185&partnerID=8YFLogxK
U2 - 10.1016/0014-5793(95)00774-4
DO - 10.1016/0014-5793(95)00774-4
M3 - Article
C2 - 7649279
AN - SCOPUS:0028984185
VL - 369
SP - 315
EP - 320
JO - FEBS Letters
JF - FEBS Letters
SN - 0014-5793
IS - 2-3
ER -