DISSOCIATION BETWEEN EXOCYTOSIS AND CA2+-CHANNEL ACTIVITY IN MOUSE PANCREATIC BETA-CELLS STIMULATED WITH CALMIDAZOLIUM (COMPOUND R24571)

被引：9

作者：

KINDMARK, H ^{[1
]}

KOHLER, M ^{[1
]}

LARSSON, O ^{[1
]}

KHAN, A ^{[1
]}

BERGGREN, PO ^{[1
]}

机构：

[1] KAROLINSKA INST,KAROLINSKA HOSP,DEPT MOLEC MED,ROLF LUFT CTR DIABET RES,S-17176 STOCKHOLM,SWEDEN

来源：

FEBS LETTERS | 1995年 / 369卷 / 2-3期

关键词：

VOLTAGE-GATED CA2+ CHANNEL; CALMIDAZOLIUM; INSULIN SECRETION; PROTEIN KINASE A;

D O I：

10.1016/0014-5793(95)00774-4

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

Calmidazolium, a calmodulin inhibitor, suppressed influx of Ca2+ through voltage-gated Ca2+ channels in mouse pancreatic beta-cells. Despite this fact, calmidazolium stimulated insulin release from beta-cells at basal glucose concentration. This effect mas not mediated by protein kinase C (PBC), since it persisted in PKC-depleted cells. R(p)cAMPS significantly attenuated the calmidazolium-stimulated insulin secretion, indicating that calmidazolium acts, at least partly, through PKA. The compound also stimulated insulin secretion from electropermeabilized beta-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.

引用

页码：315 / 320

页数：6

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