Involvement of calmodulin in the activation of store-operated Ca2+ entry in rat hepatocytes

FEBS Letters
Y Cao, J Y Chatton

Abstract

The possible participation of calmodulin in the activation of store-operated Ca2+ entry (SOC) in single rat hepatocytes was investigated microspectrofluorimetrically. SOC was triggered after discharging intracellular Ca2+ stores using the endoplasmic reticulum Ca2+-ATPase inhibitor thapsigargin in the absence of external Ca2+. Re-admission of bath Ca2+ caused a rapid and pronounced Ca2+ entry. The calmodulin antagonists calmidazolium or CGS 9343B applied before the thapsigargin treatment inhibited SOC, whereas they were ineffective when added after the thapsigargin-induced Ca2+ transient. This study suggests that activation of calmodulin after the elevation of cytosolic Ca2+ associated with the emptying of Ca2+ stores is involved in the triggering of SOC in hepatocytes.

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Citations

Feb 7, 2009·Clinical and Experimental Pharmacology & Physiology·Greg J BarrittGrigori Y Rychkov
Nov 12, 2009·Journal of Receptor and Signal Transduction Research·Yazhen Xu, Xin Xie
Feb 23, 2008·Biochimica Et Biophysica Acta·Gregory J BarrittGrigori Y Rychkov
Jun 14, 2006·British Journal of Pharmacology·Anthony P AlbertWilliam A Large
Jul 11, 2006·Journal of Cellular Physiology·Klaus Lange, Joachim Gartzke
Mar 25, 2005·Physiological Reviews·Anant B Parekh, James W Putney
Jun 28, 2002·Physiological Reviews·Michael C Ashby, Alexei V Tepikin
Dec 22, 2004·The Journal of Biological Chemistry·Ben MoreauAnant B Parekh
Jan 19, 2000·Toxicology and Applied Pharmacology·C R Jan, C J Tseng

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