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.
journal_name
FEBS Lettjournal_title
FEBS lettersauthors
Cao Y,Chatton JYdoi
10.1016/s0014-5793(98)00133-1subject
Has Abstractpub_date
1998-03-06 00:00:00pages
33-6issue
1-2eissn
0014-5793issn
1873-3468pii
S0014-5793(98)00133-1journal_volume
424pub_type
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