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A role for a pertussis toxin‐sensitive trimeric G‐protein in store‐operated Ca 2+ inflow in hepatocytes
Author(s) -
Leise A. Berven,
Greg J. Barritt
Publication year - 1994
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/0014-5793(94)00481-1
Subject(s) - thapsigargin , pertussis toxin , microinjection , chemistry , inositol , gtp' , guanosine , biophysics , g protein , intracellular , biochemistry , microbiology and biotechnology , biology , signal transduction , receptor , enzyme
The mechanism of store‐operated Ca 2+ inflow in hepatocytes was investigated using fluo‐3 and fura‐2 to monitor changes in the concentration of intracellular free Ca 2+ in single cells, and 1‐(α‐glycerophosphoryl)‐ myo ‐inositol 4,5‐diphosphate, P 4(5) ‐1‐(2‐nitrophenyl)ethyl ester (‘caged’ GPIP 2 ) and ‘caged’ guanosine 5′‐[γthio]triphosphate (GTPγS) (introduced into the cytoplasmic space by microinjection), thapsigargin and 2,5‐di‐ tert ‐butylhydroquinone (DBHQ) to stimulate Ca 2+ inflow. Photolysis of ‘caged’ GPIP 2 or ‘caged’ GTPγS stimulated Ca 2+ inflow. The abilities of GPIP 2 , thapsigargin and DBHQ to stimulate Ca 2+ inflow were inhibited by the pre‐treatment of hepatocytes with pertussis toxin in vivo for 36 h. Thapsigargin‐stimulated Ca 2+ inflow was also inhibited by guanosine 5′‐[β‐thio]diphosphate (GDPβS) (introduced by microinjection). It is concluded that, in hepatocytes, store‐operated Ca 2+ inflow induced by the actions of either inositol 1,4,5‐trisphosphate, thapsigargin or DBHQ requires a pertussis toxin‐sensitive trimeric G‐protein.