A role for a pertussis toxin-sensitive trimeric G-protein in store-operated Ca2+ inflow in hepatocytes

Leise A. Berven, Greg J. Barritt

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    21 Citations (Scopus)


    The mechanism of store-operated Ca2+ inflow in hepatocytes was investigated using fluo-3 and fura-2 to monitor changes in the concentration of intracellular free Ca2+ in single cells, and 1-(α-glycerophosphoryl)-myo-inositol 4,5-diphosphate, P4(5)-1-(2-nitrophenyl)ethyl ester ('caged' GPIP2) and 'caged' guanosine 5′-[γthio]triphosphate (GTPγS) (introduced into the cytoplasmic space by microinjection), thapsigargin and 2,5-di-tert-butylhydroquinone (DBHQ) to stimulate Ca2+ inflow. Photolysis of 'caged' GPIP2 or 'caged' GTPγS stimulated Ca2+ inflow. The abilities of GPIP2, thapsigargin and DBHQ to stimulate Ca2+ inflow were inhibited by the pre-treatment of hepatocytes with pertussis toxin in vivo for 36 h. Thapsigargin-stimulated Ca2+ inflow was also inhibited by guanosine 5′-[β-thio]diphosphate (GDPβS) (introduced by microinjection). It is concluded that, in hepatocytes, store-operated Ca2+ inflow induced by the actions of either inositol 1,4,5-trisphosphate, thapsigargin or DBHQ requires a pertussis toxin-sensitive trimeric G-protein.

    Original languageEnglish
    Pages (from-to)235-240
    Number of pages6
    JournalFEBS Letters
    Issue number2-3
    Publication statusPublished - 13 Jun 1994


    • Ca inflow
    • Hepatocyte
    • Inositol trisphosphate
    • Pertussis toxin
    • Trimeric G-protein


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