Abstract:
: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-(alpha-glycerophosphoryl)-myo-inositol 4,5-diphosphate, P4(5)-1-(2-nitrophenyl)ethyl ester ('caged' GPIP2) and 'caged' guanosine 5'-[gamma thio]triphosphate (GTP gamma S) (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' GTP gamma S 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'-[beta-thio]diphosphate (GDP beta S) (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.
journal_name
FEBS Lettjournal_title
FEBS lettersauthors
Berven LA,Barritt GJdoi
10.1016/0014-5793(94)00481-1subject
Has Abstractpub_date
1994-06-13 00:00:00pages
235-40issue
2-3eissn
0014-5793issn
1873-3468pii
0014-5793(94)00481-1journal_volume
346pub_type
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