CCK activates RhoA and Rac1 differentially through Galpha13 and Galphaq in mouse pancreatic acini.

ABSTRACT: Cholecystokinin (CCK) has been shown to activate RhoA and Rac1, as well as reorganize the actin cytoskeleton and, thereby, modify acinar morphology and amylase secretion in mouse pancreatic acini. The aim of the present study was to determine which heterotrimeric G proteins activate RhoA and Rac1 upon CCK stimulation. Galpha(13), but not Galpha(12), was identified in mouse pancreatic acini by RT-PCR and Western blotting. Using specific assays for RhoA and Rac1 activation, we showed that only active Galpha(13) activated RhoA. By contrast, active Galpha(13) and Galpha(q), but not Galpha(s), slightly increased GTP-bound Rac1 levels. A greater increase in Rac1 activation was observed when active Galpha(13) and active Galpha(q) were coexpressed. Galpha(i) was not required for CCK-induced RhoA o

SUBMITTER: Sabbatini ME 

PROVIDER: S-EPMC2838570 | biostudies-literature | 2010 Mar

REPOSITORIES: biostudies-literature