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Cholecystokinin‐Induced PKC α Activation Mediates the Translocation of RhoA in Mouse Pancreatic Acini
Author(s) -
SABBATINI MARIA EUGENIA,
WILLIAMS JOHN A
Publication year - 2010
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.24.1_supplement.867.5
Subject(s) - rhoa , protein kinase c , chromosomal translocation , cholecystokinin , cytosol , microbiology and biotechnology , chemistry , phorbol , signal transduction , endocrinology , biology , receptor , biochemistry , enzyme , gene
RhoA is a small G protein belonging to the Rho family that cycle between an inactive GDP‐bound and an active GTP‐bound forms. In previous work we showed that cholecystokinin (CCK) induces RhoA activation and translocation from the cytosol to the membrane. Aim To study which intracellular signals are involved in CCK‐induced RhoA translocation in mouse pancreatic acini. Results The PKC stimulator phorbol 12‐myristate 13‐acetate increased the amount of RhoA in the membrane fraction and the PKC inhibitor GF‐203109X blocked CCK‐induced RhoA translocation while agents affecting calcium or cAMP had no effect. In order to test which isoform of PKC mediated the effect of CCK, we infected acini with adenoviruses expressing dominant negative (DN) isoforms of PKC α, δ and ε. Only in DN PKC α‐expressing acini was the effect of CCK on RhoA translocation reduced. Conclusion PKC α, but not calcium or cAMP, is required for CCK‐induced RhoA translocation.