Elucidation of the roles of the Src kinases in pancreatic acinar cell signaling.

摘要: Recent studies report the Src-family kinases (SFK's) are important in a number of physiological and pathophysiological responses pancreatic acinar cells (pancreatitis, growth, apoptosis); however, role SFKs various signaling cascades mediating these cell functions is either not investigated or unclear. To address this we action rat acini by modulating SFK activity using three methods: adenovirus-induced expression an inactive dominant-negative CSK (Dn-CSK-Advirus) wild-type (Wt-CSK-Advirus), which activate inhibit SFK, respectively, chemical inhibitor, PP2, with its control, PP3. CCK (0.3, 100 nM) TPA (1 μM) activated altered activation FAK proteins (PYK2, p125FAK), adaptor (p130CAS, paxillin), MAPK (p42/44, JNK, p38), Shc, PKC (PKD, MARCKS), Akt but GSK3-β. Changes methods altering affected CCK/TPAs PYK2, p125FAK, p130CAS, paxillin, p42/44, p38, MARCKS) With inhibition active control analogue, PP3, showed effects. For all stimulated changes pre-incubation both adenoviruses similar effects to activity. In conclusion, different approaches Src allowed us define fully for first time roles signaling. Our results show that cells, play much wider than previously reported activating cellular shown be responses. J. Cell. Biochem. 116: 22–36, 2015. Published 2014. This article U.S. Government work public domain USA.