Gab1 amplifies signaling in response to low‐intensity stimulation by HGF

• DOI: 10.1002/cbin.10511
• Publication Date: 2015-07-04T06:35:56Z
• Authors: Monica Aasrum; John Ødegård; Gunn Hege Thoresen; Ingvild J. Brusevold; Dagny L. Sandnes; Thoralf Christoff...
• Keywords: 0303 health sciences; 03 medical and health sciences; Hepatocyte Growth Factor; Hepatocytes; Animals; Rats, Wistar; Phosphoproteins; Cells, Cultured; Signal Transduction

Abstract The receptor tyrosine kinases EGFR and Met induce phosphorylation of the docking protein Gab1, there is evidence that Gab1 may have a role in signaling from these receptors. Studying hepatocytes, we previously found although mechanistically interacted different ways with Met, it was involved mitogenic induced by both EGF HGF. It has been reported EGFR, required particularly at low dose EGF. Whether this also applies to HGF/Met not investigated. We studied activation Akt ERK pathways low‐ high‐intensity stimulation HGF cultured hepatocytes. In cells where depleted specific Gab1‐directed siRNA, EGF‐induced lowered HGF‐induced substantially reduced. These effects were more marked low‐dose stimulation. inhibitory consequence depletion pronounced for phosphorylation. results suggest an important signal amplifier low‐intensity