| First Author | Hartmann G | Year | 1994 |
| Journal | J Biol Chem | Volume | 269 |
| Issue | 35 | Pages | 21936-9 |
| PubMed ID | 8071312 | Mgi Jnum | J:20013 |
| Mgi Id | MGI:68130 | Doi | 10.1016/s0021-9258(17)31736-2 |
| Citation | Hartmann G, et al. (1994) The motility signal of scatter factor/hepatocyte growth factor mediated through the receptor tyrosine kinase met requires intracellular action of Ras. J Biol Chem 269(35):21936-9 |
| abstractText | Scatter factor/hepatocyte growth factor (SF/HGF) has various biological effects upon different cells, i.e. induces increased motility and proliferation as well as invasiveness and morphogenesis. The signals given to epithelial cells by SF/HGF are all mediated through the Met receptor tyrosine kinase (Weidner, K. M., Sachs, M., and Birchmeier, W. (1993) J. Cell Biol. 111, 145-154) suggesting that signal diversity is due to the interplay of different downstream pathways. It has also been shown that SF/HGF activates the protooncogene product Ras, i.e. stimulates guanine nucleotide exchange. In order to examine whether Ras is involved in mediating the dissociation and motility signal of SF/HGF to epithelial cells, we have expressed in Madin-Darby canine kidney cells the dominant-negative N17Ras under the control of a modified metallothionein promoter. Induced expression of N17Ras by the addition of Zn2+ clearly prevented dissociation of the cells by SF/HGF. These data indicate that the Ras pathway is indeed essential to mediate the motility signal of SF/HGF-Met to the cell-cell adhesion system and the cytoskeleton of epithelial cells. |
