| Autor: |
Laird, A D, Morrison, D K, Shalloway, D |
| Zdroj: |
Journal of Biological Chemistry; February 1999, Vol. 274 Issue: 7 p4430-9, 10p |
| Abstrakt: |
We have used site-directed mutagenesis to explore the mechanisms underlying Raf-1 activation in mitosis, and we have excluded most previously characterized activating interactions. Our results indicate that the primary locus of activation lies in the carboxyl-half of the molecule, although the extent of activation can be influenced by the amino-proximal region, particularly by the Raf-1 zinc finger. We also found that Raf-1 is hyperphosphorylated in mitosis at multiple sites within residues 283-302 and that these hyperphosphorylations are not required for activation. In addition, neither Mek1 nor Mek2 are stably activated in coordination with Raf-1 in nocodazole-arrested cells. Overall, the data suggest that the mechanism(s) responsible for activating Raf-1 during mitosis, and the subsequent downstream effects, are distinct from those involved in growth factor stimulation. |
| Databáze: |
Supplemental Index |
| Externí odkaz: |
|
