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Oncogenic mutations in B-Raf: some losses yield gains.

   
Author Hubbard, Stevan R
Citation Information Cell, 116: 764-6 (2004), : (2004)
Related Products 07-453, 14-530, 17-358, 14-557, 17-359, 07-583
Pub Med ID 15035978
   

Abstract

A study by Wan et al. in this issue of Cell demonstrates that the majority of oncogenic mutations in the B-Raf protein kinase result in increased catalytic activity, through disruption of the autoinhibited state of the kinase domain. Surprisingly, several mutations lead to impaired B-Raf kinase activity, yet these mutants are nevertheless capable of stimulating downstream signaling through transactivation of C-Raf.