Proto-Oncogene Proteins c-raf

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  Subject Areas on Research

  • A requirement for the rac1 GTPase in the signal transduction pathway leading to cardiac myocyte hypertrophy. 
  • A role for MAPK in feedback inhibition of Tcrb recombination. 
  • Activation of mitogen-activated protein kinase kinase by v-Raf in NIH 3T3 cells and in vitro. 
  • Activation of mitogen-activated protein kinase pathway by the antiandrogen hydroxyflutamide in androgen receptor-negative prostate cancer cells. 
  • Activation of the mitogen-activated protein kinase pathway through p75NTR: a common mechanism for the neurotrophin family. 
  • C-Raf antagonizes apoptosis induced by IFN-alpha in human lung cancer cells by phosphorylation and increase of the intracellular content of elongation factor 1A. 
  • COT drives resistance to RAF inhibition through MAP kinase pathway reactivation. 
  • Differential regulation of hepatocyte DNA synthesis by cAMP in vitro in vivo. 
  • Distribution, levels and phosphorylation of Raf-1 in Alzheimer's disease. 
  • Erbin suppresses the MAP kinase pathway. 
  • Expression of constitutively active Raf-1 in the mitochondria restores antiapoptotic and leukemogenic potential of a transformation-deficient BCR/ABL mutant. 
  • Gain-of-function RAF1 mutations cause Noonan and LEOPARD syndromes with hypertrophic cardiomyopathy. 
  • Human homologue of Drosophila CNK interacts with Ras effector proteins Raf and Rlf. 
  • Inactivation of Icmt inhibits transformation by oncogenic K-Ras and B-Raf. 
  • Insulin activates a novel adipocyte mitogen-activated protein kinase kinase kinase that shows rapid phasic kinetics and is distinct from c-Raf. 
  • JAK2 is required for induction of the murine DUB-1 gene. 
  • Modulation of oncogene and tumor suppressor gene expression in a hamster model of chronic lung injury with varying degrees of pulmonary neuroendocrine cell hyperplasia. 
  • Mutant forms of growth factor-binding protein-2 reverse BCR-ABL-induced transformation. 
  • Mutations of the BRAF gene in human cancer. 
  • Rearrangements of the RAF kinase pathway in prostate cancer, gastric cancer and melanoma. 
  • The GPCR-β-arrestin complex allosterically activates C-Raf by binding its amino terminus. 
  • The MEK pathway is required for stimulation of p21(WAF1/CIP1) by transforming growth factor-beta. 
  • The c-FLIPL cleavage product p43FLIP promotes activation of extracellular signal-regulated kinase (ERK), nuclear factor κB (NF-κB), and caspase-8 and T cell survival.