Author:

Keywords:

Science & Technology, Life Sciences & Biomedicine, Biochemistry & Molecular Biology, B-RAF, ACTIVATION, PATHWAY, CELLS, Capillary Permeability, Endothelial Cells, Intercellular Junctions, Permeability, Proto-Oncogene Proteins B-raf, 0304 Medicinal and Biomolecular Chemistry, 0601 Biochemistry and Cell Biology, 1101 Medical Biochemistry and Metabolomics, 3101 Biochemistry and cell biology, 3205 Medical biochemistry and metabolomics, 3404 Medicinal and biomolecular chemistry

Abstract:

The RAF/MEK/ERK signal transduction pathway is commonly deregulated in cancer and is activated by various stimuli regulating a variety of cell responses. In wild-type endothelial cells, upon permeability stimuli, ROKα, RAF1, BRAF, and RAP1 become activated, inducing a cascade of reactions resulting in F-actin remodeling and increased cell permeability. Here, Dorard et al. showed that BRAF ablated cells had more RAF1/ROKα dimerization and relocalization to VE-cadherin occurred, ultimately leading to less F-actin content and reduced vessel permeability.