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BRAF , A gatekeeper controlling endothelial permeability
Author(s) -
Declercq Mathias,
Treps Lucas
Publication year - 2019
Publication title -
the febs journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.981
H-Index - 204
eISSN - 1742-4658
pISSN - 1742-464X
DOI - 10.1111/febs.14861
Subject(s) - microbiology and biotechnology , mapk/erk pathway , permeability (electromagnetism) , chemistry , signal transduction , actin , endothelial stem cell , cancer research , biology , in vitro , biochemistry , membrane
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.