IndraLab

Statements

RAF binds BRAF and RAF1. 5 / 5
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sparser
"The results of both groups support a model in which the BRAF-specific inhibitors induce RAS-GTP-dependent RAF1 activation via the formation of BRAF-RAF heterodimers or RAF1 homodimers followed by recruitment of RAF1 to the plasma membrane, triggering the MEK-ERK pathway ( xref ; xref )."
20149136
sparser
"Analysis of the mechanisms of cutaneous toxicities (notably, cuSCC) suggest that in BRAF wt cells, BRAF inhibitors cause formation of RAF dimers that lead to signaling through CRAF, particularly in those with an upstream mutation such as RAS . xref – xref Studies have shown frequent mutations in HRAS , and to a lesser extent NRAS , in benign and malignant (cuSCCs) proliferative lesions resected from patients on BRAF inhibitors, at higher rates than in lesions from patients not treated with inhibitors. xref – xref "
23251089
sparser
"It was recently reported that imatinib and nilotinib can bind to B-RAF and C-RAF leading to the formation of RAF hetero- and homo-dimers, and stimulate paradoxical activation of BRAF and CRAF in the presence of activated RAS xref ."
27293031
sparser
"The paradoxical activation of MAPK signaling observed in Ras mutant cells following BRAF inhibitor treatment occurs following the increased formation of Raf dimers consisting of either CRAF homodimer pairs or dimers between drug-bound BRAF and CRAF ( xref , xref ) ( xref )."
23069660
sparser
"Packer et al. [42] reported that the binding of weak RAF inhibitors (imatinib, nilotinib and dasatinib) to BRAF and CRAF drives BRAF:CRAF heterodimer as well as BRCF and CRAF homodimer formation in the presence of oncogenetic RAS, thus leading to paradoxical activation of both BRAF and CRAF, followed by the activation of MEK and ERK."
23825585