Sandbox Reserved 707: Difference between revisions

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	In a second study, Poulikakos and al. reported that six ATP-competitive RAF inhibitors induce ERK activation in cells with activated RAS and wild-type B-RAF but inhibit signaling in activated mutant B-RAF cells. B-RAF and C-RAF form homo- and heterodimers following RAS activation. PLX4032 and PLX4720, RAF kinase inhibitors, induce the phosphorylation of MEK and ERK in wild-type and B-RAF -/- mouse embryonic fibroblasts. The response is diminished in C-RAF -/- fibroblasts, arguing on the importance of C-RAF in paradoxical MEK-ERK activation. <br />		In a second study, Poulikakos and al. reported that six ATP-competitive RAF inhibitors induce ERK activation in cells with activated RAS and wild-type B-RAF but inhibit signaling in activated mutant B-RAF cells<ref>PMID:20179705</ref>. B-RAF and C-RAF form homo- and heterodimers following RAS activation. PLX4032 and PLX4720, RAF kinase inhibitors, induce the phosphorylation of MEK and ERK in wild-type and B-RAF -/- mouse embryonic fibroblasts. The response is diminished in C-RAF -/- fibroblasts, arguing on the importance of C-RAF in paradoxical MEK-ERK activation. <br />

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