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BRAF activates phosphorylated ERK. 13 / 13
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"Disruption of BRAF dimerization with the R509H mutation almost completely abolishes induction of p-MEK and p-ERK by class 3 BRAF mutants, but not by dimer independent BRAF (V600E) (XREF_FIG and XREF_FIG)."

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"Overexpression of Braf rapidly led to MAPK activation with increased pERK, cell dedifferentiation, and disruption of follicular organization."

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"f Western blot analyses showing that B-Raf can activate p-ERK and that treatment with 20 muM HO-1 inhibitor ( ZnPPIX ) for 12 h can rescue the p-ERK expression of B-Raf ."

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"Pharmacological inhibition of BRAF with vemurafenib and MEK with PD0325901 markedly reduced basal phospho-ERK (pERK) in melanoma cells while increasing SOX2, and this induction was specific to the inhibitor treatment as it was time dependent (XREF_FIG)."

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"Transfection of follicular thyroid or BRAF PTC cells with BRAF induced p-ERK1/2 and enhanced uptake of dextran and albumin (Fig. 3A-C; Supplementary Fig. S3A-B)."

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"We demonstrated that BRAF and RAF1 variants increased p-ERK and enhanced sprouting capacity relative to wild type, and that biochemistry and morphology reversal could be achieved by MEK inhibition (Extended Data Fig. 1a–d)."

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"Thus, we concluded that the ~100‐fold shift in MEKi potency for pERK activated by EGFR when compared with BRAF V600E activated pERK (Figs  xref and xref ) primarily arises in the second step as a result of a lower rate of phosphorylation rate of MEKi‐uMEK by BRAF V600E compared with apo uMEK."

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"Intriguingly, RKO had only partial inhibition of pERK at 1microM (60% by densitometry); however dual PI3K and BRAF inhibition reduced pERK further (90% inhibition)."

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"In contrast, introduction of the P124S MEK1 mutant into human cells (HEK293) lacking oncogenic BRAF increased phospho-ERK signaling, suggesting that the oncogenic BRAF in melanoma cells was dominant over the 2 exon 3 MEK1 mutants with regard to ERK activation."

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"Thus, we concluded that the ~100‐fold shift in MEKi potency for pERK activated by EGFR when compared with BRAF activated pERK (Figs 2A and EV3A) primarily arises in the second step as a result of a lower rate of phosphorylation rate of MEKi‐uMEK by BRAF compared with apo uMEK.Additionally, we found that, at high concentrations of RAFi (Fig 4D, rightmost diagram), step B3 (blue) had high gain (due to low DUSP activity) under conditions in which the channel transmitted no signal and was functionally inactive (due to RAFi‐BRAF binding)."

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"Next, we analyzed the protein expression of MAPK and ERK signaling which regulates cell proliferation and differentiation, and we observed that FAM83F increased BRAF levels and induced the activation of pERK (XREF_FIG)."

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"BRAF siRNA reduced BRAF and p-ERK in transfected melanoma cells."

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"In the MAPK pathway-dependence mechanism, B-Raf or MEK inhibitor concentrations that normally suppress cell growth can reactivate p-ERK."