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Mutated BRAF activates ERK. 55 / 55
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"Accordingly, the present data show an inverse correlation between the activities of MEK-ERK-RSK signaling and AMPK in BRAF V600E CRC cells, suggesting that BRAF mutations activate phospho-MEK, Erk, and p90RSK without activating AMPK (XREF_FIG upper panel) and that inhibition of BRAF using selective BRAF inhibitors leads to inactivation of phospho-MEK, Erk, and p90RSK and activation of AMPK (XREF_FIG lower panel)."
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"The missense BRAF mutation that results in a valine (V) to glutamic acid (E) substitution at codon 600 (BRAF p.V600E) constitutively activates MAPK/ERK pathway [21] (Figure 1B)."
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"A clinically relevant dose of Dabrafenib, a type I RAF-inhibitor, in HEK293T cells reduced ERK activity induced by BRAF mutations conferring high kinase activity in the presence and absence of CRAF."
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"BRAF mutation activates ERK1/2 which in turn up-regulates Brn-2, a molecule highly over-expressed in BRAF mutant melanoma cells, but not in melanocytes or melanoblasts XREF_BIBR."
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"BRAF mutations are present in about 50% of melanomas, causing an over-activation of the MAPK and ERK pathway involved in cell proliferation and survival."
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"This result may explain why H1666 and H508 cells are more sensitive to Trametinib than to Selumetinib, as BRAF mutations in these cell lines activate the ERK pathway in a CRAF dependent manner, similarly to KRAS mutated cells."
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"Do all BRAF mutations induce constitutive ERK activation?"
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"Aberrant cell cycle related proteins such as Cyclin D1 has been shown to be reversible using chemical inhibitors suggesting that expression is not a constitutive disease trait but elicited by MEK and [MISSING/INVALID CREDENTIALS: limited to 200 char for Elsevier]"
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"KRAS and BRAF mutations were significantly correlated to early stage (I/II), grade (p = 0.004), histotype (p = 0.0014), and activated ERK (p < 0.001) [16]."
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"To investigate the effect of Dabrafenib on ERK signaling induced by different BRAF mutations, we transiently expressed 13 BRAF mutants singly or with CRAF in HEK293T cells; we then evaluated the ERK activation status after 2 h of Dabrafenib treatment (2.5 muM)."
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"The overexpression of Kidins220 resulting in sustained activation of MEK and ERK signalling rather than BRAF mutation, has been identified as leading to acral lentiginous melanoma tumourigenesis."
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"XREF_BIBR, XREF_BIBR While inhibitors of mutant BRAF monomers suppress the ERK signaling, they relieve ERK dependent negative feedback and reactivate ligand dependent EGFR and RAS signaling upon wild-type RAF dimers in melanoma cells."
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"In melanoma cells, MEK and ERK1/2 can be activated by active mutations of BRAF in 2D cultures."
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"Activating BRAF mutations and fusion products constitutively activates the MAPK/ERK pathway (also known as the RAS-RAF-MEK-ERK pathway) that communicates receptor signaling to the DNA in the nucleus of the cell [23]."
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"Small molecule inhibitors of mutant BRAF were developed to block protein kinase activity and prevent activation of MAPK and ERK signaling in tumor cells (XREF_FIG)."
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"A number of the BRAF mutations that have been identified in melanoma, including D594V, G596R and G466V, do not activate the catalytic activity of BRAF, but do result in activation of MEK and ERK."
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"Mutant BRAF constitutively activates the downstream kinases, MEK and ERK, within the mitogen activated protein kinase (MAPK) pathway, leading to uncontrolled cell proliferation."
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"Further, investigators have shown that most BRAF mutants with reduced kinase activity can still activate MEK and ERK via transactivation of CRAF."
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"Oncogenic BRAF mutations lead to overactivity of its downstream effectors MEK and ERK 32."
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"Next, to evaluate a potential interplay between mutant BRAF-induced ERK1/2 signaling and BMP-induced SMAD signaling pathways in the melanoma, we analyzed patient survivals as a function of high versus low expression of BMP1, BMP2, and BMP6 in two patient groups: BRAF mutant and BRAF-wildtype."
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"Paradoxically, most BRAF mutants with reduced kinase activity still activate MEK and ERK via transactivation of CRAF."
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"These data suggest that in some class 2 BRAF mutants, while mutant BRAF activates ERK, an additional contribution to ERK activation can come from upstream signaling."
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"Furthermore, Dabrafenib also inhibited ERK activity induced by BRAF mutants conferring impaired kinase activity co-expressed with CRAF."
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"The most common BRAF mutation (BRAF V600E), found in about 8% of human tumors and more than 50% of melanomas, results in ERK signaling upregulation, independent of RAS activity."
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"Overexpression of this BRAF mutant (BRAF-A481F and AAAA) did not stimulate ERK activation suggesting that these residues are critical for the ability of kinase-dead BRAF to stimulate ERK."
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"Thus, ERK signalling driven by low activity or kinase-dead BRAF mutants is RAS dependent and regulated by upstream signalling."
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"Pratilas et al. evaluated ERK dependent transcriptional output and feedback signaling in tumor cells in which ERK signaling is driven by mutant BRAF and in tumor cells in which ERK is driven by upstream receptors like EGFR or HER2."
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"Kinase-active Mutant BRAF induces MEK and ERK pathway activation in HEK293T cells."
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"However co-expression of class 3 BRAF mutants with wild-type CRAF in these cells induced ERK signalling (XREF_FIG)."
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"These differences suggest that although both BRAF mutation and the RET and PTC1 rearrangement are able to activate the MEK and ERK signal transduction pathway, other pathways not affected by PD0325901 may be involved in PTC cells with the RET and PTC rearrangements."
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"Furthermore, certain BRAF V600E -mutant melanomas and colorectal carcinomas appear to develop a dependence or ' addiction ' to Bim repression, since inhibition of mutant BRAF driven ERK1/2 signalling results in Bim accumulation and Bim mediated apoptosis."
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"Mutant BRAF led to deregulated activation of downstream MEK and ERK effectors in melanoma patients."
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"Commonly found BRAF mutants stimulate constitutive RAF and MEK (mitogen activated ERK activating kinase)/ERK (extracellular signal regulated kinase) pathway activation and act as transforming oncogenes in NIH-3T3 cells and immortalized murine melanocytes."
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"The BRAF mutation activates the MEK and ERK pathway by means of its effectors, which are the production and promotion of the malignant phenotype through genetic expression and proliferation [XREF_BIBR]."
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"WNT signalling is known to play a crucial role in thyroid carcinogenesis, and several mechanisms of its deregulation have been described, including inhibition of the β-catenin degradation complex via its phosphorylation by RET/PTC, inhibition of E-cadherin expression through the MAPK/ERK pathway activated by BRAF mutations, and activation of both canonical and non-canonical Wnt pathways by RAS mutations ."
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"BRAF mutations constitutively activate ERK signaling through hyperactivation of the RAS-ERK pathway, resulting in enhanced cell proliferation and survival (Brose et al., 2002; Naoki et al., 2002)."
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"BRAF mutations are known to activate ERK and should not be classified as wild-type Ras."
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"Ikenoue et al. [XREF_BIBR] indicated that the BRAF mutations of CRC can promote the activation of ERK, which activates downstream transcription factors to induce a range of biochemical processes including cell differentiation, proliferation, growth, while acting as the inhibitor of apoptosis."
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"Indeed, the persistent expression of mutant BRAF was responsible for rebound activation of ERK, as the addition of a BRAF V600E inhibitor or specific knockdown of mutant BRAF inhibited reactivation of ERK after treatment with AUY922."
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"The most common oncogenic BRAF mutation in melanomas, V600E (formerly called V599E), results in constitutive ERK signalling in vivo and can transform immortal fibroblasts (Davies et al, 2002) and immortal mouse melanocytes (Wellbrock et al, 2004)."
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"XREF_BIBR, XREF_BIBR BRAF mutations increase MEK and ERK activity, promoting tumour proliferation and growth."
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"In the BRAF mutant cells, AKT and ERK are regulated by similar positive and negative pathways as that in the KRAS mutant cells, except that ERK is activated by the mutant BRAF instead of KRAS."
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"Dr. Thakur 's reason that if vemurafenib were withheld at this point the extra ERK stimulating signal from new liberated mutant BRAF might cause ERK is an effective as under active ERK for shutting cell cycle down."
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"A recent study demonstrated that the MAPK/ERK signaling pathway activated by the BRAF mutation was able to induce epigenetic aberrations by H3K27me3 and MYC [44]."
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"In HEK293T cells, Trametinib modestly decreased ERK activity induced by BRAF mutations conferring elevated kinase activity while strongly inhibited kinase impaired BRAF and CRAF induced ERK activation."
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"Thus, activated BRAF mutants significantly increase ERK signaling despite causing feedback inhibition of RAS activity to almost undetectable levels."
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"Experimental evidence has suggested that BRAF mutations cause BRAF kinase activity and increased ERK signaling, leading to cell proliferation in melanoma cells (Davies et al., 2002; Dong et al., 2003;[MISSING/INVALID CREDENTIALS: limited to 200 char for Elsevier]"
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"Mutant BRAF triggers constitutive activation of the MAPK and ERK pathway and is typically mutually exclusive of activating RAS mutations in tumors [XREF_BIBR, XREF_BIBR]."
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"Singly, Dabrafenib only weakly suppresses mutant BRAF induced ERK signaling and can induce ERK paradoxical activation in CRAF overexpressing cells."
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"BRAF mutations are known to activate ERK and should not be classified as wild-type Ras (Oikonomou et al., 2014)."
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"Whether mult-HCL has entirely by passed any requirements for BCR, possibly due to mutant BRAF constitutively activating the ERK1/2 pathway, remains at present speculative."
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"In about half of all melanoma patients, tumor growth is driven by gain-of-function mutations of BRAF (v-rat fibrosarcoma (Raf) murine sarcoma viral oncogene homolog B), which results in constitutive ERK activation."
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"These BRAF mutations exhibit impaired kinase activity but induce ERK signaling by dimerizing with and activating CRAF."
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"These data indicate that RBJ may provoke MEK and ERK activation initiated either by Ras / Braf mutations or by other upstream signals activating MEK and ERK."
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"10 One of the most common genetic alterations found in approximately 40-50% of melanomas is the constitutively activating mutation of the Braf serine/threonine kinase, which leads to unchecked stimulation of the mitogen activated kinase and extracellular signal regulated kinase (MEK) and extracellular signal regulated kinase (ERK) pathway."
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