IndraLab

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Mutated RAS activates ERK. 41 / 41
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"Suppression of Erk activation and in vivo growth in esophageal cancer cells by the dominant negative Ras mutant, N116Y."
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"Most oncogenic activities that lead to constitutive activation of ERK1/2 signalling occur upstream of ERK1/2 activation, including overexpression of receptor tyrosine kinases such as epidermal growth factor receptor (EGFR), activating mutations in receptor tyrosine kinases, sustained autocrine or paracrine production of activating ligands, as well as Ras mutations and B-Raf mutations, resulting in enhanced or constitutive downstream activation of the Raf-MEK-ERK pathway."
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"Furthermore, PLX4032 may enhance the growth of tumors in which the ERK pathway is activated by RAS mutation or upstream receptor kinases."
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"In a simple linear view of RAS‐to‐ERK transduction, the mutant RAS GTPase activities being 50‐ to 800‐fold lower than wild type would be expected to produce correspondingly large changes in both pre‐stimulus and stimulated ERK activity."
33073539
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"The RAS mutations resulted in persistent activation of MAPK and ERK in these cells despite FLT3 inhibition."
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"First, our systematic dataset reconciles previously conflicting observations of ERK activity driven by RAS mutations."
33073539
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"Perhaps not surprisingly then, the earlier assumptions that pharmacologic inhibition of ERK activation at the level of either Raf or MEK would be equivalent, and would be effective to block ERK activation driven by mutant Ras, have proven incorrect."
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"In a majority of human cancers, the PI3K and AKT pathway is frequently activated by the activating mutations of PI3K p110alpha (PIK3CA) and the loss or inactivating mutation of PTEN, whereas hyper activation of MEK and ERK signaling driven by mutant RAS and BRAF is also a common oncogenic event in a variety of cancers [XREF_BIBR, XREF_BIBR]."
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"Papillary and nonpapillary cancers contained similar frequencies of activating RAS mutations (5-10%) [XREF_BIBR], which also function to promote downstream ERK activation."
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"Thus, it is assumed that the mutation of Ras finally cause the constitutive activation of the ERK signal transduction pathway."
10027757
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"However, none of the TKI resistant cell lines showed mutations of the most affected regions of the genes (amino acids 12, 13 and 60 in K-RAS, amino acids 12, 13, and 61 in N-RAS; data not shown), a finding which was scarcely unexpected because RAS mutations would not only stimulate PI3K, but also ERK1/2 in an imatinib-insensitive manner."
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"RAS mutations constitutively activate MAPK/ERK pathway, as shown in Figure 1C.Interestingly, some studies have also reported somatic oncogenic mutations in normal endometrium and breast cells of healthy women [7, 8]."
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"In fact, 85-90% of papillary carcinomas possess RET, NTRK1, BRAF or RAS mutations that induce MEK and ERK signaling."
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"Conversely, dominant negative mutant of Ras inhibited the protective effects of ERK."
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"Dominant negative mutants of Ras (but not Rac or Cdc42) specifically inhibited ERK activation by v-Fps and Myr-Fes, demonstrating that ERK activation occurs exclusively downstream of Ras."
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"Similarly, M-Ras, with its ability to activate both the MAPK and PI3K pathways, is an excellent candidate gene to be found mutated in human cancer.In cell lines derived from a wide variety of tumor ty[MISSING/INVALID CREDENTIALS: limited to 200 char for Elsevier]"
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"XREF_BIBR RAS mutations hyperactivate PAK1 and initiate PAK1 and ERK or PAK1 and PI3K cascades."
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"That more robust ERK activation is deleterious to cancer development is also supported by the nonoverlapping occurrence of RAS mutations with mutations in BRAF, NF1, or EGFR (cBioPortal)."
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"The dysregulation of these pathways is very common in many cancer types : Receptor Tyrosine Kinases (RTKs) amplification and mutations, PIK3CA or Ras mutations, and loss-of-function mutations in negative regulators such as PTEN, collaborate to constitutively activate either PI3K and Akt or Ras and ERK signaling coupled to mTOR signaling."
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"ERK MAPK activation induced by the Tpl2 protein is blocked by dominant negative mutants of Ras and Raf-1, and a kinase deficient Tpl2 mutant downregulates mitogenic signals induced by v-Ha-Ras or v-Ra[MISSING/INVALID CREDENTIALS: limited to 200 char for Elsevier]"
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"Nevertheless, a dominant negative mutant of Ras, Ras DN, completely blocked the stochastic ERK activity pulses."
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"ERK on the other hand is activated mainly by the mutant RAS, while inhibited by another feedback mechanism through CRAF."
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"MRAS targets SHOC2-PP1 to dephosphorylate the S259 site of RAF proteins when bound to other molecules of RAS (or RRAS members) and plays a critical contribution to ERK activation by RTKs and mutant RA[MISSING/INVALID CREDENTIALS: limited to 200 char for Elsevier]"
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"Whereas a RAS mutation in other carcinomas might activate both ERK and PI3K signaling, we propose that prostate tumors have an alternative way to activate these pathways : PTEN deletion (PI3K and AKT activation) coupled with oncogenic ETS-overexpression (activation of RAS and ERK target genes)."
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"Ectopic expression of the constitutively active mutant Ras form N-RasD12 in autoreactive cells raises active Erk, halts receptor editing via PI3 kinase, and promotes differentiation via Erk, breaking central tolerance."
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"Nevertheless, a dominant negative mutant of Ras suppressed the ERK activity pulses, strongly suggesting that the noise is evoked at the level of Raf binding to Ras."
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"In addition, a lack of sensitivity to MEK inhibition is consistent with the observation that mutant Ras often does not drive aberrant activation of ERK in cancer cells XREF_BIBR."
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"Oncogenic RAS mutations, which activate both the RAF-MAPK/ERK (mitogen-activated protein kinase) and phosphoinositide 3-kinase (PI3K)-AKT signalling pathways, are among the most prevalent genetic changes found in human cancers, occurring in approximately 20% of human tumors [13,14]."
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"However, when ERK1/2 was selectively activated by an oncogenic RAS mutant, ERK5 phosphorylation at Thr732 was induced without affecting the phosphorylation status at TEY or Ser769/773/775."
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"The CAM dependent step in the Erk1/2 activation cascade is downstream of Ras activation, because inhibitors of CAM antagonize Erk1/2 activation induced by constitutively activated mutants of Ras and c-Src but not by constitutively activated mutants of Raf and MEK (mitogen and extracellular signal regulated kinase)."
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"ERK activation was shown to be dependent on the phosphorylation of the MUC1-CT and could be abolished by a dominant negative Ras mutant or by a MEK inhibitor, thus arguing that the MUC1-CT mediates the Grb2-SOS-Ras-MEK-ERK signaling cascade which leads to cell division."
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"This contrasts with observations made in the majority of cell models of Ras transformation, in which ectopic expression of mutant Ras causes persistent ERK activation."
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"It has been shown that the oncogenic Ras mutant, RasV12, activates ERK1/2 strongly, and that the constitutively active MEK5 mutant, MEK5D, selectively activates ERK5 XREF_BIBR, XREF_BIBR."
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"These results suggest that the wild-type p53 has a weak effect on RAS expression and that the RAS mutants V12, S35 and E38 activate the ERK cascade and weaken p53 activity to promote proliferation and apoptosis resistance, while C40 activates the AKT cascade and has little effect on p53 expression and thus inhibits anti-apoptotic processes and proliferation."
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"Ras mutation results in constitutive activation of Erk1/2 and PI3K and Akt pathways leading to increased cell proliferation and decreased apoptosis in pancreatic cancer cells."
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"Oncogenic RAS mutations and the BRAF V599E mutation induce constitutive ERK activity when cDNAs encoding the mutant versions are expressed in tissue culture cells."
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"Co-expression of wild-type Aurora-A and mutant Ras enhances the signaling of the MEK and ERK, AKT and RalA activity."
20003375
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"Cotransfection of RasN17, a dominant negative Ras mutant, prevented DA induced activation of both ERK and JNK."
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"RAS mutants only moderately elevate ERK activity, and only without stimulation."
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"These results reinforce the notion that an activating Ras mutation, as present in PANC-1 cells, is not sufficient to constitutively activate the ERK pathway."
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"Overexpression of CrkL also enhanced SDF-1-induced activation of the Raf-1/MEK/Erk signaling pathway as well as that of the small GTPases Ras, Rap1, and Rac, while a dominant negative mutant of Ras or Rac suppressed CrkL enhanced Erk activation."
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