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TranscriptomicsDual-mechanism ERK1/2 inhibitors exploit a distinct binding mode to block phosphorylation and nuclear accumulation of ERK1/2, resulting in enhanced potency
Here we have characterized the MoA of Erk inhibitors in terms of Erk1/2 signalling, gene expression and antiproliferative efficacy in BRAF and RAS mutant cell lines.
ORGANISM(S): Homo sapiens 
2020-10-08 | E-MTAB-7959 | biostudies-arrayexpress
UnknownERK1/2 signalling protects against apoptosis following endoplasmic reticulum stress but cannot provide long-term protection against BAX/BAK-independent cell death.
Not available
S-EPMC5607168 | biostudies-literature
UnknownERK1/2-dependent phosphorylation of BimEL promotes its rapid dissociation from Mcl-1 and Bcl-xL.
Not available
S-EPMC1894764 | biostudies-literature
UnknownERK1/2 inhibitors act as monovalent degraders inducing ubiquitylation and proteasome-dependent turnover of ERK2, but not ERK1.
Not available
S-EPMC10212521 | biostudies-literature
TranscriptomicsCharacterising the cellular activity of new Fibroblast Growth Factor Receptor tyrosine kinase inhibitors and identification of a gatekeeper mutation in FGFR3 as a mechanism of acquired resistance.
Fibroblast growth factor receptors (FGFRs) can act as driving oncoproteins in certain cancers due to mutation, over-expression or activating gene fusions and are therefore attractive drug targets. Here we have characterized tumour cell responses to three new inhibitors of FGFR1-3, AZ12576089, AZ129...
ORGANISM(S): Homo sapiens 
2012-10-02 | E-TABM-1222 | biostudies-arrayexpress
UnknownColorectal cancer cells with the BRAF(V600E) mutation are addicted to the ERK1/2 pathway for growth factor-independent survival and repression of BIM.
Not available
S-EPMC2643813 | biostudies-literature
UnknownAn mTORC1-to-CDK1 Switch Maintains Autophagy Suppression during Mitosis.
Not available
S-EPMC6964153 | biostudies-literature
UnknownIdentification of DYRK1B as a substrate of ERK1/2 and characterisation of the kinase activity of DYRK1B mutants from cancer and metabolic syndrome.
Not available
S-EPMC4735261 | biostudies-literature
UnknownOver-expressed, N-terminally truncated BRAF is detected in the nucleus of cells with nuclear phosphorylated MEK and ERK.
Not available
S-EPMC6304467 | biostudies-literature
UnknownMEK1/2 inhibitor withdrawal reverses acquired resistance driven by BRAF<sup>V600E</sup> amplification whereas KRAS<sup>G13D</sup> amplification promotes EMT-chemoresistance.
Not available
S-EPMC6497655 | biostudies-literature
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