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Activation of the ERK1/2 pathway by aberrant RAS/RAF signalling, DNA damage, and oxidative stress leads to cellular senescence. [12] Low doses of DNA damage resulting from cancer therapy cause ERK1/2 to induce senescence, whereas higher doses of DNA damage fail to activate ERK1/2, and thus induce cell death by apoptosis. [12]
The signal that starts the MAPK/ERK pathway is the binding of extracellular mitogen to a cell surface receptor.This allows a Ras protein (a Small GTPase) to swap a GDP molecule for a GTP molecule, flipping the "on/off switch" of the pathway.
The protein encoded by this gene is a member of the MAP kinase family. MAP kinases, also known as extracellular signal-regulated kinases (ERKs), act as an integration point for multiple biochemical signals, and are involved in a wide variety of cellular processes such as proliferation, differentiation, transcription regulation and development.
26417 Ensembl ENSG00000102882 ENSMUSG00000063065 UniProt P27361 Q63844 RefSeq (mRNA) NM_001040056 NM_001109891 NM_002746 NM_011952 RefSeq (protein) NP_001035145 NP_001103361 NP_002737 NP_036082 Location (UCSC) Chr 16: 30.11 – 30.12 Mb Chr 7: 126.36 – 126.36 Mb PubMed search Wikidata View/Edit Human View/Edit Mouse Mitogen-activated protein kinase 3, also known as p44MAPK and ERK1, is an ...
Inhee Mook-Jung is a South Korean Neuroscientist.She works on Alzheimer's disease pathogenesis.Professor Mook drew attention in 2006 for discovery that ERK1/2 proteins were involved in the regulation of beta amyloid, a substance that causes dementia. [1]
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SHOC2 ubiquitination mediated by HUWE1 is triggered by growth factor activation of the ERK1/2 pathway and is a prerequisite for the subsequent ubiquitination of the RAF-1 kinase associated with SHOC2. [5]
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