Meaningful relationships: the regulation of the Ras/Raf/MEK/ERK pathway by protein interactions.

By Walter Kolch. Biochemical Journal, 2000

1,503 citations recorded by the source corpus.

View Paper: https://www.semanticscholar.org/paper/a553ba9a74821128e29f081475e76ec7ca0dc4c6

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Citations in the corpus

ERK/MAPK signalling pathway and tumorigenesis (2020, background): “Activated ERK may enter the nucleus and bind to transcription factors that induce gene expression in response to extracellular stimuli, and regulate cell proliferation, differentiation, apoptosis and transcription (4,80-83).”
Kinase-Dead BRAF and Oncogenic RAS Cooperate to Drive Tumor Progression through CRAF (2010, background): “Active RAS recruits RAF to the membrane for activation through a complex process involving changes in phosphorylation and binding to other enzymes and scaffold proteins (Kolch, 2000).”
Abscisic Acid and Abiotic Stress Tolerance in Crop Plants (2016, background): “Phosphorylation and activation events in these kinases are modulated through their nonkinase domain by dimerization, binding of other regulatory proteins or phosphorylation by upstream MAPKKK kinases (Kolch, 2000).”
Chaperoning signaling pathways: molecular chaperones as stress-sensing 'heat shock' proteins. (2002, background): “Chaperones and the Ras/Raf-1 signal transduction pathway The Ras/Raf-1 signaling pathway has an important role in proliferation, cell differentiation, growth arrest and death (Campbell et al., 1998; Kolch, 2000).”
Mutations of the BRAF gene in human cancer (2002, background): “The three RAF genes code for cytoplasmic serine/threonine kinases that are regulated by binding RA”
Targeting the RAS/RAF/MAPK pathway for cancer therapy: from mechanism to clinical studies (2023, background): “83 Many modulators mediate the negative or positive regulation of RAF activity through the formation of signaling complexes, which play critical roles in cancer growth and progression.”
Transcriptional regulation of collagenase (MMP-1, MMP-13) genes in arthritis: integration of complex signaling pathways for the recruitment of gene-specific transcription factors (2001, background): “The JNKs and p38 kinases are activated in response to inflammatory cytokines, osmotic stress and apoptotic signals [20], while the ERKs respond to cytokines, growth factors and phorbol esters [19,21] (Fig.”
Mechanism of activation of the RAF-ERK signaling pathway by oncogenic mutations of B-RAF. (2004, background): “…RAF phosphorylation that combine to stimu-3 Section of Gene Function and Regulation late its serine/threonine kinase activity, triggering se-The Institute of Cancer Research quential phosphorylation and activation of MEK andChester Beatty Laboratories ERK (Kolch, 2000; Morrison and Cutler, 1997).”