The extracellular signal-regulated kinase: Multiple substrates regulate diverse cellular functions
By Seunghee Yoon, R. Seger. Growth Factors, 2006
1,333 citations recorded by the source corpus.
Subfields: Molecular Biology
View Paper: https://www.semanticscholar.org/paper/15d01f2a30e07f84d12af6b04930e951eb4a1a00
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Citations in the corpus
- Epidermal Growth Factor Receptor Cell Proliferation Signaling Pathways (2017, background): “Unlike the narrow substrate specificity of RAF and MEK, ERK has over one hundred downstream cytoplasmic and nuclear substrates [205].”
- The ERK1/2 mitogen-activated protein kinase pathway as a master regulator of the G1- to S-phase transition (2007, background): “ERK1/ERK2, which are expressed ubiquitously in mammalian cells, are multifunctional serine/threonine kinases that phosphorylate a vast array of substrates localized in all cellular compartments (Lewis et al., 1998; Pearson et al., 2001; Yoon and Seger, 2006).”
- The MAPK cascades: signaling components, nuclear roles and mechanisms of nuclear translocation. (2011, background): “Aside from the role of ERK1/2 in the induction of immediate early transcription upon stimulation, they were also shown to play a role in the regulation of many other transcription factors or transcription repressors [5].”
- Matrix density-induced mechanoregulation of breast cell phenotype, signaling, and gene expression through a FAK-ERK linkage (2009, positive): “The ERK/mitogen-activated protein kinase (MAPK) pathway has been implicated in multiple cellular processes such as proliferation, migration and apoptosis (Dhillon et al., 2007; Turjanski et al., 2007; Yoon & Seger, 2006).”
- The MEK/ERK cascade: from signaling specificity to diverse functions. (2007, background): “Upon stimulation, ERKs have been demonstrated to phosphorylate a large number of substrates [9].”
- ERK promotes tumorigenesis by inhibiting FOXO3a via MDM2-mediated degradation (2008, background): “Ras, PI(3)k and mTOR signalling controls tumour cell growth.”
- Reactive Oxygen Species Signaling and Oxidative Stress: Transcriptional Regulation and Evolution (2024, background): “This activation is essential for cellular responses to DNA is vulnerable to numerous lesions like base modi fi cations, single-strand breaks (SSBs) or double-strand breaks (DSBs), ultimately posing a risk of mutations and genomic instability [86]. stimuli such as growth [81].”
- MAP kinase signalling pathways in cancer (2007, background): “ERK signalling can, depending on the particular cell type, regulate processes such diverse as proliferation, differentiation, survival, migration, angiogenesis and chromatin remodelling (Dunn et al., 2005; Yoon and Seger, 2006).”
- Differential regulation and properties of MAPKs (2007, background): “Activation of ERK1/2 is involved in many cellular responses such as cell motility, proliferation, differentiation and survival (Lewis et al., 1998; Chen et al., 2001; Johnson and Lapadat, 2002; Yoon and Seger, 2006).”
- ERK1/2 MAP kinases in cell survival and apoptosis (2006, background): “These substrates can be categorized as transcription factors, protein kinases, protein phosphatases, cytoskeletal proteins, scaffold-ing proteins, receptors, signaling molecules, apoptosis-related proteins, as well as other types of proteins (Table 1) ( 22 ).”
- Targeting the Raf-MEK-ERK mitogen-activated protein kinase cascade for the treatment of cancer (2007, background): “Activated ERKs phosphorylate and regulate the activities of an ever growing roster of substrates that are estimated to comprise over 160 proteins (Yoon and Seger, 2006).”
- HIPPIE v2.0: enhancing meaningfulness and reliability of protein–protein interaction networks (2016, background): “All terminal nodes in pink (ELK1, MYC, JUN, TP53, SREBF1/2) are known substrates of ERK1 (52).”