Molecular interpretation of ERK signal duration by immediate early gene products

By Leon O. Murphy, Sallie W. Smith, Rey-Huei Chen, D. Fingar, J. Blenis. Nature Cell Biology, 2002

1,006 citations recorded by the source corpus.

View Paper: https://www.semanticscholar.org/paper/dfa3dc89d30bc1b734f817c261b6b0136bd729d3

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Citations in the corpus

Activation and Function of the MAPKs and Their Substrates, the MAPK-Activated Protein Kinases (2011, background): “essential for osteosarcoma formation in mice (52, 80, 245).”
Regulation of PDGF and its receptors in fibrotic diseases. (2004, background): “have shown that the immediate early gene product c-Fos functions as a sensor for ERK signal duration, c-Fos (and perhaps other immediate early genes) is phosphorylated by still-active ERK in PDGF-stimulated cells to function in cell-cycle progression [135].”
Growth factor-induced MAPK network topology shapes Erk response determining PC-12 cell fate (2007, methodology): “A model for the molecular interpretation of Erk signal strength and duration by immediate early gene (IEG) products was propose”
The MAPK pathway across different malignancies: A new perspective (2014, background): “When the MAPK/ERK signal is transient, c-FOS is unstable and degraded in the nucleus; but, if the signal is sustained, then c-FOS is phosphorylated, and specific domains are exposed, promoting more ERK activation.(25)”
Feedback regulation of EGFR signalling: decision making by early and delayed loops (2011, background): “These differences, along with differences in the stability of IEG products induced by EGF- or NGF-induced ERK activatio”
Encoding and Decoding Cellular Information through Signaling Dynamics (2013, neutral): “In the ERK pathway, transient and persistent ERK dynamics are distinguished by a set of ‘‘immediate early gene products’’ that accumulate in response to activated ERK (Murphy et al., 2002, 2004).”
The Molecular Bases of Training Adaptation (2007, background): “Moreover, the role of ERK1/2 in regulating immediate early gene (IEG) responses and the cell cycle programme has been shown to be dependent on the strength and duration of the signal (Wu et al. 2000b; Assoian 2002; Murphy et al. 2002; Murphy et al. 2004).”
The RSK family of kinases: emerging roles in cellular signalling (2008, background): “Upon activation, a fraction of the activated ERKs and RSKs enter the nucleus, and this translocation correlates with the induction of immediate-early gene expressio”
ERK1/2 MAP kinases: structure, function, and regulation. (2012, background): “c-Fos phosphorylation catalyzed by ERK1/2 at Ser374 and that catalyzed by their downstream MAPKAP kinase RSK at Ser362 stabilizes c-Fos for several hours [88,89].”
The interplay between the glucocorticoid receptor and nuclear factor-kappaB or activator protein-1: molecular mechanisms for gene repression. (2003, background): “with activation of JNK and ERK1/2 (via increased MKP1 levels), which prevented AP-1 phosphorylation (283, 286, 552, 553) (Fig.”
Signal transduction in cancer. (2015, background): “Elk1, for example, in combination with the SRF transcription factor, induces the immediate early gene FOS, whose product is also stabilized by ERK phosphorylation (Murphy et al. 2002).”
The MAPK cascades: signaling components, nuclear roles and mechanisms of nuclear translocation. (2011, background): “ylation by nuclear ERK1/2 and their downstream RSKs on Ser374 and Ser362 in the C-terminus of c-Fos is the first step in its stabilization [97].”
The MEK/ERK cascade: from signaling specificity to diverse functions. (2007, background): “[71,86,96], who demonstrated that signal duration is likely to influence the transcription and activity of immediate early genes, such as c-Fos, c-Jun, c-Myc and Egr1.”