Differential regulation of MAP kinase signalling by dual-specificity protein phosphatases
By DM Owens, S. Keyse. Oncogene, 2007
827 citations recorded by the source corpus.
Subfields: Molecular Biology
View Paper: https://www.semanticscholar.org/paper/498120784ca0f9c1a5b2dff9a71a0e96c57053ca
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In Molecular Biology
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Citations in the corpus
- Phosphatase‐mediated crosstalk between MAPK signaling pathways in the regulation of cell survival (2008, neutral): “amino terminus kinase-binding domain (70).”
- Vitamin D Inhibits Monocyte/macrophage Pro-inflammatory Cytokine Production by Targeting Mitogen-Activated Protein Kinase Phosphatase 1 (2012, background): “The phosphorylation of three subfamilies of MAPK— ERK, JNK, and p38—was examined by flow cytometry.”
- V600EBRAF is associated with disabled feedback inhibition of RAF–MEK signaling and elevated transcriptional output of the pathway (2009, background): “Among those genes most changed in response to MEK inhibition were ERK targets such as CCND1, multiple transcription factors, and genes involved in the feedback inhibition of MEK/ERK signaling [dual specificity phosphatase 6 (DUSP6), DUSP4, SPRY2, SPRY4, and SPRED2] (21, 22).”
- MicroRNA control in the immune system: basic principles. (2009, background): “Dual specificity phosphatases DUSP5 and DUSP6 dephosphorylate and inactivate the kinase ERK, with the former acting in the nucleus and the latter acting in the cytoplasm (Owens and Keyse, 2007; Tanzola and Kersh, 2006).”
- Cisplatin nephrotoxicity: mechanisms and renoprotective strategies. (2008, background): “Activation of MAPKs regulates cellular homeostasis and processes including proliferation, differentiation, and apoptosis.(87,88) ERK, p38, and JNK/SAPK are activated in various experimental models of cisplatin nephrotoxicity.”