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Tumor cells with KRAS or BRAF mutations or ERK5/MAPK7 amplification are not addicted to ERK5 activity for cell proliferation.
Cell Cycle. 2016;15(4):506-18. doi: 10.1080/15384101.2015.1120915.
Cell Cycle. 2016.
PMID: 26959608
Free PMC article.
Stimulating translational research: several European life science institutions put their heads together.
Bentires-Alj M, Rajan A, van Harten W, van Luenen HG, Kubicek S, Andersen JB, Saarela J, Cook SJ, Van Minnebruggen G, Roman-Roman S, Maurer C, Erler JT, Bertero MG.
Bentires-Alj M, et al.
Trends Mol Med. 2015 Sep;21(9):525-7. doi: 10.1016/j.molmed.2015.07.002. Epub 2015 Aug 5.
Trends Mol Med. 2015.
PMID: 26254816
Item in Clipboard
ERK5 and its role in tumour development.
Lochhead PA, Gilley R, Cook SJ.
Lochhead PA, et al.
Biochem Soc Trans. 2012 Feb;40(1):251-6. doi: 10.1042/BST20110663.
Biochem Soc Trans. 2012.
PMID: 22260700
Review.
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CDK1, not ERK1/2 or ERK5, is required for mitotic phosphorylation of BIMEL.
Gilley R, Lochhead PA, Balmanno K, Oxley D, Clark J, Cook SJ.
Gilley R, et al.
Cell Signal. 2012 Jan;24(1):170-80. doi: 10.1016/j.cellsig.2011.08.018. Epub 2011 Sep 8.
Cell Signal. 2012.
PMID: 21924351
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ERK1/2, but not ERK5, is necessary and sufficient for phosphorylation and activation of c-Fos.
Gilley R, March HN, Cook SJ.
Gilley R, et al.
Cell Signal. 2009 Jun;21(6):969-77. doi: 10.1016/j.cellsig.2009.02.006. Epub 2009 Feb 25.
Cell Signal. 2009.
PMID: 19249353
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