Gilley R - Search Results

1

MEK1/2 inhibitor withdrawal reverses acquired resistance driven by BRAF^V600E amplification whereas KRAS^G13D amplification promotes EMT-chemoresistance.

Sale MJ, Balmanno K, Saxena J, Ozono E, Wojdyla K, McIntyre RE, Gilley R, Woroniuk A, Howarth KD, Hughes G, Dry JR, Arends MJ, Caro P, Oxley D, Ashton S, Adams DJ, Saez-Rodriguez J, Smith PD, Cook SJ. Sale MJ, et al. Among authors: gilley r. Nat Commun. 2019 May 2;10(1):2030. doi: 10.1038/s41467-019-09438-w. Nat Commun. 2019. PMID: 31048689 Free PMC article.

2

The duration of ERK1/2 activity determines the activation of c-Fos and Fra-1 and the composition and quantitative transcriptional output of AP-1.

Chalmers CJ, Gilley R, March HN, Balmanno K, Cook SJ. Chalmers CJ, et al. Among authors: gilley r. Cell Signal. 2007 Apr;19(4):695-704. doi: 10.1016/j.cellsig.2006.09.001. Epub 2006 Sep 15. Cell Signal. 2007. PMID: 17052890

3

ERK1/2-dependent phosphorylation of BimEL promotes its rapid dissociation from Mcl-1 and Bcl-xL.

Ewings KE, Hadfield-Moorhouse K, Wiggins CM, Wickenden JA, Balmanno K, Gilley R, Degenhardt K, White E, Cook SJ. Ewings KE, et al. Among authors: gilley r. EMBO J. 2007 Jun 20;26(12):2856-67. doi: 10.1038/sj.emboj.7601723. Epub 2007 May 24. EMBO J. 2007. PMID: 17525735 Free PMC article.

4

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

5

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

6

ERK5 and its role in tumour development.

Lochhead PA, Gilley R, Cook SJ. Lochhead PA, et al. Among authors: gilley r. Biochem Soc Trans. 2012 Feb;40(1):251-6. doi: 10.1042/BST20110663. Biochem Soc Trans. 2012. PMID: 22260700 Review.

7

Adaptation to chronic mTOR inhibition in cancer and in aging.

Gilley R, Balmanno K, Cope CL, Cook SJ. Gilley R, et al. Biochem Soc Trans. 2013 Aug;41(4):956-61. doi: 10.1042/BST20130080. Biochem Soc Trans. 2013. PMID: 23863163 Review.

8

Adaptation to mTOR kinase inhibitors by amplification of eIF4E to maintain cap-dependent translation.

Cope CL, Gilley R, Balmanno K, Sale MJ, Howarth KD, Hampson M, Smith PD, Guichard SM, Cook SJ. Cope CL, et al. Among authors: gilley r. J Cell Sci. 2014 Feb 15;127(Pt 4):788-800. doi: 10.1242/jcs.137588. Epub 2013 Dec 20. J Cell Sci. 2014. PMID: 24363449

9

Tumor cells with KRAS or BRAF mutations or ERK5/MAPK7 amplification are not addicted to ERK5 activity for cell proliferation.

Lochhead PA, Clark J, Wang LZ, Gilmour L, Squires M, Gilley R, Foxton C, Newell DR, Wedge SR, Cook SJ. Lochhead PA, et al. Among authors: gilley r. Cell Cycle. 2016;15(4):506-18. doi: 10.1080/15384101.2015.1120915. Cell Cycle. 2016. PMID: 26959608 Free PMC article.

10

Visualization of Endogenous ERK1/2 in Cells with a Bioorthogonal Covalent Probe.

Sipthorp J, Lebraud H, Gilley R, Kidger AM, Okkenhaug H, Saba-El-Leil M, Meloche S, Caunt CJ, Cook SJ, Heightman TD. Sipthorp J, et al. Among authors: gilley r. Bioconjug Chem. 2017 Jun 21;28(6):1677-1683. doi: 10.1021/acs.bioconjchem.7b00152. Epub 2017 May 12. Bioconjug Chem. 2017. PMID: 28449575 Free article.

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