Recent, selected publications
Little AS, Balmanno K, Sale MJ, Smith PD, Cook SJ (In press) Tumour cell responses to MEK1/2 inhibitors - acquired resistance and pathway remodeling.
Biochemical Society Transactions
Lochhead PA, Gilley R, Cook SJ (|In press) ERK5 and its role in tumour development.
Biochemical Society Transactions
Gilley R, Lochhead PA, Balmanno K, Oxley D, Clark J, Cook SJ (In press) CDK1, not ERK1/2 or ERK5, regulates mitotic phosphorylation of BIMEL.
Cellular Signalling
Wiggins CM, Tsvetkov P, Johnson M, Joyce CL, Lamb CA, Bryant NJ, Komander D, Shaul Y, Cook SJ (2011) BIMEL, an intrinsically disordered protein, is degraded by 20S proteasomes in the absence of poly-ubiquitylation.
Journal of Cell Science 124 969-977
http://dx.doi.org/10.1242/jcs.058438
Little AS, Balmanno K, Sale MJ, Newman S, Dry JR, Hampson M, Edwards PAW, Smith PD, Cook SJ (2011) Amplification of the driving oncogene, KRAS or BRAF, underpins acquired resistance to MEK1/2 inhibitors in colorectal cancer cells.
Science Signaling 4 ra17 (Correction: Science Signaling, 2011, vol. 4, no. 170, p. er2)
http://dx.doi.org/10.1126/scisignal.2001752
Carragher LAS, Snell KR, Giblett SM, Aldridge VSS, Patel B, Cook SJ, Winton DJ, Marais R, Pritchard CA (2010) V600EBraf induces gastrointestinal crypt senescence and promotes tumour progression through enhanced CpG methylation of p16INK4a.
EMBO Molecular Medicine 2 458-471
http://dx.doi.org/10.1002/emmm.201000099
Wiggins CM, Johnson M, Cook SJ (2010) Refining the minimal sequence required for ERK1/2-dependent poly-ubiquitination and proteasome-dependent turnover of BIM.
Cellular Signalling 22 801-808
http://dx.doi.org/10.1016/j.cellsig.2010.01.004
Knights V, Cook SJ (2010) De-regulated FGF receptors as therapeutic targets in cancer.
Pharmacology and Therapeutics 125 105-117
http://dx.doi.org/10.1016/j.pharmthera.2009.10.001
Gillings AS, Balmanno K, Wiggins CM, Johnson M, Cook SJ (2009) Apoptosis and autophagy: BIM as a mediator of tumour cell death in response to oncogene-targeted therapeutics.
FEBS Journal 276 6050-6062
http://dx.doi.org/10.1111/j.1742-4658.2009.07329.x
Balmanno K, Chell SD, Gillings AS, Hayat S, Cook SJ (2009) Intrinsic resistance to the MEK1/2 inhibitor AZD6244 (ARRY-142886) is associated with weak ERK1/2 signalling and/or strong PI3K signalling in colorectal cancer cell lines.
International Journal of Cancer 125 2332-2341
http://dx.doi.org/10.1002/ijc.24604
Balmanno K, Cook SJ (2009) Tumour cell survival signalling by the ERK1/2 pathway.
Cell Death and Differentiation 16 368-377
http://dx.doi.org/10.1038/cdd.2008.148
Gilley R, March HN, Cook SJ (2009) ERK1/2, but not ERK5, is necessary and sufficient for phosphorylation and activation of c-Fos.
Cellular Signalling 21 969-977
http://dx.doi.org/10.1016/j.cellsig.2009.02.006
Densham RM, Todd DE, Balmanno K, Cook SJ (2008) ERK1/2 and p38 cooperate to delay progression through G1 by promoting cyclin D1 protein turnover.
Cellular Signalling 20 1986-94
http://dx.doi.org/10.1016/j.cellsig.2008.07.005
Wickenden JA, Jin H, Johnson M, Gillings AS, Newson C, Austin M, Chell SD, Balmanno K, Pritchard CA, Cook SJ 2008) Colorectal cancer cells with BRAFV600E mutation are addicted to the ERK1/2 pathway for growth factor-independent survival and repression of BIM.
Oncogene 27 7150-61
http://dx.doi.org/10.1038/onc.2008.335
Roderick HL, Cook SJ (2008) Ca2+ signalling checkpoints in cancer; remodelling Ca2+ for cancer cell proliferation and survival.
Nature Reviews Cancer 8 361-375
http://dx.doi.org/10.1038/nrc2374
Arkell RS, Dickinson RJ, Squires M, Hayat S, Keyse SM, Cook SJ (2008) DUSP6/MKP-3 inactivates ERK1/2 but fails to bind and inactivate ERK5.
CellularSignalling 20 836-843
http://dx.doi.org/10.1016/j.cellsig.207.12.014
Wiggins CM, Band H, Cook SJ (2007) c-Cbl is not required for ERK1/2-dependent degredation of BimEL.
Cellular Signalling 19 2605-2611
http://dx.doi.org/10.1016/j.cellsig.2007.08.008
Ewings KE, Hadfield-Moorhouse K, Wiggins CM, Wickenden JA, Balmanno K, Gilley R, Degenhardt K, White E, Cook SJ (2007) ERK1/2-dependent phosphorylation of BimEL promotes its rapid dissociation from Mcl-1 and Bcl-xL.
EMBO Journal 26 2856-2867
http://dx.doi.org/10.1038/sj.emboj.7601723
Ley R, Ewings KE, Hadfield K, Cook SJ (2005) Regulatory phosphorylation of Bim: sorting out the ERK from the JNK.
Cell Death and Differentiation 12 1008-1014
http://dx.doi.org/10.1038/sj.cdd.4401688
Ley R, Hadfield K, Howes EA, Cook SJ (2005) Identification of a DEF-type docking domain for extracellular signal-regulated kinases 1/2 that directs phosphorylation and turnover of the BH3-only protein BimEL.
Journal of Biological Chemistry 280 17657-17663
http://dx.doi.org/10.1074/jbc.M412342200
Ley R, Ewings KE, Hadfield K, Howes EA, Balmanno K, Cook SJ (2004) Extracellular signal-related kinases 1/2 are serum-stimulated "BimEL-kinases" that bind to the BH3-only protein BimEL causing its phosphorylation and turnover.
Journal of Biological Chemistry 279 8837-8847
http://dx.doi.org/10.1074/jbc.M311578200
Todd DE, Densham RM, Molton SA, Balmanno K, Newson C, Weston CR, Garner AP, Scott L, Cook SJ (2004) ERK1/2 and p38 cooperate to induce a p21CIP1-dependent G1 cell cycle arrest.
Oncogene 23 3284-3295
http://dx.doi.org/10.1038/sj.onc.1207467
Balmanno K, Millar T, McMahon M, Cook SJ (2003) ΔRaf-1:ER* bypasses the cyclic AMP block of extracellular signal-regulated kinase 1 and 2 activation but not CDK2 activation or cell cycle reentry.
Molecular and Cellular Biology 23 9303-9317
http://dx.doi.org/10.1128/MCB.23.24.9303-9317.2003
Ley R, Balmanno K, Hadfield K, Weston CR, Cook SJ (2003) Activation of the ERK1/2 signaling pathway promotes phosphorylation and proteasome-dependent degradation of the BH3-only protein, Bim.
Journal of Biological Chemistry 278 18811-18816
http://dx.doi.org/10.1074/jbc.M301010200
Weston CR, Balmanno K, Chalmers C, Hadfield K, Molton SA, Ley R, Wagner EF, Cook SJ (2003) Activation of ERK1/2 by ΔRaf-1:ER* represses Bim expression independently of the JNK or PI3K pathways.
Oncogene 22 1281-1293
http://dx.doi.org/10.1038/sj.onc.1206261
Updated 1 September, 2011