Andrew KidgerOriginally from Sheffield, Andrew completed a BSc honours degree in Biology at the University of Bath, graduating in 2012. His interest in mitogen activated protein (MAP) kinase signalling was stimulated by a research project he undertook during his BSc to develop a system to characterise the binding partners of ERK2 with Dr Jim Caunt.
Following this Andrew moved North of the border to complete his PhD with Professor Stephen Keyse at the University of Dundee studying the regulation of MAP kinase signalling by MAP kinase phosphatases (MKPs/DUSPs). His project investigated the role of the ERK1/2-specific phosphatases DUSP5 & DUSP6 in modulating the development of mutant RAS-driven cancers.
Andrew is now continuing his interest in ERK signalling in the Cook lab, where he is investigating the functional consequences of the differences in mechanisms of action of a range of published ERK inhibitors.
Cook SJ, Stuart K, Gilley R
The FEBS journal
Sipthorp J, Lebraud H, Gilley R
Galloway A, Saveliev A, Łukasiak S
Science (New York, N.Y.)
352 1095-9203:453-9 (2016)
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
Cell cycle (Georgetown, Tex.)
15 1551-4005:506-18 (2016)
Branco MR, King M, Perez-Garcia V
36 1878-1551:152-63 (2016)
Caunt CJ, Sale MJ, Smith PD
Nature reviews. Cancer
15 1474-1768:577-92 (2015)
Identification of DYRK1B as a substrate of ERK1/2 and characterisation of the kinase activity of DYRK1B mutants from cancer and metabolic syndrome.
Ashford AL, Dunkley TP, Cockerill M
Cellular and molecular life sciences : CMLS
DYRK1A-mediated Cyclin D1 Degradation in Neural Stem Cells Contributes to the Neurogenic Cortical Defects in Down Syndrome.
Najas S, Arranz J, Lochhead PA
2 2352-3964:120-34 (2015)
Epigenetic memory of the first cell fate decision prevents complete ES cell reprogramming into trophoblast.
F Cambuli, A Murray, W Dean
26 5:5538 (2014)
Sale MJ, Cook SJ
Biochemical Society transactions
42 1470-8752:776-83 (2014)
The increase in BIK expression following ERK1/2 pathway inhibition is a consequence of G₁ cell-cycle arrest and not a direct effect on BIK protein stability.
Sale MJ, Cook SJ
The Biochemical journal
459 1470-8728:513-24 (2014)
Oncogenic K-Ras suppresses IP3-dependent Ca2+ release through remodeling of IP3Rs isoform composition and ER luminal Ca2+ levels in colorectal cancer cell lines.
C Pierro, SJ Cook, TC Foets
Journal of cell science