Anne AshfordAnne grew up in Sheffield and did her first degree at the University of Oxford. She then worked at Novartis Pharmaceuticals in Sussex where she discovered her love of cell signalling (for which she is currently receiving counselling). Still failing to escape ‘the South’, she is now embarking on an AstraZeneca/BBSRC CASE PhD Studentship in the Cook laboratory. In her spare time she likes to read and occasionally dabbles in art (specializing in disproportioned honey bees). She has done fencing in the past (the one with sharp pointy things, not the one with planks of wood) and is now learning archery – enemies and PhD supervisors beware!
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