Pamela LochheadPam’s interest in Signal Transduction started with her PhD in the MRC PPU, University of Dundee with Calum Sutherland studying insulin regulation of gene expression. She then moved to the Beatson Intitute for Cancer Research in Glasgow where she defined the activation mechanism of DYRKs and characterised somatic mutations in the ROCK protein kinases, with Vaughn Cleghon and Mike Olson. Keen to pursue her interest in signal transduction and cancer she was lured into the Signalling & Cell Fate ISP at the Babraham Institute, and is now investigating the role of ERK5 in cancer, whilst retaining an interest in DYRKs. Pam is enjoying the science, Simon’s tolerance of Scottish people and the climate, but misses the fine cuisine of her homeland! Outside work Pam enjoys spending time with her young daughter, cycling, cooking and embracing English culture.
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