Kathryn BalmannoKathy comes from Sarf London and spent 7 years at the Institute of Cancer Research in Sutton before moving to the Cancer Research Unit at The University of Newcastle Upon Tyne. During this time she completed a part time degree in Cell and Molecular Biology and an MPhil by research, working on various aspects of anti-cancer drug development. Kathy joined the Cook laboratory in 1997 as its founder member! She has worked on a range of projects and is interested in how nutritional cues integrate with growth factor signalling pathways to control cell survival and cell proliferation. Kathy’s outside interests include jogging, reading, music and film.
ERK1/2 signalling protects against apoptosis following endoplasmic reticulum stress but cannot provide long-term protection against BAX/BAK-independent cell death.
Darling NJ, Balmanno K, Cook SJ
12 1932-6203:e0184907 (2017)
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)