Hannah JohnsonHannah entered into science due to a fascination with mass spectrometry techniques and how they can be used to gain quantitative insight into cellular signalling. During her PhD in Professor Simon Gaskell’s lab at the University of Manchester she developed methodologies for the absolute quantification of phosphorylation stoichiometry. From there, to put her love of mass spectrometry to the test, she worked as a post-doc in the lab of Forest White at MIT where she applied mass spectrometric methodologies to understand the effects of deregulated receptor tyrosine kinases on tyrosine phosphorylation signalling in human glioblastoma. Hannah hopes to further develop her skill set in the Cook lab by aiming to understand how cancer cells become resistant to small molecule inhibitors to receptor tyrosine kinases such as FGFR. Hannah’s outside interests include embroidery, reading, and movies.
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