Life Sciences Research for Lifelong Health

Simon Cook

One of the keys to understanding lifelong health is to understand the signalling pathways that operate inside cells and govern key fate decisions such as cell death, cell survival, cell division or cell senescence (collectively cell longevity).  These signalling pathways involve enzymes called ‘protein kinases’ that attach phosphate groups to specific cellular proteins, thereby controlling their activity, location or abundance. In this way protein kinases orchestrate the cellular response to growth factors, nutrient availability or stress and damage.

Ageing results in part from the imbalance between cellular damage, accrued throughout life, and the progressive decline in stress response and repair pathways. We are interested in how protein kinases function in stress responses, the removal of damaged cellular components (e.g. autophagy, see also Nicholas Ktistakis and Oliver Florey) and the control of cellular lifespan. We believe this will enhance our understanding of how the normal declines in these processes drive ageing.

Signalling pathways are frequently de-regulated in certain age-related diseases – notably in cancer, inflammation and neurodegeneration – and many protein kinases are attractive drug targets. Consequently we translate our basic knowledge of signalling through collaborations with charities and pharmaceutical companies (e.g. AstraZeneca and MISSION Therapeutics).

Latest Publication:
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, Gilmour L, Squires M, Gilley R, Foxton C, Newell DR, Wedge SR, Cook SJ. Cell Cycle.
2016 Feb 16;15(4):506-18. doi: 10.1080/15384101.2015.1120915.

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Latest Publications

RNA-binding proteins ZFP36L1 and ZFP36L2 promote cell quiescence.

Galloway A, Saveliev A, Łukasiak S

Science (New York, N.Y.)
352 1095-9203:453-9 (2016)

PMID: 27102483

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)

PMID: 26959608

Maternal DNA Methylation Regulates Early Trophoblast Development.

Branco MR, King M, Perez-Garcia V

Developmental cell
36 1878-1551:152-63 (2016)

PMID: 26812015

MEK1 and MEK2 inhibitors and cancer therapy: the long and winding road.

Caunt CJ, Sale MJ, Smith PD

Nature reviews. Cancer
15 1474-1768:577-92 (2015)

PMID: 26399658

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
1420-9071: (2015)

PMID: 26346493

Intrinsic and acquired resistance to MEK1/2 inhibitors in cancer.

Sale MJ, Cook SJ

Biochemical Society transactions
42 1470-8752:776-83 (2014)

PMID: 25109957