Simon CookSimon became interested in Signal Transduction during his Biochemistry degree at Royal Holloway College, University of London. He did his PhD in Michael Wakelam’s laboratory at the University of Glasgow, studying signalling by Phospholipase-C and -D. A chance meeting over a beer (several beers actually) at a conference led to his move in 1991 to Post-Doc with Frank McCormick at ONYX Pharmaceuticals in the San Francisco Bay Area where he studied the then emerging RAS-RAF-MEK-ERK1/2 pathway. After his Post-Doc Simon stayed on at ONYX as a Staff Scientist, member of the RAS Group Steering Committee and Project Manager for the Inflammation Project. In 1997 he took a Group Leader post at the Babraham Institute. From 2000-2006 he held a CRUK Senior Cancer Research Fellowship and is currently a Group Leader in the Signalling Programme. He also coordinates Knowledge Exchange and Commercialisation activities within the Institute. His hobbies include birdwatching, walking, reading, music, cinema and undermining the system from within.
Myers SM, Miller DC, Molyneux L
European journal of medicinal chemistry
178 1768-3254:530-543 (2019)
MEK1/2 inhibitor withdrawal reverses acquired resistance driven by BRAF amplification whereas KRAS amplification promotes EMT-chemoresistance.
Sale MJ, Balmanno K, Saxena J
10 2041-1723:2030 (2019)
Over-expressed, N-terminally truncated BRAF is detected in the nucleus of cells with nuclear phosphorylated MEK and ERK.
Hey F, Andreadi C, Noble C
4 2405-8440:e01065 (2018)
Targeting IKKβ in Cancer: Challenges and Opportunities for the Therapeutic Utilisation of IKKβ Inhibitors.
Prescott JA, Cook SJ
7 2073-4409: (2018)
Kidger AM, Sipthorp J, Cook SJ
Pharmacology & therapeutics
Kidger AM, Cook SJ
The FEBS journal
285 1742-4658:42-45 (2018)
Calcium phosphate particles stimulate interleukin-1β release from human vascular smooth muscle cells: A role for spleen tyrosine kinase and exosome release.
Dautova Y, Kapustin AN, Pappert K
Journal of molecular and cellular cardiology
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)