Emma MinihaneEmma grew up on the island of Jersey and went on to study Molecular & Cellular Biology at the University of Bath. Her interest in signalling sparked from a research project she undertook with Dr Jim Caunt, studying ERK1/2 and PKB responses to nerve growth factor in the PC12 model system.
After a 5-month stint travelling in the USA (visiting 23/50 States), Emma re-entered the world of science and joined the Cook lab in 2016. Her work is in collaboration with AstraZeneca, focusing on combining BH3 mimetics with kinase inhibitors in cancer.
Still an islander at heart, Emma enjoys many water sports and misses being by the sea. She is a jazz drummer (yes really!) and is also currently teaching herself how to play the guitar (very badly).
Note from Editor.
It is unclear from Emma’s account if she is very bad at teaching herself or very bad at playing the guitar. No doubt such ambiguity in writing will be sorted by the time she comes to write her thesis.
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)