Emma DuncanEmma comes from Lincolnshire and did her degree in Human Biology at Loughborough University, followed by a masters in Molecular Biology at the University of Nottingham. She moved down to London in 2010 to become a research assistant for a couple of years at Queen Mary University of London, where she worked on the regulation of cholesterol biosynthesis with Prof Carol Shoulders.
Emma stayed at Queen Mary University for another 4 years to do a PhD with Prof Paul Chapple, where she identified that cell organelle defects and disruptions to protein homeostasis are implicated in a rare cerebellar ataxia.
She is now in her first post-doc position with Simon where she is investigating the role that DYRKs have in the regulation of the signalling scaffold protein p62/SQSTM1, which is important for autophagy, nutrient sensing and cellular stress responses.
Outside work Emma enjoys many sports including cycling, rock climbing, swimming and running.
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)
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)