Rebecca Gilley

发表

An mTORC1-to-CDK1 Switch Maintains Autophagy Suppression during Mitosis

S. Cook, D. Oxley, K. Balmanno, 2019, Molecular cell.

ERK1/2‐dependent phosphorylation of BimEL promotes its rapid dissociation from Mcl‐1 and Bcl‐xL

Ceri M. Wiggins, S. Cook, E. White, 2007, The EMBO journal.

Tumor cells with KRAS or BRAF mutations or ERK5/MAPK7 amplification are not addicted to ERK5 activity for cell proliferation

S. Cook, S. Wedge, D. Newell, 2016, Cell cycle.

Targeting melanoma’s MCL1 bias unleashes the apoptotic potential of BRAF and ERK1/2 pathway inhibitors

S. Cook, J. Dry, Paul D. Smith, 2019, Nature Communications.

MEK1/2 inhibitor withdrawal reverses acquired resistance driven by BRAFV600E amplification whereas KRASG13D amplification promotes EMT-chemoresistance

D. Adams, J. Saez-Rodriguez, R. McIntyre, 2019, Nature Communications.

Control of cell death and mitochondrial fission by ERK1/2 MAP kinase signalling

S. Cook, Rebecca H. Gilley, K. Stuart, 2017, The FEBS journal.

CDK1, not ERK1/2 or ERK5, is required for mitotic phosphorylation of BIMEL.

S. Cook, D. Oxley, K. Balmanno, 2012, Cellular signalling.

Adaptation to mTOR kinase inhibitors by amplification of eIF4E to maintain cap-dependent translation

S. Cook, Paul D. Smith, S. Guichard, 2014, Journal of Cell Science.

Adaptation to chronic mTOR inhibition in cancer and in aging.

S. Cook, K. Balmanno, Rebecca H. Gilley, 2013, Biochemical Society transactions.