K. Balmanno

发表

Pharmacokinetics and pharmacodynamics of prolonged oral etoposide in women with metastatic breast cancer

M. Millward, D. Newell, K. Yuen, 2004, Cancer Chemotherapy and Pharmacology.

Activation of ERK1/2 by ΔRaf-1 : ER* represses Bim expression independently of the JNK or PI3K pathways

E. Wagner, S. Cook, K. Balmanno, 2003, Oncogene.

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.

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

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

Extracellular Signal-regulated Kinases 1/2 Are Serum-stimulated “BimEL Kinases” That Bind to the BH3-only Protein BimEL Causing Its Phosphorylation and Turnover*

S. Cook, K. Balmanno, K. Hadfield, 2004, Journal of Biological Chemistry.

Pharmacokinetics of Carboplatin in Children and the Development of a Paediatric Dose Equation

D. Newell, K. Balmanno, A. Calvert, 1991 .

Over-expressed, N-terminally truncated BRAF is detected in the nucleus of cells with nuclear phosphorylated MEK and ERK

David T. W. Jones, V. P. Collins, S. Cook, 2018, Heliyon.

Apoptosis and autophagy: BIM as a mediator of tumour cell death in response to oncogene‐targeted therapeutics

Ceri M. Wiggins, S. Cook, K. Balmanno, 2009, The FEBS journal.

Phase I and pharmacokinetic study of a water-soluble etoposide prodrug, etoposide phosphate (BMY-40481).

M. Millward, D. Newell, K. Balmanno, 1995, European journal of cancer.

Resistance to ERK1/2 pathway inhibitors; sweet spots, fitness deficits and drug addiction

S. Cook, K. Balmanno, Matthew J. Sale, 2019, Cancer drug resistance.

Carboplatin pharmacokinetics in children: the development of a pediatric dosing formula. The United Kingdom Children's Cancer Study Group.

M. Stevens, C. R. Pinkerton, I. Lewis, 1993, Journal of clinical oncology : official journal of the American Society of Clinical Oncology.

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

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

1H NMR studies of human urine: Urinary elimination of the anticancer drug carboplatin

P. Sadler, D. Newell, K. Balmanno, 1991 .

Delta MEKK3:ER* activation induces a p38 alpha/beta 2-dependent cell cycle arrest at the G2 checkpoint.

S. Cook, K. Balmanno, C. Weston, 2002, Oncogene.

RNA-binding proteins ZFP36L1 and ZFP36L2 promote cell quiescence

Manuel D. Díaz-Muñoz, S. Cook, S. Andrews, 2016, Science.

ΔRaf-1:ER* Bypasses the Cyclic AMP Block of Extracellular Signal-Regulated Kinase 1 and 2 Activation but Not CDK2 Activation or Cell Cycle Reentry

S. Cook, M. McMahon, K. Balmanno, 2003, Molecular and Cellular Biology.

Amplification of the Driving Oncogene, KRAS or BRAF, Underpins Acquired Resistance to MEK1/2 Inhibitors in Colorectal Cancer Cells

P. Edwards, S. Cook, J. Dry, 2011, Science Signaling.

Sustained MAP kinase activation is required for the expression of cyclin D1, p21Cip1 and a subset of AP-1 proteins in CCL39 cells

S. Cook, K. Balmanno, 1999, Oncogene.

IKKα plays a major role in canonical NF-κB signalling in colorectal cells

S. Cook, K. Balmanno, Jennifer P. Mitchell, 2022, The Biochemical journal.

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.

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.

Activation of the ERK1/2 Signaling Pathway Promotes Phosphorylation and Proteasome-dependent Degradation of the BH3-only Protein, Bim*

S. Cook, K. Balmanno, C. Weston, 2003, Journal of Biological Chemistry.

ΔMEKK3:ER* activation induces a p38α/β2-dependent cell cycle arrest at the G2 checkpoint

S. Cook, K. Balmanno, C. Weston, 2002, Oncogene.

Tumour cell responses to MEK1/2 inhibitors: acquired resistance and pathway remodelling.

S. Cook, Paul D. Smith, K. Balmanno, 2012, Biochemical Society transactions.

Identification of DYRK1B as a substrate of ERK1/2 and characterisation of the kinase activity of DYRK1B mutants from cancer and metabolic syndrome

S. Cook, Mark Cockerill, T. Dunkley, 2015, Cellular and Molecular Life Sciences.

Intrinsic resistance to the MEK1/2 inhibitor AZD6244 (ARRY‐142886) is associated with weak ERK1/2 signalling and/or strong PI3K signalling in colorectal cancer cell lines

S. Cook, K. Balmanno, S. Hayat, 2009, International journal of cancer.

Dual-Mechanism ERK1/2 Inhibitors Exploit a Distinct Binding Mode to Block Phosphorylation and Nuclear Accumulation of ERK1/2

S. Cook, K. Balmanno, H. Saini, 2019, Molecular Cancer Therapeutics.

Resistance to ERK 1 / 2 pathway inhibitors ; sweet spots , fitness deficits and drug addiction

S. Cook, K. Balmanno, Matthew J. Sale, 2019 .

ERK1/2 signalling protects against apoptosis following endoplasmic reticulum stress but cannot provide long-term protection against BAX/BAK-independent cell death

S. Cook, K. Balmanno, Nicola J. Darling, 2017, PloS one.

University of Dundee ERK 1 / 2 signalling protects against apoptosis following endoplasmic reticulum stress but cannot provide long-term protection against BAX / BAK-independent cell

S. Cook, K. Balmanno, Nicola J. Darling, 2017 .

ERK1/2 and p38 cooperate to induce a p21CIP1-dependent G1 cell cycle arrest

S. Cook, K. Balmanno, C. Weston, 2004, Oncogene.

Regulation of MEK/ERK pathway output by subcellular localization of B-Raf.

S. Cook, C. Pritchard, K. Balmanno, 2012, Biochemical Society transactions.

The conditional kinase ΔMEKK1:ER* selectively activates the JNK pathway and protects against serum withdrawal-induced cell death

S. Cook, K. Balmanno, C. Weston, 2005 .

The duration of ERK1/2 activity determines the activation of c-Fos and Fra-1 and the composition and quantitative transcriptional output of AP-1.

S. Cook, K. Balmanno, Claire J Chalmers, 2007, Cellular signalling.

Thrombin inhibits Bim (Bcl-2-interacting mediator of cell death) expression and prevents serum-withdrawal-induced apoptosis via protease-activated receptor 1.

S. Cook, K. Balmanno, Claire J Chalmers, 2003, The Biochemical journal.

Identification of DYRK1B as a substrate of ERK1/2 and characterisation of the kinase activity of DYRK1B mutants from cancer and metabolic syndrome

S. Cook, Mark Cockerill, T. Dunkley, 2015, Cellular and Molecular Life Sciences.

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

D. Adams, J. Sáez-Rodríguez, R. McIntyre, 2019, Nature Communications.

Tumour cell survival signalling by the ERK1/2 pathway

S. Cook, K. Balmanno, K. Balmanno, 2009, Cell Death and Differentiation.

Colorectal cancer cells with the BRAFV600E mutation are addicted to the ERK1/2 pathway for growth factor-independent survival and repression of BIM

S. Cook, C. Pritchard, M. Johnson, 2008, Oncogene.

Tumour cell responses to new fibroblast growth factor receptor tyrosine kinase inhibitors and identification of a gatekeeper mutation in FGFR3 as a mechanism of acquired resistance

S. Cook, K. Balmanno, K. Balmanno, 2013, Oncogene.

Amplification of the Driving Oncogene, KRAS or BRAF, Underpins Acquired Resistance to MEK1/2 Inhibitors in Colorectal Cancer Cells

P. Edwards, S. Cook, J. Dry, 2011, Science Signaling.

Intrinsic resistance to the MEK1/2 inhibitor AZD6244 (ARRY‐142886) is associated with weak ERK1/2 signalling and/or strong PI3K signalling in colorectal cancer cell lines

S. Cook, K. Balmanno, S. Hayat, 2009, International Journal of Cancer.

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.