Simon J. Cook

13.5k total citations · 4 hit papers
131 papers, 10.9k citations indexed

About

Simon J. Cook is a scholar working on Molecular Biology, Oncology and Cell Biology. According to data from OpenAlex, Simon J. Cook has authored 131 papers receiving a total of 10.9k indexed citations (citations by other indexed papers that have themselves been cited), including 107 papers in Molecular Biology, 33 papers in Oncology and 17 papers in Cell Biology. Recurrent topics in Simon J. Cook's work include Melanoma and MAPK Pathways (45 papers), Protein Kinase Regulation and GTPase Signaling (39 papers) and Cell death mechanisms and regulation (25 papers). Simon J. Cook is often cited by papers focused on Melanoma and MAPK Pathways (45 papers), Protein Kinase Regulation and GTPase Signaling (39 papers) and Cell death mechanisms and regulation (25 papers). Simon J. Cook collaborates with scholars based in United Kingdom, United States and Germany. Simon J. Cook's co-authors include Kathryn Balmanno, Frank McCormick, H. Llewelyn Roderick, Michael J.O. Wakelam, Kathryn Hadfield, Matthew J. Sale, Paul D. Smith, Nicola J. Darling, Katherine Ewings and Claire R. Weston and has published in prestigious journals such as Science, Journal of Biological Chemistry and Nature Communications.

In The Last Decade

Simon J. Cook

129 papers receiving 10.8k citations

Hit Papers

Inhibition by cAMP of Ras-Dependent Activation of Raf 1993 2026 2004 2015 1993 2008 2003 2015 250 500 750

Peers — A (Enhanced Table)

Peers by citation overlap · career bar shows stage (early→late) cites · hero ref

Name h Career Trend Papers Cites
Simon J. Cook United Kingdom 55 8.3k 2.1k 1.4k 1.3k 1.1k 131 10.9k
Sylvain Meloche Canada 54 7.3k 0.9× 1.9k 0.9× 1.1k 0.8× 1.4k 1.1× 1.3k 1.2× 151 10.6k
Christian Rommel United States 44 7.3k 0.9× 1.7k 0.8× 1.0k 0.8× 2.1k 1.6× 913 0.8× 88 10.2k
Richard B. Pearson Australia 61 9.6k 1.2× 2.1k 1.0× 1.5k 1.1× 889 0.7× 1.3k 1.2× 136 12.4k
Ana Cuenda Spain 43 7.9k 0.9× 2.1k 1.0× 1.4k 1.0× 1.9k 1.4× 1.6k 1.4× 76 11.5k
Peter Juo United States 20 7.3k 0.9× 1.4k 0.7× 842 0.6× 1.4k 1.1× 1.3k 1.1× 33 8.8k
Lucio Cocco Italy 58 8.8k 1.1× 1.8k 0.9× 2.1k 1.5× 1.2k 0.9× 1.2k 1.1× 344 12.0k
Gilles Pagès France 58 7.2k 0.9× 2.2k 1.1× 1.1k 0.8× 1.3k 1.0× 2.1k 1.9× 173 11.3k
Stephan Wullschleger Switzerland 21 6.3k 0.8× 1.3k 0.6× 950 0.7× 967 0.7× 871 0.8× 26 8.8k
Senji Shirasawa Japan 48 5.8k 0.7× 2.7k 1.3× 804 0.6× 920 0.7× 2.0k 1.8× 191 9.3k
Lynn E. Heasley United States 50 6.0k 0.7× 2.7k 1.3× 743 0.5× 1.2k 0.9× 1.3k 1.2× 141 9.2k

Countries citing papers authored by Simon J. Cook

Since Specialization
Citations

This map shows the geographic impact of Simon J. Cook's research. It shows the number of citations coming from papers published by authors working in each country. You can also color the map by specialization and compare the number of citations received by Simon J. Cook with the expected number of citations based on a country's size and research output (numbers larger than one mean the country cites Simon J. Cook more than expected).

Fields of papers citing papers by Simon J. Cook

Since Specialization
Physical SciencesHealth SciencesLife SciencesSocial Sciences

This network shows the impact of papers produced by Simon J. Cook. Nodes represent research fields, and links connect fields that are likely to share authors. Colored nodes show fields that tend to cite the papers produced by Simon J. Cook. The network helps show where Simon J. Cook may publish in the future.

Co-authorship network of co-authors of Simon J. Cook

This figure shows the co-authorship network connecting the top 25 collaborators of Simon J. Cook. A scholar is included among the top collaborators of Simon J. Cook based on the total number of citations received by their joint publications. Widths of edges represent the number of papers authors have co-authored together. Node borders signify the number of papers an author published with Simon J. Cook. Simon J. Cook is excluded from the visualization to improve readability, since they are connected to all nodes in the network.

All Works

20 of 20 papers shown
1.
Batie, Michael, et al.. (2025). NF-κB is a central regulator of hypoxia-induced gene expression. EMBO Reports. 27(2). 416–432.
2.
Stuart, Kate, et al.. (2024). Reporter cell lines to screen for inhibitors or regulators of the KRAS-RAF-MEK1/2-ERK1/2 pathway. Biochemical Journal. 481(6). 405–422.
3.
Channathodiyil, Prasanna, et al.. (2022). Escape from G1 arrest during acute MEK inhibition drives the acquisition of drug resistance. NAR Cancer. 4(4). zcac032–zcac032. 3 indexed citations
4.
Shah, Izhar Hussain, et al.. (2022). Environmental Sustainability and Supply Resilience of Cobalt. Sustainability. 14(7). 4124–4124. 23 indexed citations
5.
Lochhead, Pamela A., Julie A. Tucker, Natalie J. Tatum, et al.. (2020). Paradoxical activation of the protein kinase-transcription factor ERK5 by ERK5 kinase inhibitors. Nature Communications. 11(1). 1383–1383. 33 indexed citations
6.
Kidger, Andrew M., Joanne M. Munck, Harpreet K. Saini, et al.. (2019). Dual-Mechanism ERK1/2 Inhibitors Exploit a Distinct Binding Mode to Block Phosphorylation and Nuclear Accumulation of ERK1/2. Molecular Cancer Therapeutics. 19(2). 525–539. 17 indexed citations
7.
Sale, Matthew J., Kathryn Balmanno, & Simon J. Cook. (2019). Resistance to ERK1/2 pathway inhibitors; sweet spots, fitness deficits and drug addiction. Cancer Drug Resistance. 2(2). 365–380. 5 indexed citations
8.
Ficz, Gabriella, Timothy A. Hore, Fátima Santos, et al.. (2013). FGF signalling inhibition in ESCs drives rapid genome-wide demethylation to the epigenetic ground state of pluripotency. Clinical Epigenetics. 5(S1). 154 indexed citations
9.
Ficz, Gabriella, Timothy A. Hore, Fátima Santos, et al.. (2013). FGF Signaling Inhibition in ESCs Drives Rapid Genome-wide Demethylation to the Epigenetic Ground State of Pluripotency. Cell stem cell. 13(3). 351–359. 301 indexed citations
10.
Gilley, Rebecca, Kathryn Balmanno, Matthew J. Sale, et al.. (2013). Adaptation to mTOR kinase inhibitors by amplification of eIF4E to maintain cap-dependent translation. Journal of Cell Science. 127(Pt 4). 788–800. 66 indexed citations
11.
Gilley, Rebecca, H. Nikki March, & Simon J. Cook. (2009). ERK1/2, but not ERK5, is necessary and sufficient for phosphorylation and activation of c-Fos. Cellular Signalling. 21(6). 969–977. 42 indexed citations
12.
Krueger, Felix, Zofia E. Madeja, Myriam Hemberger, et al.. (2009). Down-regulation of Cdx2 in colorectal carcinoma cells by the Raf–MEK–ERK 1/2 pathway. Cellular Signalling. 21(12). 1846–1856. 25 indexed citations
13.
14.
Roderick, H. Llewelyn & Simon J. Cook. (2008). Ca2+ signalling checkpoints in cancer: remodelling Ca2+ for cancer cell proliferation and survival. Nature reviews. Cancer. 8(5). 361–375. 598 indexed citations breakdown →
15.
Dickinson, Robin J., et al.. (2007). DUSP6/MKP-3 inactivates ERK1/2 but fails to bind and inactivate ERK5. Cellular Signalling. 20(5). 836–843. 72 indexed citations
16.
18.
Todd, Daniel E., Ruth M. Densham, Sarah A Molton, et al.. (2004). ERK1/2 and p38 cooperate to induce a p21CIP1-dependent G1 cell cycle arrest. Oncogene. 23(19). 3284–3295. 74 indexed citations
19.
Balmanno, Kathryn & Simon J. Cook. (1999). Sustained MAP kinase activation is required for the expression of cyclin D1, p21Cip1 and a subset of AP-1 proteins in CCL39 cells. Oncogene. 18(20). 3085–3097. 195 indexed citations
20.
Braselmann, Sylvia, Timothy M. Palmer, & Simon J. Cook. (1997). Signalling enzymes: Bursting with potential. Current Biology. 7(8). R470–R473. 9 indexed citations

Rankless uses publication and citation data sourced from OpenAlex, an open and comprehensive bibliographic database. While OpenAlex provides broad and valuable coverage of the global research landscape, it—like all bibliographic datasets—has inherent limitations. These include incomplete records, variations in author disambiguation, differences in journal indexing, and delays in data updates. As a result, some metrics and network relationships displayed in Rankless may not fully capture the entirety of a scholar's output or impact.

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