Author

Almudena Serrano-Benítez

University of CambridgeORCID 0000-0002-7263-6863Unclaimed ORCID profile · follow to get notified of new preprints

Biology Disciplines

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Biochemistry· 1 Cell Biology· 1 Molecular Biology· 1

Signature Assays, Organisms & Methods

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Organism:human· 3 Research Focus:cell type annotation· 2 Research Focus:differential expression· 2 Approach:experimental assay· 2 Research Focus:gene regulatory network inference· 2 Research Focus:drug response / drug discovery· 1 Approach:genetic perturbation / CRISPR· 1 Assay:metagenomics· 1

Frequent Co-Authors

Stephen P. JacksoniD· 2 shared Alexandra SapetschnigiD· 1 shared Amy R. Wanders· 1 shared Bianca Pierattini· 1 shared C. J. BlumiD· 1 shared Chloe S. Palma-Chaundler· 1 shared Christopher J. CarnieiD· 1 shared David JordaniD· 1 shared

Activity by Year

2024-2026 · peak 1/yr

Co-Author Collaboration Network

10 top collaborators · 17 mutual co-author links

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2 shared papersMolecular Biology

Stephen P. JacksonORCID

Mutual co-authors in cluster

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3 papers

Recent·Most cited

Molecular BiologybioRxivPreprintJul 15, 2026

Insights into mechanisms of ATM activation via constitutively active mutants

Md Saiful Islam, Verena G. Gautsch, Rimma Belotserkovskaya…·Roger Lee Williams

This study identifies PRD mutants of ATM that are constitutively active, showing increased phosphorylation of targets without requiring MRN/DNA, and suggests potential for small-molecule modulators.

DOI 10.64898/2026.07.15.738190

humanexperimental assay

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BiochemistrybioRxivPreprintOct 13, 2025

Compensatory tRNA Modification by DUS3L Confers Resistance to METTL1 Loss in Oesophageal Cancer

Helena Santos-Rosa, Jonathan L. Price, Georgia Tsagkogeorga…·Eric Alexander Miska

The paper identifies a compensatory tRNA modification pathway mediated by DUS3L that allows oesophageal cancer cells to resist METTL1 loss, suggesting DUS3L as a biomarker and therapeutic target.

DOI 10.1101/2025.10.13.682082

humanproteomics

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Cell BiologyThe EMBO JournalPeer-reviewedMay 17, 2024

The dCMP deaminase DCTD and the E3 ligase TOPORS are central mediators of decitabine cytotoxicity

Christopher J. Carnie, Maximilian J. Götz, Chloe S. Palma-Chaundler…·Stephen P. Jackson

This study identifies DCTD and TOPORS as key factors in decitabine cytotoxicity by showing their roles in DPC formation and repair.

41 citationstop 3%

humangenetic perturbation / CRISPR

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