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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Signature Assays, Organisms & Methods

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Approach:experimental assay· 2 Organism:human· 2 Research Focus:cell type annotation· 1 Research Focus:differential expression· 1 Research Focus:gene regulatory network inference· 1 Assay:metagenomics· 1 Assay:proteomics· 1

Frequent Co-Authors

Alexandra SapetschnigiD· 1 shared Bianca Pierattini· 1 shared David JordaniD· 1 shared Dénes Buzafalvi· 1 shared Eric Alexander MiskaiD· 1 shared Georgia TsagkogeorgaiD· 1 shared Helena Santos-Rosa· 1 shared Jonathan L. PriceiD· 1 shared

Activity by Year

2025-2026 · peak 1/yr

Co-Author Collaboration Network

10 top collaborators · 29 mutual co-author links

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1 shared paperBiochemistry

Alexandra SapetschnigORCID

Mutual co-authors in cluster

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2 papers

Recent·Most cited

Insights into mechanisms of ATM activation via constitutively active mutants

Md Saiful Islam, Verena G. Gautsch, Rimma Belotserkovskaya, Almudena Serrano-Benítez, Dénes Buzafalvi, Olga Perišić, Stephen P. Jackson, 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.

bioRxiv · Jul 15, 2026 · PreprintMolecular Biology

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

Helena Santos-Rosa, Jonathan L. Price, Georgia Tsagkogeorga, Alexandra Sapetschnig, Bianca Pierattini, David Jordan, Paula Milán-Rois, Almudena Serrano-Benítez, Katherine M. Stott, Namshik Han, Tony Kouzarides, 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.

bioRxiv · Oct 13, 2025 · PreprintBiochemistry