Author

M. E. Duenas

Listed by name: these papers carry no ORCID for this author, so different people with the same name may be mixed together.

Biology Disciplines

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Biochemistry· 1 Cancer Biology· 1 Immunology· 1

Signature Assays, Organisms & Methods

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Research Focus:drug response / drug discovery· 3 Organism:human· 3 Assay:proteomics· 3 Approach:experimental assay· 2 Approach:statistical model· 2 Research Focus:benchmarking· 1 Research Focus:cell type annotation· 1 Approach:deep learning· 1

Frequent Co-Authors

M. Trost· 3 shared J. L. Marin-Rubio· 2 shared J. Scott· 2 shared A. C. M. Khan· 1 shared A. I. Gardner· 1 shared A. J. Simpson· 1 shared A. L. George· 1 shared B. J. Thompson· 1 shared

Activity by Year

2021-2023 · peak 2/yr

Co-Author Collaboration Network

10 top collaborators · 26 mutual co-author links

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3 shared papersBiochemistry

M. Trost

Mutual co-authors in cluster

Author profile →

3 papers

Recent·Most cited

A Comparison of Quantitative Mass Spectrometric Methods for Drug Target Identification by Thermal Proteome Profiling

A. L. George, F. R. Sidgwick, J. E. Watt, M. P. Martin, M. Trost, J. L. Marin-Rubio, M. E. Duenas

This study compares DIA-based label-free quantification methods with TMT-DDA for thermal proteome profiling, finding DIA approaches are comparable or better for detecting drug target engagement.

bioRxiv · Feb 15, 2023Biochemistry

A MALDI-TOF assay identifies nilotinib as an inhibitor of inflammation in acute myeloid leukaemia

J. L. Marin-Rubio, R. E. Heap, T. Heunis, M. E. Duenas, J. Inns, J. Scott, A. J. Simpson, J. M. Allan, H. Blair, O. Heidenreich, B. Saxty, M. Trost

This study identifies nilotinib as an anti-inflammatory drug using a MALDI-TOF assay in AML-derived monocytes, showing it inhibits the p38-MK2/3 signaling axis.

bioRxiv · Mar 29, 2021 · PreprintCancer Biology

Delayed induction of type I and III interferons mediates nasal epithelial cell permissiveness to SARS-CoV-2

C. F. Hatton, R. A. Botting, M. E. Duenas, I. J. Haq, B. Verdon, B. J. Thompson, J. Stremenova Spegarova, F. Gothe, E. A. Stephenson, A. I. Gardner, S. Murphy, J. Scott, J. P. Garnett, S. Carrie, J. Powell, , C. J. A. Duncan

This study shows that delayed type I and III interferon responses in nasal epithelial cells allow SARS-CoV-2 replication, but pre-infection IFN treatment restricts virus and preserves barrier integrity.

bioRxiv · Feb 17, 2021Immunology