Author

H. C. Scott

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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Cancer Biology· 2 Biochemistry· 1 Cell Biology· 1

Signature Assays, Organisms & Methods

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Approach:experimental assay· 4 Organism:human· 4 Assay:proteomics· 4 Research Focus:cancer & tumor microenvironment· 3 Research Focus:cell type annotation· 3 Research Focus:cell signaling & trafficking· 2 Research Focus:drug response / drug discovery· 1 Research Focus:metabolism & bioenergetics· 1

Frequent Co-Authors

A. Pinto-Fernandez· 4 shared B. M. Kessler· 4 shared A. Damianou· 2 shared D. Komander· 2 shared G. Vere· 2 shared H. Greenwood· 2 shared M. Gersch· 2 shared M. J. Clague· 2 shared

Activity by Year

2020-2023 · peak 3/yr

Co-Author Collaboration Network

10 top collaborators · 41 mutual co-author links

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4 shared papersCancer Biology

A. Pinto-Fernandez

Mutual co-authors in cluster

Author profile →

4 papers

Recent·Most cited

USP16 is an ISG15 cross-reactive deubiquitinase targeting a subset of metabolic pathway-related proteins

J. Gan, A. Pinto-Fernandez, D. Flierman, J. J. L. L. Akkermans, D. P. O'Brien, H. Greenwood, H. C. Scott, J. Neefjes, G. Fritz, K.-P. Knobeloch, H. van Dam, B. M. Kessler, H. Ovaa, P. P. Geurink, A. Sapmaz

This study identifies USP16 as an ISG15 cross-reactive deubiquitinase that regulates metabolic pathway-related proteins during type I interferon responses.

bioRxiv · Jun 26, 2023 · PreprintBiochemistry

USP28 deletion and small molecule inhibition destabilises c-Myc and elicits regression of squamous cell lung carcinoma

E. J. Ruiz, A. Pinto-Fernandez, A. P. Turnbull, L. Lan, T. M. Charlton, H. C. Scott, A. Damianou, G. Vere, E. M. Riising, C. Da Costa, W. W. Krajewski, D. Guerin, J. Kearns, S. Ioannidis, M. Katz, , A. Behrens

This study shows that deleting or inhibiting USP28 reduces c-Myc levels and causes regression of lung squamous cell carcinoma in mice and human xenografts.

bioRxiv · Nov 17, 2020Cancer Biology

A novel USP30 inhibitor recapitulates genetic loss of USP30 and sets the trigger for PINK1-PARKIN amplification of mitochondrial ubiquitylation.

E. Rusilowicz-Jones, J. Jardine, A. Kallinos, A. Pinto-Fernandez, F. Guenther, M. Giurrandino, F. G. Barone, K. McCarron, C. J. Burke, A. Murad, A. Martinez, E. Marcassa, M. Gersch, A. Buckmelter, K. Kayser-Bricker, , M. J. Clague

The paper identifies a USP30 inhibitor that mimics genetic loss of USP30, revealing its role in regulating mitochondrial ubiquitylation and mitophagy through TOM complex components.

Life Science Alliance · Jul 7, 2020Peer-reviewedCell Biology

Deep analysis of the USP18-dependent ISGylome and proteome unveils important roles for USP18 in tumour cell antigenicity and radiosensitivity

A. Pinto-Fernandez, M. Salio, T. Partridge, J. Chen, G. Vere, H. Greenwood, C. S. Olie, A. Damianou, H. C. Scott, H. J. Pegg, A. Chiarenza, L. Diaz-Saez, P. Smith, C. Gonzalez-Lopez, B. Patel, , B. M. Kessler

This study identifies novel ISGylation targets regulated by USP18, showing its role in enhancing tumour cell antigenicity and reducing radiosensitivity in CML cells.

bioRxiv · Mar 31, 2020 · PreprintCancer Biology