Author

R. M. Densham

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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Cell Biology· 2 Cancer Biology· 1

Signature Assays, Organisms & Methods

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Research Focus:chromatin & epigenetic regulation· 3 Approach:experimental assay· 3 Organism:human· 3 Research Focus:cancer & tumor microenvironment· 2 Assay:DNA methylation· 2 Research Focus:cell signaling & trafficking· 1 Research Focus:cell type annotation· 1 Assay:ChIP-seq· 1

Frequent Co-Authors

J. R. Morris· 3 shared K. Starowicz· 3 shared A. J. Garvin· 2 shared A. K. Walker· 2 shared A. S. Chauhan· 2 shared H. L. Mackay· 2 shared H. R. Stone· 2 shared M. Jamshad· 2 shared

Activity by Year

2018-2024 · peak 1/yr

Co-Author Collaboration Network

10 top collaborators · 41 mutual co-author links

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3 shared papersCell Biology

J. R. Morris

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Author profile →

3 papers

Recent·Most cited

USP50 suppresses alternative RecQ helicase use and deleterious DNA2 activity during replication.

H. L. Mackay, H. R. Stone, K. Ellis, G. Ronson, K. Starowicz, A. J. Garvin, P. Van Eijk, A. Aitsiankova, S. Vijayendran, J. Beesley, E. Petermann, E. Brown, R. M. Densham, S. H. Reed, F. Dobbs, , J. R. Morris

This study identifies USP50 as a ubiquitin-binding protein that regulates helicase and nuclease activities during DNA replication to prevent fork collapse and maintain genomic stability.

bioRxiv · Jan 10, 2024Cancer Biology

The deSUMOylase SENP2 coordinates homologous recombination and non-homologous end joining by independent mechanisms.

A. J. Garvin, A. K. Walker, R. M. Densham, A. S. Chauhan, H. R. Stone, H. L. MacKay, M. Jamshad, K. Starowicz, M. Daza-Martin, J. R. Morris

This study identifies SENP2 as a deSUMOylase that differentially regulates homologous recombination and non-homologous end joining through distinct mechanisms, impacting DSB repair and radioresistance.

Genes & Development · Feb 22, 2019Peer-reviewedCell Biology

PIN1 isomerisation of BRCA1 promotes replication fork protection.

M. R. Daza-Martin, M. Jamshad, K. Starowicz, A. S. Chauhan, J. F. J. Beesley, J. Coles, G. S. Stewart, R. M. Densham, J. R. Morris

This study identifies PIN1-mediated BRCA1 isomerisation as a regulator of replication fork protection through enhanced BRCA1-BARD1-RAD51 interaction, distinct from BRCA1's role in homologous recombination.

bioRxiv · Nov 28, 2018 · PreprintCell Biology