Author

A. Vindigni

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

Signature Assays, Organisms & Methods

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Assay:DNA methylation· 2 Approach:experimental assay· 2 Organism:human· 2 Research Focus:cancer & tumor microenvironment· 1 Research Focus:cell signaling & trafficking· 1 Research Focus:chromatin & epigenetic regulation· 1 Research Focus:development & morphogenesis· 1 Assay:proteomics· 1

Frequent Co-Authors

J. Jackson· 2 shared B. Teodoro-Castro· 1 shared E. Antony· 1 shared E. Berthiaume· 1 shared E. Shashkova· 1 shared J. Calvo· 1 shared K. Cong· 1 shared K. M. Hadden· 1 shared

Activity by Year

2019-2021 · peak 1/yr

Co-Author Collaboration Network

10 top collaborators · 25 mutual co-author links

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2 shared papersCancer Biology

J. Jackson

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Author profile →

2 papers

Recent·Most cited

A-type lamins are critical for the recruitment of RPA and RAD51 to stalled replication forks to maintain fork stability

S. Graziano, N. Coll-Bonfill, B. Teodoro-Castro, S. Kuppa, J. Jackson, E. Shashkova, U. Mahajan, A. Vindigni, E. Antony, S. Gonzalo

This study shows A-type lamins are essential for recruiting RPA and RAD51 to stalled replication forks, preventing replication fork instability during replication stress.

bioRxiv · Jun 22, 2021 · PreprintCancer Biology

Replication gaps are a cancer vulnerability counteracted by translesion synthesis

S. Nayak, J. Calvo, K. Cong, E. Berthiaume, J. Jackson, R. C. Dash, A. Vindigni, K. M. Hadden, S. Cantor

The paper identifies that oncogene expression creates replication gaps, which are suppressed by translesion synthesis (TLS), and shows that inhibiting TLS reduces cancer cell fitness.

bioRxiv · Sep 25, 2019Cancer Biology