Author

James A. DeCaprio

Brigham and Women's HospitalORCID 0000-0002-0896-167XUnclaimed ORCID profile · follow to get notified of new preprints

Biology Disciplines

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Signature Assays, Organisms & Methods

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Organism:human· 2 Assay:bulk RNA-seq· 1 Research Focus:database / resource· 1 Research Focus:differential expression· 1 Approach:experimental assay· 1 Research Focus:gene regulatory network inference· 1 Organism:mouse· 1 Approach:statistical model· 1

Frequent Co-Authors

Fatmata F. SesayiD· 1 shared Konstantin RiegeiD· 1 shared Larisa LitovchickiD· 1 shared Laurence A. FlorensiD· 1 shared Martin FischeriD· 1 shared Michael P. WashburniD· 1 shared Mikhail G. DozmoroviD· 1 shared Robert J. SchwarziD· 1 shared

Activity by Year

2019-2022 · peak 1/yr

Co-Author Collaboration Network

10 top collaborators · 24 mutual co-author links

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1 shared paperMolecular Biology

Fatmata F. SesayORCID

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2 papers

Recent·Most cited

TargetGeneReg 2.0: a comprehensive web-atlas for p53, p63, and cell cycle-dependent gene regulation

Martin Fischer, Robert J. Schwarz, Konstantin Riege, James A. DeCaprio, Steve Hoffmann

TargetGeneReg 2.0 expands its database to include non-coding genes and new transcription factors, enabling analysis of gene regulation by p53, ΔNp63, and cell cycle signaling.

NAR Cancer · Jan 13, 2022Peer-reviewedBioinformatics

DYRK1A regulates the recruitment of 53BP1 to the sites of DNA damage in part through interaction with RNF169

Vijay Menon, Varsha Ananthapadmanabhan, Selene K. Swanson, Siddharth Saini, Fatmata F. Sesay, Vasily A. Yakovlev, Laurence A. Florens, James A. DeCaprio, Michael P. Washburn, Mikhail G. Dozmorov, Larisa Litovchick

This paper identifies DYRK1A's role in DNA repair by regulating RNF169-mediated 53BP1 recruitment to DSB sites, with implications for DNA damage therapy response.

Cell Cycle · Feb 17, 2019Peer-reviewedMolecular Biology