Author

C. Boumendil

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

Biology Disciplines

Click to filter author papers

Cell Biology· 3

Signature Assays, Organisms & Methods

Click to filter · or open tag

Approach:experimental assay· 3 Research Focus:cell signaling & trafficking· 2 Research Focus:development & morphogenesis· 2 Research Focus:host-pathogen & immune response· 2 Organism:human· 2 Research Focus:chromatin & epigenetic regulation· 1 Assay:DNA methylation· 1 Organism:mouse· 1

Frequent Co-Authors

W. A. Bickmore· 2 shared A. Quintanilla· 1 shared B. M. Bartlett· 1 shared D. R. FitzPatrick· 1 shared G. Olley· 1 shared J. C. Acosta· 1 shared J.-C. Acosta· 1 shared K. Olsen· 1 shared

Activity by Year

2018-2024 · peak 1/yr

Co-Author Collaboration Network

10 top collaborators · 15 mutual co-author links

Click any collaborator node to inspect or filter shared papers

Focal author (center)Selected co-authorORCID co-authorUnlinked name

Curved chords = mutual co-authorship

2 shared papersCell Biology

W. A. Bickmore

Mutual co-authors in cluster

Author profile →

3 papers

Recent·Most cited

TPR is required for cytoplasmic chromatin fragment formation during senescence

B. M. Bartlett, Y. Kumar, S. Boyle, T. Chowdhury, A. Quintanilla, C. Boumendil, J. C. Acosta, W. A. Bickmore

The paper shows TPR is required for early NF-κB activation during oncogene-induced senescence, leading to cytoplasmic chromatin fragment formation and SASP activation.

bioRxiv · Apr 18, 2024Cell Biology

Cornelia-de-Lange syndrome-associated mutations cause a DNA damage signalling and repair defect

G. Olley, M. M. Pradeepa, D. R. FitzPatrick, W. A. Bickmore, C. Boumendil

This study shows that BRD4 mutations linked to Cornelia de Lange Syndrome impair DNA damage signalling and repair, and similar effects are observed in NIPBL-deficient cells.

bioRxiv · May 9, 2019Cell Biology

Nuclear pore density controls heterochromatin reorganization during senescence

W. Bickmore, C. Boumendil, P. Hari, K. Olsen, J.-C. Acosta

This study shows that increased nuclear pore density during oncogene-induced senescence drives SAHF formation, which is essential for SASP expression but not cell cycle arrest.

bioRxiv · Jul 21, 2018Cell Biology