Author

J.-S. Hoffmann

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

Cancer Biology· 3 Cell Biology· 1

Signature Assays, Organisms & Methods

Click to filter · or open tag

Approach:experimental assay· 4 Organism:human· 4 Research Focus:chromatin & epigenetic regulation· 2 Assay:proteomics· 2 Assay:bulk RNA-seq· 1 Research Focus:cancer & tumor microenvironment· 1 Research Focus:cell signaling & trafficking· 1 Research Focus:cell type annotation· 1

Frequent Co-Authors

M.-J. Pillaire· 3 shared C. Ribeyre· 2 shared M. Madrid-Mencia· 2 shared V. Bergoglio· 2 shared V. Pancaldi· 2 shared A. Constantinou· 1 shared A. El kaoutari· 1 shared A. Frances· 1 shared

Activity by Year

2019-2021 · peak 2/yr

Co-Author Collaboration Network

10 top collaborators · 38 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

3 shared papersCancer Biology

M.-J. Pillaire

Mutual co-authors in cluster

Author profile →

4 papers

Recent·Most cited

Cytidine deaminase protects pancreatic cancer cells from replicative stress and drives resistance to DNA-targeting drugs

A. Lumeau, N. Bery, A. Frances, M. Gayral, C. Ribeyre, C. Lopez, A. Nevot, A. El kaoutari, G. Labrousse, M. Madrid-Mencia, M.-J. Pillaire, V. Pancaldi, V. Bergoglio, N. J. V. Dusetti, J.-S. Hoffmann, , P. Cordelier

This study shows that Cytidine deaminase (CDA) protects pancreatic cancer cells from replication stress and contributes to resistance against DNA-targeting drugs.

bioRxiv · Oct 23, 2021 · PreprintCancer Biology

A catalytic-independent function of human DNA polymerase Kappa controls the pool of the Checkpoint Kinase 1

M. Dall'Osto, L. Pierini, N. Valery, J.-S. Hoffmann, M.-J. Pillaire

This study identifies a catalytic-independent role of Pol kappa in maintaining Chk1 protein stability, crucial for replication checkpoint function.

bioRxiv · Feb 9, 2021Cell Biology

Low replication stress leads to specific replication timing advances associated to chromatin remodelling in cancer cells

L. Courtot, E. Bournique, C. Maric, L. Guitton-Sert, M. Madrid-Mencia, V. Pancaldi, J.-C. Cadoret, J.-S. Hoffmann, V. Bergoglio

The paper examines how low replication stress affects replication timing in cancer cells, revealing chromatin remodelling and inheritance of timing advances.

bioRxiv · Aug 19, 2020 · PreprintCancer Biology

KDM5 histone-demethylases contribute to replication stress response and tolerance.

M. Vandromme, S. Gaillard, V. Charasson, C. Ribeyre, K. Salifou, M.-J. Pillaire, J.-S. Hoffmann, A. Constantinou, D. Trouche

This study shows KDM5A and KDM5B contribute to replication stress response and tolerance through mechanisms independent of their demethylase activity.

bioRxiv · Dec 16, 2019 · PreprintCancer Biology