Author

J. C. Marie

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

Immunology· 2

Signature Assays, Organisms & Methods

Click to filter · or open tag

Approach:experimental assay· 2 Organism:mouse· 2 Research Focus:cell signaling & trafficking· 1 Research Focus:cell type annotation· 1 Research Focus:cell-cell communication· 1 Research Focus:chromatin & epigenetic regulation· 1 Research Focus:development & morphogenesis· 1 Research Focus:differential expression· 1

Frequent Co-Authors

H. Hernandez-Vargas· 2 shared A. H. Abid· 1 shared C. Barrachina· 1 shared C. Goldsmith· 1 shared D. Bauche· 1 shared E. Dubois· 1 shared J. Perrault· 1 shared M. I. Matias· 1 shared

Activity by Year

2021-2023 · peak 1/yr

Co-Author Collaboration Network

10 top collaborators · 25 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 papersImmunology

H. Hernandez-Vargas

Mutual co-authors in cluster

Author profile →

2 papers

Recent·Most cited

Single molecule DNA methylation and hydroxymethylation reveal unique epigenetic identity profiles of T helper cells

C. Goldsmith, O. Fesneau, V. Thevin, M. I. Matias, J. Perrault, A. H. Abid, N. Taylor, V. Dardalhon, J. C. Marie, H. Hernandez-Vargas

The paper develops a method to profile DNA methylation and hydroxymethylation in T helper cells, revealing their role in cell identity and potential for studying autoimmune disease mechanisms.

bioRxiv · Feb 3, 2023 · PreprintImmunology

SMAD4 governs a feedforward regulation of the TGF-beta effects in CD8 T cells that contributes to preventing chronic intestinal inflammation

R. Igalouzene, H. Hernandez-Vargas, N. Benech, D. Bauche, C. Barrachina, E. Dubois, J. C. Marie, S. M. SOUDJA

This study shows SMAD4 in CD8 T cells prevents chronic intestinal inflammation through a TGF-beta-independent feedforward mechanism by repressing TGF-beta imprinting and promoting IL-7 response and integrin expression.

bioRxiv · Feb 19, 2021 · PreprintImmunology