Author

J. Messeant

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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Pathology· 1 Physiology· 1

Signature Assays, Organisms & Methods

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Approach:experimental assay· 2 Organism:mouse· 2 Research Focus:cell type annotation· 1 Research Focus:differential expression· 1 Research Focus:host-pathogen & immune response· 1 Organism:human· 1 Assay:proteomics· 1

Frequent Co-Authors

A. Ferry· 2 shared A. Brull· 1 shared A. F. Klein· 1 shared A. Lilienbaum· 1 shared A. Parlakian· 1 shared C. Coirault· 1 shared C. Delacroix· 1 shared D. Furling· 1 shared

Activity by Year

2019-2020 · peak 1/yr

Co-Author Collaboration Network

10 top collaborators · 25 mutual co-author links

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2 shared papersPhysiology

A. Ferry

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2 papers

Recent·Most cited

Lamin-related congenital muscular dystrophy alters mechanical signaling and skeletal muscle growth

D. J. Owens, J. Messeant, S. Moog, M. Viggars, A. Ferry, K. Mamchaoui, E. Lacene, N. Romero, A. Brull, G. Bonne, G. S. Butler-Bowne, C. Coirault

This study investigates how LMNA mutations affect skeletal muscle growth and mechanical signaling in muscle stem cells and mouse models, finding impaired differentiation and hypertrophy in LMNA-CMD.

bioRxiv · Aug 6, 2020Physiology

Desmin is a modifier of dystrophic muscle features in Mdx mice

A. Ferry, J. Messeant, A. Parlakian, M. Lemaitre, P. Roy, C. Delacroix, A. Lilienbaum, Y. Hovhannisyan, D. Furling, A. F. Klein, Z. Li, O. Agbulut

This study shows that desmin deletion in Mdx mice worsens muscle weakness, fragility, and fatigue resistance, while desmin gene transfer improves these features.

bioRxiv · Aug 23, 2019 · PreprintPathology