Author

I. Scionti

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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Cell Biology· 1 Physiology· 1

Signature Assays, Organisms & Methods

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Approach:experimental assay· 2 Organism:mouse· 2 Assay:ATAC-seq· 1 Assay:bulk RNA-seq· 1 Research Focus:cancer & tumor microenvironment· 1 Research Focus:cell signaling & trafficking· 1 Research Focus:cell type annotation· 1 Assay:ChIP-seq· 1

Frequent Co-Authors

L. Schaeffer· 2 shared A. Hamiche· 1 shared A. Osseni· 1 shared A. Ravel-Chapuis· 1 shared B. J. Jasmin· 1 shared C. Papin· 1 shared D. Dalkara· 1 shared E. Belotti· 1 shared

Activity by Year

2019-2022 · peak 1/yr

Co-Author Collaboration Network

10 top collaborators · 27 mutual co-author links

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2 shared papersPhysiology

L. Schaeffer

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Author profile →

2 papers

Recent·Most cited

Pharmacological inhibition of HDAC6 downregulates TGF-β via Smad2/3 acetylation and improves dystrophin-deficient muscles.

A. Osseni, A. Ravel-Chapuis, I. Scionti, Y.-G. Gangloff, V. Moncollin, R. Mounier, P. Leblanc, B. J. Jasmin, L. Schaeffer

This study shows that inhibiting HDAC6 with tubastatin A improves dystrophin-deficient muscle by reducing fibrosis and restoring microtubules and NMJ through Smad2/3 acetylation and TGF-β signaling inhibition.

bioRxiv · Jan 21, 2022 · PreprintPhysiology

H2A.Z is dispensable for both basal and activated transcription in post-mitotic mouse muscles

E. Belotti, N. Lacoste, T. Simonet, C. Papin, K. Padmanabhan, L. Ramos, D. Dalkara, I. Scionti, A. Hamiche, S. Dimitrov, L. Schaeffer

This study shows H2A.Z is not required for transcription in post-mitotic muscle cells, challenging its role as an activator and suggesting it is a marker of active promoters.

bioRxiv · Oct 30, 2019Cell Biology