Author

M. Borczyk

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

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Pathology· 1

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Assay:bulk RNA-seq· 1 Research Focus:cell type annotation· 1 Research Focus:differential expression· 1 Research Focus:gene regulatory network inference· 1 Organism:human· 1 Organism:mouse· 1 Approach:statistical model· 1

Frequent Co-Authors

A. Occhipinti· 1 shared C. Angione· 1 shared C. Pinset· 1 shared D. C. Gorecki· 1 shared J. Rog· 1 shared L. Bozycki· 1 shared M. Korostynski· 1 shared M. R. Gosselin· 1 shared

Activity by Year

2021-2021 · peak 1/yr

Co-Author Collaboration Network

10 top collaborators · 45 mutual co-author links

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1 shared paperPathology

A. Occhipinti

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1 paper

Recent·Most cited

Loss of full-length dystrophin expression results in major cell-autonomous abnormalities in proliferating myoblasts

M. R. Gosselin, V. Mournetas, M. Borczyk, S. Verma, A. Occhipinti, J. Rog, L. Bozycki, M. Korostynski, S. Robson, C. Angione, C. Pinset, D. C. Gorecki

This study shows that loss of full-length dystrophin in myoblasts causes cell-autonomous defects in gene expression, proliferation, chemotaxis, and differentiation, contributing to muscle regeneration failure in Duchenne muscular dystrophy.

bioRxiv · Aug 24, 2021Pathology