Author

M. Spinazzi

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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Assay:bulk RNA-seq· 2 Research Focus:cell type annotation· 2 Research Focus:differential expression· 2 Approach:experimental assay· 2 Research Focus:gene regulatory network inference· 2 Organism:mouse· 2 Assay:ATAC-seq· 1 Research Focus:cell-cell communication· 1

Frequent Co-Authors

A. Girona· 1 shared A. VU Hong· 1 shared C.-A. Assenmacher· 1 shared D. Israeli· 1 shared E. Banerjee· 1 shared E. Gicquel· 1 shared E. Massourides· 1 shared E. Radaelli· 1 shared

Activity by Year

2021-2022 · peak 1/yr

Co-Author Collaboration Network

10 top collaborators · 21 mutual co-author links

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1 shared paperCell Biology

A. Girona

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Author profile →

2 papers

Recent·Most cited

Mitochondrial defects leading to arrested spermatogenesis and ferroptosis in a mouse model of Leigh Syndrome

E. Radaelli, C.-A. Assenmacher, E. Banerjee, F. Manero, S. Khiati, A. Girona, G. Lopez-Lluch, P. Navas, M. Spinazzi

This study shows that PARL deficiency in mice causes testicular atrophy and male infertility due to ferroptosis in spermatocytes, independent of neurodegeneration.

bioRxiv · Nov 22, 2022Cell Biology

Dlk1-Dio3 cluster miRNAs regulate mitochondrial functions in Duchenne muscular dystrophy

A. VU Hong, N. Bourg, P. Sanatine, J. Poupiot, K. Charton, E. Gicquel, E. Massourides, M. Spinazzi, I. Richard, D. Israeli

This study identifies DD-miRNAs as regulators of mitochondrial dysfunction in DMD, showing their upregulation and epigenetic control in dystrophic muscle.

bioRxiv · Oct 20, 2021 · PreprintPhysiology