Author

T. Vitali

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· 2

Signature Assays, Organisms & Methods

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Research Focus:cell type annotation· 2 Approach:experimental assay· 2 Research Focus:cell signaling & trafficking· 1 Research Focus:development & morphogenesis· 1 Research Focus:differential expression· 1 Organism:Drosophila· 1 Organism:human· 1 Assay:imaging· 1

Frequent Co-Authors

A. A. Mironov· 1 shared C. Gellera· 1 shared C. Paiardi· 1 shared D. Grifoni· 1 shared F. Taroni· 1 shared G. Licata· 1 shared G. Yan· 1 shared J. Swift· 1 shared

Activity by Year

2019-2022 · peak 1/yr

Co-Author Collaboration Network

10 top collaborators · 24 mutual co-author links

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1 shared paperCell Biology

A. A. Mironov

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2 papers

Recent·Most cited

Vimentin intermediate filaments provide structural stability to the mammalian Golgi apparatus

T. Vitali, T. M. Witkos, M. F. Cutiongco, G. Yan, A. A. Mironov, J. Swift, M. Lowe

This study shows vimentin intermediate filaments support Golgi structural stability, with GORAB mediating this interaction, affecting Golgi disassembly and reassembly dynamics.

bioRxiv · Aug 25, 2022 · PreprintCell Biology

Glutamine Synthetase-1 induces autophagy-lysosomal degradation of huntingtin aggregates and ameliorates animal motility in a Drosophila model for Huntington’s disease

L. Vernizzi, C. Paiardi, G. Licata, T. Vitali, S. Santarelli, M. Raneli, V. Manelli, M. Rizzetto, M. Gioria, M. E. Pasini, D. Grifoni, M. A. Vanoni, C. Gellera, F. Taroni, P. Bellosta

This study shows that GS1 expression in Drosophila neurons reduces huntingtin aggregates and improves motility in a Huntington’s disease model by enhancing autophagy and inhibiting TOR signaling.

bioRxiv · Apr 30, 2019Cell Biology