Author

Nadia D’Ambrosi

University of Rome Tor VergataORCID 0000-0002-6646-7653Unclaimed ORCID profile · follow to get notified of new preprints

Biology Disciplines

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Molecular Biology· 1 Neuroscience· 1

Signature Assays, Organisms & Methods

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Approach:experimental assay· 2 Organism:mouse· 2 Research Focus:cell-cell communication· 1 Research Focus:differential expression· 1 Organism:Drosophila· 1 Research Focus:drug response / drug discovery· 1 Research Focus:gene regulatory network inference· 1 Organism:human· 1

Frequent Co-Authors

Gianluca CestraiD· 2 shared Ilaria Della ValleiD· 2 shared Mauro CozzolinoiD· 2 shared Michela Di SalvioiD· 2 shared Adelaide Riccardi· 1 shared Anna GarbelliiD· 1 shared Annalucia SerafinoiD· 1 shared Erica D’Avorio· 1 shared

Activity by Year

2025-2025 · peak 2/yr

Co-Author Collaboration Network

10 top collaborators · 37 mutual co-author links

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2 shared papersMolecular Biology

Gianluca CestraORCID

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2 papers

Recent·Most cited

DNA damage response defects induced by the formation of TDP-43 and mutant FUS cytoplasmic inclusions and their pharmacological rescue.

Stefania Modafferi, Stefania Farina, Francesca Esposito, Ornella Brandi, Michela Di Salvio, Ilaria Della Valle, Sara D’Uva, Eveljn Scarian, Giada Cicio, Adelaide Riccardi, Federica Pisati, Anna Garbelli, Tiziana Santini, Orietta Pansarasa, Mariangela Morlando, , Sofia Francia

This study shows that TDP-43 and FUS cytoplasmic inclusions impair DNA damage response and repair, and that pharmacological stimulation of DDR can rescue these defects in ALS models.

Cell Death and Differentiation · May 28, 2025Peer-reviewedMolecular Biology

Cytoplasmic accumulation of a splice variant of hnRNP A2/B1 contributes to FUS-associated toxicity in a mouse model of ALS

Simona Rossi, Martina Milani, Ilaria Della Valle, S. Bisegna, Valeria Durante, M. Addesse, Erica D’Avorio, Michela Di Salvio, Annalucia Serafino, Gianluca Cestra, Savina Apolloni, Nadia D’Ambrosi, Mauro Cozzolino

This study shows that FUS-induced splicing changes lead to cytoplasmic accumulation of hnRNP A2b/B1 splice variants, promoting stress granule formation and motor neuron toxicity in a mouse model of ALS.

Cell Death and Disease · Mar 29, 2025Peer-reviewedNeuroscience