Author

Ilaria Della Valle

University of Rome Tor VergataORCID 0009-0007-7136-066XUnclaimed ORCID profile · follow to get notified of new preprints

Biology Disciplines

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Molecular Biology· 1 Neuroscience· 1 Physiology· 1

Signature Assays, Organisms & Methods

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Approach:experimental assay· 3 Organism:mouse· 3 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 Research Focus:host-pathogen & immune response· 1

Frequent Co-Authors

Nadia D’AmbrosiiD· 3 shared Gianluca CestraiD· 2 shared Martina MilaniiD· 2 shared Mauro CozzolinoiD· 2 shared Michela Di SalvioiD· 2 shared Savina ApolloniiD· 2 shared Adelaide Riccardi· 1 shared Andrea Ninni· 1 shared

Activity by Year

2024-2025 · peak 2/yr

Co-Author Collaboration Network

10 top collaborators · 33 mutual co-author links

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3 shared papersMolecular Biology

Nadia D’AmbrosiORCID

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3 papers

Recent·Most cited

Molecular BiologyCell Death and DifferentiationPeer-reviewedMay 28, 2025

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…·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.

14 citationstop 2%

humanmouse

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NeuroscienceCell Death and DiseasePeer-reviewedMar 29, 2025

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…·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.

6 citations

mouseexperimental assay

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PhysiologyLife Science AlliancePeer-reviewedApr 17, 2024

Frataxin Deficiency Drives a Shift from Mitochondrial Metabolism to Glucose Catabolism, Triggering an Inflammatory Phenotype in Microglia

Francesca Sciarretta, Fabio Zaccaria, Andrea Ninni…·Daniele Lettieri‐Barbato

This study shows that frataxin deficiency in microglia shifts metabolism to glucose catabolism, causing inflammation, which is mitigated by butyrate treatment.

15 citations

mousescRNA-seq

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