Author

Antonia G. Vitalo

Harvard University

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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Genetics· 2

Signature Assays, Organisms & Methods

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Approach:experimental assay· 2 Organism:mouse· 2 Research Focus:benchmarking· 1 Research Focus:drug response / drug discovery· 1 Organism:human· 1

Frequent Co-Authors

Eduarda Mota‐SilvaiD· 2 shared Marina V. KovalenkoiD· 2 shared Ricardo Mouro PintoiD· 2 shared Vanessa Chantal WheeleriD· 2 shared Zoe N. Burch· 2 shared Anh M. NhuiD· 1 shared António Azevedo· 1 shared Brigitte Demelo· 1 shared

Activity by Year

2021-2025 · peak 1/yr

Co-Author Collaboration Network

10 top collaborators · 39 mutual co-author links

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2 shared papersGenetics

Eduarda Mota‐SilvaORCID

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2 papers

Recent·Most cited

GeneticsNature GeneticsPeer-reviewedJan 22, 2025

Identification of genetic modifiers of Huntington's disease somatic CAG repeat instability by in vivo CRISPR-Cas9 genome editing

Ricardo Mouro Pinto, Ryan Murtha, António Azevedo…·Vanessa Chantal Wheeler

The paper identifies genetic modifiers of Huntington's disease somatic CAG repeat instability using CRISPR-Cas9 in HD knock-in mice, revealing new therapeutic targets.

75 citationstop 1%

mouseexperimental assay

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GeneticsNucleic Acids ResearchPeer-reviewedFeb 23, 2021

Somatic CAG expansion in Huntington's disease is dependent on the MLH3 endonuclease domain, which can be excluded via MLH3 splice redirection to suppress expansion

Jennie C. L. Roy, Antonia G. Vitalo, Marissa A Andrew…·Ricardo Mouro Pinto

This study shows that targeting the MLH3 endonuclease domain reduces somatic CAG expansion in Huntington's disease models and patient cells.

42 citations

mousehuman

𝕏 PostBluesky