🏆 Finalist — NIH Data Sharing Index (“S-Index”) Challenge

Marina Kovalenko

Massachusetts General Hospital

ORCID: 0000-0002-4296-8189
NeuroscienceBiochemistry, Genetics and Molecular Biology

Pilot corpus only

This score is computed over theSindex pilot corpus and does not cover the full scientific literature. Scores are relative to papers we have ingested — papers, authors, and institutions outside the pilot are not represented. Methodology.

Top 100%percentile
0Author DataRank

Indexed papers

0in pilot corpus
datarank_citation_only_1hop_v6· scope data_onlyMethodology

Papers

Driven by 9 papers. Top paper: “Promotion of somatic CAG repeat expansion by Fan1 knock-out in Huntington’s disease knock-in mice is blocked by Mlh1 knock-out”.

Promotion of somatic CAG repeat expansion by Fan1 knock-out in Huntington’s disease knock-in mice is blocked by Mlh1 knock-out

Human Molecular Genetics(2020)10.1093/hmg/ddaa196
N/A
2.1DataRank · unranked
95 citations

Ricardo Mouro Pinto, Kyung‐Hee Kim, Tammy Gillis, Jayalakshmi Srinidhi Mysore, Marissa A Andrew +11 more

Histone deacetylase knockouts modify transcription, CAG instability and nuclear pathology in Huntington disease mice

eLife(2020)10.7554/elife.55911
N/A
0.620DataRank · unranked
21 citations

Serkan Erdin, Marissa A Andrew, Jason St. Claire, Melissa Shaughnessey, Leroy Hubert +9 more

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

bioRxiv (Cold Spring Harbor Laboratory)(2020)10.1101/2020.10.26.356238
N/A
0DataRank · unranked
1 citations

Antonia Vitalo, Marissa A Andrew, Eduarda Mota‐Silva, Marina Kovalenko, Zoe Burch +6 more

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

Nucleic Acids Research(2021)10.1093/nar/gkab152
N/A
0DataRank · unranked
45 citations

Antonia Vitalo, Marissa A Andrew, Eduarda Mota‐Silva, Marina Kovalenko, Zoe Burch +6 more

Defective linear and circular RNAs biogenesis in Huntington’s disease: CAG repeat expansion hijacks neuronal splicing

bioRxiv (Cold Spring Harbor Laboratory)(2021)10.1101/2021.12.27.474266
N/A
0DataRank · unranked
2 citations

Alan Monziani, Takshashila Tripathi, Jessica Döring, Guendalina Bergonzoni, Emanuela Kerschbamer +12 more

CAG repeat expansion in the Huntington’s disease gene shapes linear and circular RNAs biogenesis

PLoS Genetics(2023)10.1371/journal.pgen.1010988
N/A
0DataRank · unranked
23 citations

Guendalina Bergonzoni, Alan Monziani, Takshashila Tripathi, Jessica Döring, Emanuela Kerschbamer +12 more

CircHTT(2,3,4,5,6) — co-evolving with the HTT CAG-repeat tract — modulates Huntington's disease phenotypes

Molecular Therapy — Nucleic Acids(2024)10.1016/j.omtn.2024.102234
N/A
0DataRank · unranked
11 citations

Alan Monziani, Martina Lazioli, Deborah Donzel, Jessica Döring, Claudio Oss Pegorar +17 more

In vivo CRISPR–Cas9 genome editing in mice identifies genetic modifiers of somatic CAG repeat instability in Huntington’s disease

Nature Genetics(2025)10.1038/s41588-024-02054-5
N/A
0DataRank · unranked
59 citations

Ryan Murtha, António Azevedo, Cameron J. Douglas, Marina Kovalenko, Jessica Ulloa +17 more

Huntington’s disease LIG1 modifier variant increases ligase fidelity and suppresses somatic CAG repeat expansion

bioRxiv (Cold Spring Harbor Laboratory)(2025)10.1101/2025.07.15.664798
N/A
0DataRank · unranked
0 citations

Wonju Kim, David H. Beier, Yejin Lee, Marina Kovalenko, Faaiza Saif +17 more