Marina V. Kovalenko

This study shows that knocking out Msh3 in mice with Huntington's disease slows CAG expansion and reduces pathology, with earlier intervention being more effective.

This paper investigates the protective effect of the LIG1 K845N variant in Huntington's disease by showing it increases ligase fidelity and suppresses somatic CAG repeat expansion.

This study investigates how different HTT-lowering therapies affect somatic instability in HD mice, finding that transcriptional repression and CAG repeat binding reduce SI without lowering HTT levels.

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.

This study shows splice modulators like branaplam reduce HTT CAG repeat expansion by affecting PMS1 expression, suggesting PMS1 as a new therapeutic target for Huntington's disease.

The paper shows that CAG repeat expansion in Huntington's disease disrupts splicing, reducing circular RNA production and affecting neural progenitors and striatum before symptoms appear.

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

This study shows that reducing huntingtin protein levels decreases somatic instability in CAG-expanded loci in both mouse models and human neurons.