Kärt Mätlik

This study shows that H3K27me3 maintenance in mature neurons via EZH1 has minimal impact on gene expression and chromatin accessibility.

This study shows that GDNF regulates serotonin system development and adult function, with excess GDNF linked to neuropsychiatric disorders.

This study shows that increasing GDNF in postnatal Purkinje cells enhances motor learning in mice, with findings relevant to human motor skill differences.

This study shows that Astn2 knockout mice display ASD-like behaviors and altered cerebellar circuit properties, including changes in synaptic transmission and glial volume.

The paper investigates CAG repeat expansions and their association with cell death in specific brain regions in Huntington's disease using molecular profiling.

The paper identifies layer 5a corticostriatal neurons as selectively vulnerable in Huntington's disease using single nucleus RNA sequencing and shows they have extensive mHTT-CAG expansions.

This study shows that H4K91 mutants alter chromatin occupancy and misregulate neuronal differentiation, leading to microcephaly-like phenotypes in mice.

The paper shows that histone bivalency regulates the timing of cerebellar granule cell development by controlling gene expression during migration and differentiation.

This study shows that nicotinamide riboside (NR) alleviates Parkinson's disease symptoms in animal models but reduces dopamine levels when combined with proteasome inhibition.

This study shows that excess fetal GDNF can prolong nephrogenesis in postnatal mouse kidneys without increasing tumor risk.

This paper develops methods to upregulate gene expression in vivo while preserving cell-type-specific regulation, demonstrating their use in studying gene function and disease mechanisms.