Author

Kert Mätlik

Tallinn University of TechnologyORCID 0009-0009-8542-6193Unclaimed ORCID profile · follow to get notified of new preprints

Biology Disciplines

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Neuroscience· 3

Signature Assays, Organisms & Methods

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Organism:human· 3 Research Focus:differential expression· 2 Approach:statistical model· 2 Assay:bulk RNA-seq· 1 Assay:ChIP-seq· 1 Research Focus:database / resource· 1 Assay:DNA methylation· 1 Approach:experimental assay· 1

Frequent Co-Authors

Nathaniel HeintziD· 3 shared Christina PressliD· 2 shared Maria Esterlita Siantoputri· 2 shared Matthew BaffutoiD· 2 shared Alan UmfressiD· 1 shared Chris KayiD· 1 shared Christina Maree BuchananiD· 1 shared Douglas BarrowsiD· 1 shared

Activity by Year

2025-2026 · peak 2/yr

Co-Author Collaboration Network

10 top collaborators · 25 mutual co-author links

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3 shared papersNeuroscience

Nathaniel HeintzORCID

Mutual co-authors in cluster

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3 papers

Recent·Most cited

NeurosciencebioRxivPreprintMar 24, 2026

GPCRs as Targets for Human Brain Modulation: A Multi-omic Atlas of Cell-Type Specific Expression

Alan Umfress, Patrick Wertimer, Christina Pressl…·Nathaniel Heintz

This study presents an atlas of orphan GPCR expression across the human brain for translational targeting.

DOI 10.64898/2026.03.23.713764

humanbulk RNA-seq

𝕏 PostBluesky

NeurosciencebioRxivPreprintMar 5, 2026

Loss of interruption in the HTT CAG repeat is associated with increased somatic expansion and loss of medium spiny neurons in HD

Chris Kay, Jessica Q. Dawson, Kert Mätlik…·Michael R. Hayden

The paper shows that loss of interruption in HTT CAG repeats increases somatic expansion and MSN loss in HD, with greater effects in patients with CAG-CCG LOI.

1 citation

humanstatistical model

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NeurosciencebioRxivPreprintMay 21, 2025

Epigenetic mechanisms governing cell type specific somatic expansion and toxicity in Huntington's disease

Matthew Baffuto, Kert Mätlik, Isaac Ilyashov…·Nathaniel Heintz

This study identifies epigenetic mechanisms linking cell type-specific enhancer activity to somatic CAG expansion and toxicity in Huntington's disease.

6 citations

𝕏 PostBluesky