Author

Clarisse Orniacki

University of ConnecticutORCID 0000-0002-2585-3179Unclaimed ORCID profile · follow to get notified of new preprints

Biology Disciplines

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Signature Assays, Organisms & Methods

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Approach:experimental assay· 2 Assay:bulk RNA-seq· 1 Research Focus:cell signaling & trafficking· 1 Research Focus:cell type annotation· 1 Research Focus:development & morphogenesis· 1 Research Focus:differential expression· 1 Assay:electronic health records· 1 Organism:human· 1

Frequent Co-Authors

Beata TuroňováiD· 1 shared Christian E. ZimmerliiD· 1 shared Christopher E. StoddardiD· 1 shared Clémence M Dupont-Thibert· 1 shared Dea GorkaiD· 1 shared Hans-Georg KräusslichiD· 1 shared Heather R. Glatt-DeeleyiD· 1 shared Jan Philipp KreysingiD· 1 shared

Activity by Year

2020-2024 · peak 1/yr

Co-Author Collaboration Network

10 top collaborators · 21 mutual co-author links

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1 shared paperCell Biology

Beata TuroňováORCID

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2 papers

Recent·Most cited

Cell BiologybioRxivFeb 5, 2024

Nuclear pores safeguard the integrity of the nuclear envelope

Reiya Taniguchi, Clarisse Orniacki, Jan Philipp Kreysing…·Martin Beck

This study shows that nuclear pore complexes dilate during cell differentiation and that Nup133 deficiency prevents this dilation, leading to nuclear envelope instability.

DOI 10.1038/s41556-025-01648-3

mouseelectronic health records

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GeneticsHuman Molecular GeneticsPeer-reviewedSep 18, 2020

Specific ZNF274 binding interference at SNORD116 activates the maternal transcripts in Prader-Willi syndrome neurons

Maéva Langouët, Dea Gorka, Clarisse Orniacki…·Stormy J. Chamberlain

The paper shows that disrupting ZNF274 binding at SNORD116 activates its maternal allele in PWS neurons without altering ZNF274 levels, suggesting a therapeutic strategy for Prader-Willi syndrome.

19 citations

humanbulk RNA-seq

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