Author

Miroslava Hančárová

Charles UniversityORCID 0000-0001-6772-8862Unclaimed ORCID profile · follow to get notified of new preprints

Biology Disciplines

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Genetic & Genomic Medicine· 1 Genetics· 1

Signature Assays, Organisms & Methods

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Research Focus:differential expression· 2 Organism:human· 2 Approach:statistical model· 2 Organism:Drosophila· 1 Research Focus:drug response / drug discovery· 1 Assay:electronic health records· 1 Approach:experimental assay· 1 Research Focus:gene regulatory network inference· 1

Frequent Co-Authors

Ingrid M. WentzenseniD· 2 shared Zdeněk SedláčekiD· 2 shared Alali AbdulrazakiD· 1 shared Alban C. ZiegleriD· 1 shared Alejandro D. IglesiasiD· 1 shared Amber Hogart BegtrupiD· 1 shared Amélie Bosc-RosatiiD· 1 shared Andrew A. HardiganiD· 1 shared

Activity by Year

2018-2025 · peak 1/yr

Co-Author Collaboration Network

10 top collaborators · 33 mutual co-author links

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2 shared papersGenetic & Genomic Medicine

Ingrid M. WentzensenORCID

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2 papers

Recent·Most cited

Genetic & Genomic MedicineNature CommunicationsPeer-reviewedNov 26, 2025

Unveiling the crucial neuronal role of the proteasomal ATPase subunit gene PSMC5 in neurodevelopmental proteasomopathies

Sébastien Küry, Janelle E. Stanton, Geeske M. van Woerden…·Marta Codina‐Solà

The paper identifies PSMC5 variants causing neurodevelopmental disorders and shows their impact on neuronal function and immune signaling, suggesting therapeutic targets.

3 citations

humanrat

𝕏 PostBluesky

GeneticsPLoS GeneticsPeer-reviewedNov 30, 2018

De novo mutations in the GTP/GDP-binding region of RALA, a RAS-like small GTPase, cause intellectual disability and developmental delay

Susan M. Hiatt, Matthew B. Neu, Ryne C. Ramaker…·Gregory M. Cooper

The paper identifies de novo mutations in RALA, a RAS-like GTPase, as a cause of intellectual disability and developmental delay, showing their functional impact on GTP binding and effector interactions.

35 citations

humanwhole-exome sequencing

𝕏 PostBluesky