Author

Stefan Kochanek

Universität UlmORCID 0000-0001-7494-1602Unclaimed ORCID profile · follow to get notified of new preprints

Biology Disciplines

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Signature Assays, Organisms & Methods

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Assay:bulk RNA-seq· 2 Research Focus:differential expression· 2 Organism:human· 2 Approach:statistical model· 2 Research Focus:cell-cell communication· 1 Research Focus:drug response / drug discovery· 1 Approach:experimental assay· 1 Research Focus:gene regulatory network inference· 1

Frequent Co-Authors

Manuel SeefelderiD· 2 shared Besnik Muqaku· 1 shared Enrico CalziaiD· 1 shared Fabrice A. C. KleiniD· 1 shared Patrick OeckliD· 1 shared

Activity by Year

2021-2026 · peak 1/yr

Co-Author Collaboration Network

5 top collaborators · 10 mutual co-author links

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2 shared papersMolecular Biology

Manuel SeefelderORCID

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2 papers

Recent·Most cited

Molecular BiologybioRxivPreprintJul 7, 2026

The huntingtin-HAP40 complex is a bidirectional cellular rheostat

Manuel Seefelder, Fabrice A. C. Klein, Enrico Calzia…·Stefan Kochanek

The paper shows the HTT-HAP40 complex acts as a bidirectional rheostat regulating stress response and lipid metabolism, with loss of balance linked to Huntington's disease pathogenesis.

DOI 10.64898/2026.06.03.729778

humanproteomics

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NeurosciencePLoS ONEPeer-reviewedJun 10, 2021

A meta-analysis of transcriptomic profiles from Huntington's disease patients points to a pathophysiological role of CDC42, NFY, DLX1 and PRMT3

Manuel Seefelder, Stefan Kochanek

This study identifies transcriptomic alterations in Huntington's disease, highlighting CDC42, NFY, DLX1, and PRMT3 as key genes involved in disease pathology.

26 citations

humanbulk RNA-seq

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