Author

Christina Klausen

University of Bonn

Listed by name: these papers carry no ORCID for this author, so different people with the same name may be mixed together.

Biology Disciplines

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Cell Biology· 1 Genetics· 1

Signature Assays, Organisms & Methods

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Research Focus:cell type annotation· 2 Research Focus:differential expression· 2 Approach:experimental assay· 2 Organism:mouse· 2 Research Focus:cell-cell communication· 1 Research Focus:development & morphogenesis· 1 Research Focus:drug response / drug discovery· 1 Research Focus:protein structure prediction· 1

Frequent Co-Authors

Dagmar WachteniD· 2 shared Helen May‐SimeraiD· 2 shared Bernhard SchermeriD· 1 shared Carmen Ruiz de AlmodóvariD· 1 shared Christoph ThieleiD· 1 shared Collins Osei-SarpongiD· 1 shared Dalila Juliana Silva RibeiroiD· 1 shared Elvira MassiD· 1 shared

Activity by Year

2024-2025 · peak 1/yr

Co-Author Collaboration Network

10 top collaborators · 33 mutual co-author links

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2 shared papersCell Biology

Dagmar WachtenORCID

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2 papers

Recent·Most cited

Cell BiologyThe EMBO JournalPeer-reviewedAug 20, 2025

BBSome-dependent ciliary Hedgehog signaling governs cell fate in the white adipose tissue

Katharina Sieckmann, Nora Winnerling, Dalila Juliana Silva Ribeiro…·Dagmar Wachten

This study shows that primary cilia dysfunction in Bbs8-/- mice reduces adipose stem cells and promotes fibrogenic progenitors via disrupted Hedgehog signaling, affecting adipogenesis and lipid uptake.

10 citations

mousescRNA-seq

𝕏 PostBluesky

GeneticsbioRxivPreprintMar 7, 2024

Loss of Bbs8 leads to cystic kidney disease in mice with reduced acetylation of ciliary alpha-tubulin through HDAC2

Emilia Kieckhöfer, Julia Günzler, Peter Andreas Matthiessen…·Bernhard Schermer

This study shows that loss of Bbs8 in mice causes cystic kidney disease by reducing ciliary alpha-tubulin acetylation through increased HDAC2 activity.

DOI 10.1101/2024.03.07.583949

mouseproteomics

𝕏 PostBluesky