Author

Claudia Dafinger

University of Cologne

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

Biology Disciplines

Click to filter author papers

Cell Biology· 2 Genetics· 1 Physiology· 1

Signature Assays, Organisms & Methods

Click to filter · or open tag

Research Focus:differential expression· 3 Approach:experimental assay· 3 Assay:proteomics· 3 Research Focus:cell type annotation· 2 Organism:human· 2 Organism:mouse· 2 Research Focus:cell signaling & trafficking· 1 Research Focus:cell-cell communication· 1

Frequent Co-Authors

Max C. LiebauiD· 4 shared Bernhard SchermeriD· 3 shared Thomas R. BenzingiD· 2 shared Alf HonigmanniD· 1 shared Alina Braun· 1 shared Andre KrausiD· 1 shared Andrea GrundiD· 1 shared Andreas BeyeriD· 1 shared

Activity by Year

2017-2025 · peak 2/yr

Co-Author Collaboration Network

10 top collaborators · 21 mutual co-author links

Click any collaborator node to inspect or filter shared papers

Focal author (center)Selected co-authorORCID co-authorUnlinked name

Curved chords = mutual co-authorship

4 shared papersCell Biology

Max C. LiebauORCID

Mutual co-authors in cluster

Author profile →

4 papers

Recent·Most cited

The fibrocystin C-terminal domain inhibits Src/STAT3 signal induced cystogenesis of kidney epithelia.

Fatima Hassan, Susanne T. Hahnenstein, Andre Kraus, Bjoern Buchholz, Markus Mukenhirn, Alf Honigmann, Claudia Dafinger, Max C. Liebau, Thomas Pokrant, Jan Faix, Andrea Grund, Dieter Haffner, Wolfgang H. Ziegler

This study shows that the fibrocystin C-terminal domain suppresses Src/STAT3 signaling, preventing cyst formation in kidney epithelial cells by inhibiting secretory phenotype and STAT3-dependent transcription.

bioRxiv · Aug 8, 2025 · PreprintCell Biology

The nephronophthisis protein GLIS2/NPHP7 is required for the DNA damage response in kidney tubular epithelial cells

Lena K. Ebert, Lukas Schloesser, Laura E. Frech, Manaswita Jain, Claudia Dafinger, Max C. Liebau, Thomas R. Benzing, Bernhard Schermer, Gisela G.G. Slaats

This paper shows that GLIS2 is essential for the DNA damage response in kidney cells, leading to DNA damage and cystic kidney disease in a mouse model.

American Journal of Physiology-Renal Physiology · Jul 25, 2025Peer-reviewedCell Biology

mTOR-activating mutations in RRAGD cause kidney tubulopathy and cardiomyopathy (KICA) syndrome

Karl P. Schlingmann, François Jouret, Kuang Shen, Anukrati Nigam, Francisco J. Arjona, Claudia Dafinger, Pascal Houillier, Deborah P. Jones, Felix Kleinerüschkamp, Jun Seok Oh, Nathalie Godefroid, Mehmet Eltan, Tülay Güran, Stéphane Burtey, Marie-Christine Parotte, , Jeroen H. F. de Baaij

The paper identifies mTOR-activating mutations in RRAGD causing kidney tubulopathy and cardiomyopathy (KICA) syndrome through genetic and functional analyses of patient cohorts.

bioRxiv · Mar 11, 2021 · PreprintGenetics

Individual nephron proteomes connect morphology and function in proteinuric kidney disease

Martin Höhne, Christian K. Frese, Florian Grahammer, Claudia Dafinger, Giuliano Ciarimboli, Linus Butt, Julia Binz, Matthias J. Hackl, Mahdieh Rahmatollahi, Martin Kann, Simon Schneider, Mehmet M. Altintas, Bernhard Schermer, Thomas Reinheckel, Heike Göbel, , Markus M. Rinschen

The paper develops a method to analyze individual nephron proteomes in kidney disease, identifying lysosomal protein overexpression as a key mechanism in proteinuric diseases.

bioRxiv · Sep 27, 2017 · PreprintPhysiology