Author

E. W. Kuehn

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

Pathology· 2 Physiology· 1

Signature Assays, Organisms & Methods

Click to filter · or open tag

Approach:experimental assay· 3 Organism:mouse· 3 Research Focus:host-pathogen & immune response· 2 Assay:bulk RNA-seq· 1 Research Focus:cancer & tumor microenvironment· 1 Research Focus:cell type annotation· 1 Research Focus:cell-cell communication· 1 Research Focus:development & morphogenesis· 1

Frequent Co-Authors

A. Viau· 3 shared E. Poree· 2 shared F. Bienaime· 2 shared G. Ferri· 2 shared M. Quatredeniers· 2 shared S. Braeg· 2 shared S. Saunier· 2 shared A. Aka· 1 shared

Activity by Year

2020-2022 · peak 1/yr

Co-Author Collaboration Network

10 top collaborators · 33 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

3 shared papersPathology

A. Viau

Mutual co-authors in cluster

Author profile →

3 papers

Recent·Most cited

YAP restricts renal inflammation and mitigates kidney damage in nephronothisis related kidney disease.

G. Ferri, V. Goffette, E. Poree, S. Braeg, S. Carvalho, M. Quatredeniers, E. W. Kuehn, S. Saunier, A. Viau

This study investigates the role of YAP in NPH-like kidney disease and finds that YAP inhibition is not therapeutic, suggesting LKB1 and YAP are parallel regulators of a harmful pathway.

bioRxiv · Jan 17, 2022 · PreprintPathology

The renal inflammatory network of nephronophthisis

M. Quatredeniers, F. Bienaime, G. Ferri, P. Isnard, E. Poree, K. Billot, E. Birgy, S. Ceccarelli, F. Legendre, S. Braeg, T. Nguyen-Khoa, R. Salomon, M.-C. Gubler, E. W. Kuehn, S. Saunier, A. Viau

This study identifies a CCL2-independent inflammatory network in nephronophthisis, revealing distinct immune cell infiltration and cytokine signatures compared to autosomal dominant polycystic kidney disease.

bioRxiv · Jan 7, 2021Physiology

Tubular STAT3 limits renal inflammation in autosomal dominant polycystic kidney disease

A. Viau, M. Baziz, A. Aka, C. Nguyen, E. W. Kuehn, F. Terzi, F. Bienaime

This study shows that STAT3 limits renal inflammation in ADPKD by repressing inflammatory chemokines, despite not driving cyst growth.

Journal of the American Society of Nephrology · Apr 1, 2020Peer-reviewedPathology