Author

E. Poree

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 Pathology· 1 Physiology· 1

Signature Assays, Organisms & Methods

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Approach:experimental assay· 3 Organism:mouse· 3 Research Focus:cell type annotation· 2 Research Focus:differential expression· 2 Organism:human· 2 Assay:bulk RNA-seq· 1 Research Focus:cancer & tumor microenvironment· 1 Research Focus:cell-cell communication· 1

Frequent Co-Authors

A. Viau· 3 shared S. Saunier· 3 shared E. Birgy· 2 shared E. W. Kuehn· 2 shared G. Ferri· 2 shared K. Billot· 2 shared M. Quatredeniers· 2 shared R. Salomon· 2 shared

Activity by Year

2021-2022 · peak 2/yr

Co-Author Collaboration Network

10 top collaborators · 41 mutual co-author links

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3 shared papersCell Biology

A. Viau

Mutual co-authors in cluster

Author profile →

3 papers

Recent·Most cited

Prostaglandin E1 as therapeutic molecule for Nephronophthisis and related ciliopathies

H. Garcia, A. Serafin, F. Silbermann, E. Poree, C. Mahaut, A. Viau, K. Billot, E. Birgy, M. Garfa-Traore, S. Roy, S. Cecarelli, M. Mehraz, P. C. Rodriguez, B. Deleglise, L. Furio, , S. Saunier

This study identifies PGE1 as a potential therapeutic for NPH-associated ciliopathies, showing it rescues ciliogenesis and improves kidney phenotypes in models.

bioRxiv · Jan 21, 2022Cell Biology

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