Author

A. Doucet

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

Physiology· 2 Pathology· 1

Signature Assays, Organisms & Methods

Click to filter · or open tag

Research Focus:cell type annotation· 3 Approach:experimental assay· 3 Organism:human· 3 Assay:proteomics· 3 Research Focus:differential expression· 2 Organism:mouse· 2 Organism:rat· 2 Research Focus:host-pathogen & immune response· 1

Frequent Co-Authors

G. Crambert· 3 shared A. SASSI· 2 shared C. Walter· 2 shared L. Cheval· 2 shared L. Morla· 2 shared A. Blanchard· 1 shared A. Chassot· 1 shared B. Matot· 1 shared

Activity by Year

2021-2022 · peak 2/yr

Co-Author Collaboration Network

10 top collaborators · 30 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 papersPhysiology

G. Crambert

Mutual co-authors in cluster

Author profile →

3 papers

Recent·Most cited

GDF15 mediates renal cell plasticity in response to potassium depletion

S. Lasaad, C. Walter, C. Rafael, L. Morla, A. Doucet, N. Picard, A. Blanchard, Y. Fromes, B. Matot, G. Crambert, L. Cheval

This study shows that GDF15 mediates renal cell plasticity in response to potassium depletion by regulating intercalated cell numbers and K+ retention.

bioRxiv · Dec 27, 2022 · PreprintPhysiology

Claudin-4, a core component of the tight-junctional complex along the collecting system, is induced in nephrotic syndrome

V. Olivier, A. SASSI, G. Arnoux, R. Chambrey, I. Monnay, A. Chassot, K. Udwan, E. Dizin, J. M. Rutkowski, L. Cheval, G. Crambert, C. A. Wagner, A. Doucet, D. Eladari, S. Moll, , S. K Ramakrishnan

This study shows claudin-4 expression increases in nephrotic syndrome, suggesting a shift from transcellular to paracellular chloride transport in the kidney collecting system.

bioRxiv · Jun 1, 2022 · PreprintPhysiology

A new variant of ASIC2 mediates sodium retention in nephrotic syndrome

M. Fila, A. Sassi, G. Brideau, L. Morla, P. Houillier, C. Walter, M. Gennaoui, L. Collignon, M. Keck, G. Planelles, N. Bakouh, M. Peuchmaur, G. Deschenes, I. Anegon, S. Remy, , A. Doucet

The paper identifies a truncated variant of ASIC2b responsible for sodium retention in idiopathic nephrotic syndrome, independent of ENaC and aldosterone.

bioRxiv · Feb 9, 2021Pathology