Author

C. Walter

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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Biophysics· 1 Immunology· 1 Pathology· 1 Physiology· 1

Signature Assays, Organisms & Methods

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Approach:experimental assay· 4 Research Focus:cell type annotation· 3 Organism:human· 3 Research Focus:differential expression· 2 Organism:mouse· 2 Assay:proteomics· 2 Research Focus:cell signaling & trafficking· 1 Research Focus:cell-cell communication· 1

Frequent Co-Authors

A. Doucet· 2 shared G. Crambert· 2 shared L. Morla· 2 shared A. Blanchard· 1 shared A. Pathak· 1 shared A. Sassi· 1 shared B. Heitplatz· 1 shared B. Huechtmann· 1 shared

Activity by Year

2021-2024 · peak 2/yr

Co-Author Collaboration Network

10 top collaborators · 18 mutual co-author links

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2 shared papersPhysiology

A. Doucet

Mutual co-authors in cluster

Author profile →

4 papers

Recent·Most cited

Microvascular immunity is organ-specific and concealed in peripheral blood

R. Rixen, P. Schuetz, C. Walter, B. Huechtmann, V. Van Marck, B. Heitplatz, J. Varghese, H. Pavenstaedt, K. Buscher

The paper analyzes microvascular immune cells in mouse organs and compares them to peripheral blood, finding organ-specific immune responses that are not detectable in blood or tissue samples.

bioRxiv · Apr 2, 2024 · PreprintImmunology

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

Matrix obstructions cause multiscale disruption in collective epithelial migration by suppressing physical function of leader cells

Y. L. Lee, J. Mathur, C. Walter, H. Zmuda, A. Pathak

This study shows that dense matrix obstructions disrupt collective epithelial migration by altering cell stiffness, leader-follower dynamics, and communication, with implications for disease mechanotypes.

bioRxiv · Apr 28, 2022Biophysics

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