Super‐resolved local recruitment of CLDN5 to filtration slits implicates a direct relationship with podocyte foot process effacement-Reference-Cited by-同舟云学术

Super‐resolved local recruitment of CLDN5 to filtration slits implicates a direct relationship with podocyte foot process effacement

Published:2021-06-22 Issue:16 Volume:25 Page:7631-7641
ISSN:1582-1838
Container-title:Journal of Cellular and Molecular Medicine
language:en
Short-container-title:J Cell Mol Med

Author:

Tesch Florian¹,Siegerist Florian¹^ORCID,Hay Eleonora¹²,Artelt Nadine¹,Daniel Christoph³,Amann Kerstin³,Zimmermann Uwe⁴,Kavvadas Panagiotis⁵,Grisk Olaf⁶,Chadjichristos Christos⁵,Endlich Karlhans¹,Chatziantoniou Christos⁵,Endlich Nicole¹

Affiliation:

1. Department of Anatomy and Cell Biology University Medicine Greifswald Greifswald Germany

2. Department of Mental and Physical Health and Preventive Medicine Section of Human Anatomy University of Campania “Luigi Vanvitelli” Naples Italy

3. Department of Nephropathology Institute of Pathology University of Erlangen‐Nuremberg Erlangen Germany

4. Department of Urology University Medicine Greifswald Greifswald Germany

5. UMRS 1155 INSERM Sorbonne Université Paris France

6. Institute for Physiology Medizinische Hochschule Brandenburg Theodor Fontane Neuruppin Germany

Funder

Bundesministerium für Bildung und Forschung

Publisher

Wiley

Subject

Cell Biology,Molecular Medicine

Link

https://onlinelibrary.wiley.com/doi/pdf/10.1111/jcmm.16519

Reference19 articles.

1. Positionally Cloned Gene for a Novel Glomerular Protein—Nephrin—Is Mutated in Congenital Nephrotic Syndrome

2. Differentiation of epithelial foot processes and filtration slits: sequential appearance of occluding junctions, epithelial polyanion, and slit membranes in developing glomeruli;Reeves W;Lab Invest,1978

3. Proteinuria and Perinatal Lethality in Mice Lacking NEPH1, a Novel Protein with Homology to NEPHRIN

4. NPHS2, encoding the glomerular protein podocin, is mutated in autosomal recessive steroid-resistant nephrotic syndrome

5. Congenital Nephrotic Syndrome in Mice Lacking CD2-Associated Protein

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