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Article

TRPC6 channels and their binding partners in podocytes: role in glomerular filtration and pathophysiology.

American journal of physiology. Renal physiology - 1 Oct 2010

Dryer Stuart E, Reiser Jochen

Abstract excerpt

Loss or dysfunction of podocytes is a major cause of glomerular kidney disease. Several genetic forms of glomerular disease are caused by mutations in genes that encode structural elements of the slit diaphragm or the underlying cytoskeleton of podocyte foot processes. The recent discovery that gain-of-function mutations in Ca(2+)-permeable canonical transient receptor potential-6 channels (TRPC6) underlie a...

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Topics

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Share to Calcium
Share to Glomerular Filtration Rate
Share to Glomerulosclerosis, Focal Segmental

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Mutation

Share to Podocytes

Share to Potassium Channels, Calcium-Activated

Share to TRPC Cation Channels

Share to TRPC6 Cation Channel

Source

Open in PubMed Open full text

Identifiers

PMID: 20685822
DOI: 10.1152/ajprenal.00298.2010
PMCID: PMC2957253

Genes

TRPC6

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-07.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

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TRPC6 channels and their binding partners in podocytes: role in glomerular filtration and pathophysiology.PMID 20685822Read ↗

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