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Article

Podocyte-specific overexpression of wild type or mutant trpc6 in mice is sufficient to cause glomerular disease.

PloS one - 20 Sept 2010

Krall Paola, Canales Cesar P, Kairath Pamela, Carmona-Mora Paulina, Molina Jessica, Carpio J Daniel, Ruiz Phillip, Mezzano Sergio A, Li Jing, Wei Changli, Reiser Jochen, Young Juan I, Walz Katherina

Abstract excerpt

Mutations in the TRPC6 calcium channel (Transient receptor potential channel 6) gene have been associated with familiar forms of Focal and Segmental Glomerulosclerosis (FSGS) affecting children and adults. In addition, acquired glomerular diseases are associated with increased expression levels o...

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Topics

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Share to Gene Expression
Share to Glomerulosclerosis, Focal Segmental

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Mice, Inbred CBA

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Source

Open in PubMed Open full text

Identifiers

PMID: 20877463
DOI: 10.1371/journal.pone.0012859
PMCID: PMC2942896

Genes

TRPC6

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 2 Sept 2026. Prepared record publication-20877463-2026-09-02.2. Manifest publication-graph-cohort-2026-09-02.2.

Source receipt: PubMed via Helena Literature Corpus, retrieved 2 Sept 2026.

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Podocyte-specific overexpression of wild type or mutant trpc6 in mice is sufficient to cause glomerular disease.PMID 20877463Read ↗

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