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Article

Trpc6 inactivation confers protection in a model of severe nephrosis in rats.

Journal of molecular medicine (Berlin, Germany) - 1 Jul 2018

Kim Eun Young, Yazdizadeh Shotorbani Parisa, Dryer Stuart E

Abstract excerpt

Mutations in canonical transient receptor potential-6 (TRPC6) channels give rise to rare familial forms of focal and segmental glomerulosclerosis (FSGS). Here we examined a possible role for TRPC6 in the progression of chronic puromycin aminonucleoside (PAN) nephrosis in Sprague-Dawley rats, a classic model of acquired nephrotic syndromes. We used CRISPR/Cas9 technology to delete a 239-bp region within exon 2 of...

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Source

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Identifiers

PMID: 29785489
DOI: 10.1007/s00109-018-1648-3
PMCID: PMC6015123

Genes

TRPC6
TRPC3
TRPC5

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 6 Sept 2026. Manifest publication-graph-cohort-2026-09-06.1.

Source receipt: pubmed, retrieved 6 Sept 2026.

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