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Article

TRPC6 mutations associated with focal segmental glomerulosclerosis cause constitutive activation of NFAT-dependent transcription.

American journal of physiology. Cell physiology - 1 Mar 2009

Schlöndorff Johannes, Del Camino Donato, Carrasquillo Robert, Lacey Vanessa, Pollak Martin R

Abstract excerpt

Mutations in the canonical transient receptor potential channel TRPC6 lead to an autosomal dominant form of human kidney disease characterized histologically by focal and segmental glomerulosclerosis. Several of these mutations enhance the amplitude and duration of the channel current. However, the effect of these mutations on the downstream target of TRPC6, the nuclear factor of activated T cell (NFAT)...

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Source

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Identifiers

PMID: 19129465
DOI: 10.1152/ajpcell.00077.2008
PMCID: PMC2660257

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 mutations associated with focal segmental glomerulosclerosis cause constitutive activation of NFAT-dependent transcription.PMID 19129465Read ↗

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