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Article

Overexpression of calcium-activated potassium channels underlies cortical dysfunction in a model of PTEN-associated autism.

Proceedings of the National Academy of Sciences of the United States of America - 5 Nov 2013

Garcia-Junco-Clemente Pablo, Chow David K, Tring Elaine, Lazaro Maria T, Trachtenberg Joshua T, Golshani Peyman

Abstract excerpt

De novo phosphatase and tensin homolog on chromosome ten (PTEN) mutations are a cause of sporadic autism. How single-copy loss of PTEN alters neural function is not understood. Here we report that Pten haploinsufficiency increases the expression of small-conductance calcium-activated potassium channels. The resultant augmentation of this conductance increases the amplitude of the afterspike hyperpolarization,...

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Source

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Identifiers

PMID: 24145404
DOI: 10.1073/pnas.1309207110
PMCID: PMC3831440

Genes

PTEN

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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