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Article

Mutated KCNJ5 activates the acute and chronic regulatory steps in aldosterone production.

Journal of molecular endocrinology - 1 Jul 2016

Hattangady Namita G, Karashima Shigehiro, Yuan Lucy, Ponce-Balbuena Daniela, Jalife José, Gomez-Sanchez Celso E, Auchus Richard J, Rainey William E, Else Tobias

Abstract excerpt

Somatic and germline mutations in the inward-rectifying K(+) channel (KCNJ5) are a common cause of primary aldosteronism (PA) in aldosterone-producing adenoma and familial hyperaldosteronism type III, respectively. Dysregulation of adrenal cell calcium signaling represents one mechanism for mutated KCNJ5 stimulation of aldosterone synthase (CYP11B2) expression and aldosterone production. However, the mechanisms...

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Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

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Source

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Identifiers

PMID: 27099398
DOI: 10.1530/JME-15-0324
PMCID: PMC5027885

Genes

KCNJ5
ATF2

Variants

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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