Discover Community Create You

Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Article

K+ channel mutations in adrenal aldosterone-producing adenomas and hereditary hypertension.

Science (New York, N.Y.) - 11 Feb 2011

Choi Murim, Scholl Ute I, Yue Peng, Björklund Peyman, Zhao Bixiao, Nelson-Williams Carol, Ji Weizhen, Cho Yoonsang, Patel Aniruddh, Men Clara J, Lolis Elias, Wisgerhof Max V, Geller David S, Mane Shrikant, Hellman Per, Westin Gunnar, Åkerström Göran, Wang Wenhui, Carling Tobias, Lifton Richard P

Abstract excerpt

Endocrine tumors such as aldosterone-producing adrenal adenomas (APAs), a cause of severe hypertension, feature constitutive hormone production and unrestrained cell proliferation; the mechanisms linking these events are unknown. We identify two recurrent somatic mutations in and near the selectivity filter of the potassium (K(+)) channel KCNJ5 that are present in 8 of 22 human APAs studied. Both produce...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to Adrenal Cortex Neoplasms
Share to Adrenal Glands

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Adrenocortical Adenoma

Share to Aldosterone

Share to G Protein-Coupled Inwardly-Rectifying Potassium Channels

Share to Hyperaldosteronism

Share to Hyperplasia

Share to Potassium

Source

Open in PubMed Open full text

Identifiers

PMID: 21311022
DOI: 10.1126/science.1198785
PMCID: PMC3371087

Genes

KCNJ5

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 5 Sept 2026. Manifest publication-graph-cohort-2026-09-05.1.

Source receipt: pubmed, retrieved 5 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

K+ channel mutations in adrenal aldosterone-producing adenomas and hereditary hypertension.PMID 21311022Read ↗

New insights into aldosterone-producing adenomas and hereditary aldosteronism: mutations in the K+ channel KCNJ5.Semantic proximity Read ↗

A Novel KCNJ5-insT149 Somatic Mutation Close to, but Outside, the Selectivity Filter Causes Resistant Hypertension by Loss of Selectivity for PotassiumSemantic proximity Read ↗

Hypertension with or without adrenal hyperplasia due to different inherited mutations in the potassium channel KCNJ5.Semantic proximity Read ↗

Pharmacology and pathophysiology of mutated KCNJ5 found in adrenal aldosterone-producing adenomas.Semantic proximity Read ↗

Somatic ATP1A1, ATP2B3, and KCNJ5 mutations in aldosterone-producing adenomas.Semantic proximity Read ↗

Somatic and germline CACNA1D calcium channel mutations in aldosterone-producing adenomas and primary aldosteronism.Semantic proximity Read ↗

Comprehensive re-sequencing of adrenal aldosterone producing lesions reveal three somatic mutations near the KCNJ5 potassium channel selectivity filter.Semantic proximity Read ↗

Role of KCNJ5 in familial and sporadic primary aldosteronism.Semantic proximity Read ↗

An update on novel mechanisms of primary aldosteronismSemantic proximity Read ↗

Clinical Translationality of KCNJ5 Mutation in Aldosterone Producing Adenoma.Semantic proximity Read ↗

Somatic and inherited mutations in primary aldosteronism.Semantic proximity Read ↗

Somatic mutations in ATP1A1 and ATP2B3 lead to aldosterone-producing adenomas and secondary hypertension.Semantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.