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Article

Mutation of an A-kinase-anchoring protein causes long-QT syndrome.

Proceedings of the National Academy of Sciences of the United States of America - 26 Dec 2007

Chen Lei, Marquardt Michelle L, Tester David J, Sampson Kevin J, Ackerman Michael J, Kass Robert S

Abstract excerpt

A-kinase anchoring proteins (AKAPs) recruit signaling molecules and present them to downstream targets to achieve efficient spatial and temporal control of their phosphorylation state. In the heart, sympathetic nervous system (SNS) regulation of cardiac action potential duration (APD), mediated by beta-adrenergic receptor (betaAR) activation, requires assembly of AKAP9 (Yotiao) with the I(Ks) potassium channel...

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Topics

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Share to A Kinase Anchor Proteins
Share to Binding Sites

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Cytoskeletal Proteins

Share to KCNQ1 Potassium Channel

Share to Long QT Syndrome

Share to Potassium Channels

Share to Protein Structure, Tertiary

Share to Receptors, Adrenergic, beta

Source

Open in PubMed Open full text

Identifiers

PMID: 18093912
DOI: 10.1073/pnas.0710527105
PMCID: PMC2409254

Genes

KCNQ1
AKAP9

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.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Mutation of an A-kinase-anchoring protein causes long-QT syndrome.PMID 18093912Read ↗

The A-kinase anchoring protein Yotiao facilitates complex formation between adenylyl cyclase type 9 and the IKs potassium channel in heart.Semantic proximity Read ↗

Requirement of a macromolecular signaling complex for beta adrenergic receptor modulation of the KCNQ1-KCNE1 potassium channel.Semantic proximity Read ↗

Polymorphisms/Mutations in A-Kinase Anchoring Proteins (AKAPs): Role in the Cardiovascular SystemSemantic proximity Read ↗

A590T mutation in KCNQ1 C-terminal helix D decreases IKs channel trafficking and function but not Yotiao interaction.Semantic proximity Read ↗

Dominant-negative control of cAMP-dependent IKs upregulation in human long-QT syndrome type 1.Semantic proximity Read ↗

Proarrhythmic Consequences of a KCNQ1 AKAP-Binding Domain MutationSemantic proximity Read ↗

A mutation in the cardiac KV7.1 channel possibly disrupts interaction with Yotiao protein.Semantic proximity Read ↗

Protein kinase A and phosphodiesterase-4D3 binding to coding polymorphisms of cardiac muscle anchoring protein (mAKAP).Semantic proximity Read ↗

Divergent regulation of KCNQ1/E1 by targeted recruitment of protein kinase A to distinct sites on the channel complexSemantic proximity Read ↗

Human muscle-specific A-kinase anchoring protein polymorphisms modulate the susceptibility to cardiovascular diseases by altering cAMP/PKA signaling.Semantic proximity Read ↗

Dysregulation of N-terminal acetylation causes cardiac arrhythmia and cardiomyopathySemantic proximity Read ↗

Targeting the IKs Channel PKA Phosphorylation Axis to Restore Its Function in High-Risk LQT1 Variants.Semantic proximity Read ↗

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