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

PKA and PKC partially rescue long QT type 1 phenotype by restoring channel-PIP2 interactions.

Channels (Austin, Tex.) - 1 Jan 2000

Matavel Alessandra, Medei Emiliano, Lopes Coeli M B

Abstract excerpt

Long-QT syndrome causes torsade de pointes arrhythmia, ventricular fibrillation, and sudden death. The most commonly inherited form of long-QT syndrome, LQT1, is due to mutations on the potassium channel gene KCNQ1, which forms one of the main repolarizing cardiac K(+) channels, IKs. IKs has been...

Read the complete abstract on PubMed

Topics

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

Share to Cyclic AMP-Dependent Protein Kinases
Share to GTP-Binding Protein alpha Subunits, Gq-G11
Share to KCNQ1 Potassium Channel

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Phosphatidylinositol 4,5-Diphosphate

Share to Phosphotransferases (Alcohol Group Acceptor)

Share to Protein Kinase C

Share to Romano-Ward Syndrome

Share to Xenopus

Source

Identifiers

PMID: 19934648
DOI: 10.4161/chan.4.1.10227

Genes

PIP
KCNQ1

Variants

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 2 Sept 2026. Prepared record publication-19934648-2026-09-02.2. Manifest publication-graph-cohort-2026-09-02.2.

Source receipt: PubMed via Helena Literature Corpus, retrieved 2 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

PKA and PKC partially rescue long QT type 1 phenotype by restoring channel-PIP2 interactions.PMID 19934648Read ↗

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

A molecular mechanism for adrenergic-induced long QT syndrome.Semantic proximity Read ↗

C-terminal HERG (LQT2) mutations disrupt IKr channel regulation through 14-3-3epsilon.Semantic proximity Read ↗

KCNE1 enhances phosphatidylinositol 4,5-bisphosphate (PIP2) sensitivity of IKs to modulate channel activity.Semantic proximity Read ↗

Impaired IKs channel activation by Ca(2+)-dependent PKC shows correlation with emotion/arousal-triggered events in LQT1.Semantic proximity Read ↗

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

Long QT2 mutation on the Kv11.1 ion channel inhibits current activity by ablating a protein kinase Cα consensus site.Semantic proximity Read ↗

Impaired KCNQ1-KCNE1 and phosphatidylinositol-4,5-bisphosphate interaction underlies the long QT syndrome.Semantic proximity Read ↗

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

Molecular analysis of PIP2 regulation of HERG and IKr.Semantic proximity Read ↗

Phosphorylation of protein kinase C sites in NBD1 and the R domain control CFTR channel activation by PKA.Semantic proximity Read ↗

A hERG mutation E1039X produced a synergistic lesion on IKs together with KCNQ1-R174C mutation in a LQTS family with three compound mutations.Semantic proximity Read ↗

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