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Potassium voltage-gated channel, Isk-related family, member 1

KCNE1, IsK, B55
The product of this gene belongs to the potassium channel KCNE family. Potassium ion channels are essential to many cellular functions and show a high degree of diversity, varying in their electrophysiologic and pharmacologic properties. This gene encodes a transmembrane protein known to associate with the product of the KVLQT1 gene to form the delayed rectifier potassium channel. Mutation in this gene are associated with both Jervell and Lange-Nielsen and Romano-Ward forms of long-QT syndrome. Alternatively spliced transcript variants encoding the same protein have been identified. [provided by RefSeq, Jul 2008] (from NCBI)
Top mentioned proteins: KCNQ1, HERG, CAN, HAD, SCN5A
Papers on KCNE1
KCNE1 and KCNE3: The yin and yang of voltage-gated K(+) channel regulation.
Abbott, Irvine, United States. In Gene, Feb 2016
Here, we review the often opposite effects of KCNE1 and KCNE3 on Kv channel biology, with an emphasis on regulation of KCNQ1.
Spatial Regulation of Greatwall by Cdk1 and PP2A-Tws in the Cell Cycle.
Archambault et al., Montréal, Canada. In Cell Cycle, Feb 2016
UNASSIGNED: Entry into mitosis requires the phosphorylation of multiple substrates by cyclin B-Cdk1, while exit from mitosis requires their dephosphorylation, which depends largely on the phosphatase PP2A in complex with its B55 regulatory subunit (Tws in Drosophila).
Voltage-Dependent Gating: Novel Insights from KCNQ1 Channels.
Cui, Saint Louis, United States. In Biophys J, Feb 2016
These mechanisms underlie the extraordinary KCNE1 subunit modification of the KCNQ1 channel and have significant physiological implications.
The residue I257 at S4-S5 linker in KCNQ1 determines KCNQ1/KCNE1 channel sensitivity to 1-alkanols.
Yao et al., Wuhan, China. In Acta Pharmacol Sin, Jan 2016
AIM: KCNQ1 and KCNE1 form a complex in human ventricular cardiomyocytes, which are important in maintaining a normal heart rhythm.
Pitx2c increases in atrial myocytes from chronic atrial fibrillation patients enhancing IKs and decreasing ICa,L.
Caballero et al., Madrid, Spain. In Cardiovasc Res, Jan 2016
Luciferase assays demonstrated that Pitx2c increased transcriptional activity of KCNQ1 and KCNE1 genes.
MicroRNA heterogeneity in endometrial cancer cell lines revealed by deep sequencing.
Ge et al., Nanjing, China. In Oncol Lett, Dec 2015
UNASSIGNED: The aim of the present study was to obtain comprehensive microRNA (miRNA) profiles of type I [Ishikawa (ISK)] and type II (HEC-1B) human endometrial adenocarcinoma cell lines, utilizing the latest high-throughput sequencing techniques.
Regulation of SCN3B/scn3b by Interleukin 2 (IL-2): IL-2 modulates SCN3B/scn3b transcript expression and increases sodium current in myocardial cells.
Tu et al., Wuhan, China. In Bmc Cardiovasc Disord, Dec 2015
METHODS: In the present study, we observed the effect of IL-2 by qRT-PCR on the transcription of ion channel genes including SCN2A, SCN3A, SCN4A, SCN5A, SCN9A, SCN10A, SCN1B, SCN2B, SCN3B, KCNN1, KCNJ5, KCNE1, KCNE2, KCNE3, KCND3, KCNQ1, KCNA5, KCNH2 and CACNA1C.
KCNQ1 channel modulation by KCNE proteins via the voltage-sensing domain.
Kubo et al., Okazaki, Japan. In J Physiol, Jul 2015
KCNE1, for example, slows the activation kinetics of KCNQ1 by two orders of magnitude.
A PP1-PP2A phosphatase relay controls mitotic progression.
Hagan et al., Manchester, United Kingdom. In Nature, 2015
Here we describe a mitotic phosphatase relay in which PP1 reactivation is required for the reactivation of both PP2A-B55 and PP2A-B56 to coordinate mitotic progression and exit in fission yeast.
Recent molecular insights from mutated IKS channels in cardiac arrhythmia.
Attali et al., Tel Aviv-Yafo, Israel. In Curr Opin Pharmacol, 2014
Co-assembly of KCNQ1 with KCNE1 generates the IKS potassium current that is vital for the proper repolarization of the cardiac action potential.
Regulation of transport across cell membranes by the serum- and glucocorticoid-inducible kinase SGK1.
Alesutan et al., Tübingen, Germany. In Mol Membr Biol, 2014
SGK1 is a powerful stimulator of Na(+)/K(+)-ATPase, carriers (e.g., NCC, NKCC, NHE1, NHE3, SGLT1, several amino acid transporters) and ion channels (e.g., ENaC, SCN5A, TRPV4-6, ORAI1/STIM1, ROMK, KCNE1/KCNQ1, GluR6, CFTR).
Misshapen-like kinase 1 (MINK1) is a novel component of striatin-interacting phosphatase and kinase (STRIPAK) and is required for the completion of cytokinesis.
Senga et al., Nagoya, Japan. In J Biol Chem, 2012
Misshapen-like kinase 1 (MINK1) is a novel component of striatin-interacting phosphatase and kinase (STRIPAK) and is required for the completion of cytokinesis.
Regulation of KCNQ1/KCNE1 by β-catenin.
Lang et al., Tübingen, Germany. In Mol Membr Biol, 2012
KCNE1/KCNQ1 was expressed in Xenopus oocytes with and without beta-catenin. Confocal microscopy revealed that beta-catenin enhanced the KCNE1/KCNQ1 protein abundance in the cell membrane.
A large candidate gene survey identifies the KCNE1 D85N polymorphism as a possible modulator of drug-induced torsades de pointes.
Roden et al., München, Germany. In Circ Cardiovasc Genet, 2012
The KCNE1 variant rs1805128, resulting in D85N, confers substantially increased risk for drug-induced torsades de pointes.
Characterization of KCNQ1 atrial fibrillation mutations reveals distinct dependence on KCNE1.
Kass et al., New York City, United States. In J Gen Physiol, 2012
When coexpressed with KCNE1, both mutants deactivate significantly slower than wild-type KCNQ1/KCNE1 channels.
Mutations in the potassium channel subunit KCNE1 are associated with early-onset familial atrial fibrillation.
Schmitt et al., Copenhagen, Denmark. In Bmc Med Genet, 2011
Early-onset lone atrial fibrillation is associated with mutations in the potassium current channel regulatory subunit KCNE1.
Common variants at ten loci influence QT interval duration in the QTGEN Study.
Stricker et al., Boston, United States. In Nat Genet, 2009
We observed associations at P < 5 x 10(-8) with variants in NOS1AP, KCNQ1, KCNE1, KCNH2 and SCN5A, known to be involved in myocardial repolarization and mendelian long-QT syndromes.
(Patho)physiological significance of the serum- and glucocorticoid-inducible kinase isoforms.
Vallon et al., Tübingen, Germany. In Physiol Rev, 2006
SGKs activate ion channels (e.g., ENaC, TRPV5, ROMK, Kv1.3, KCNE1/KCNQ1, GluR1, GluR6), carriers (e.g., NHE3, GLUT1, SGLT1, EAAT1-5), and the Na+-K+-ATPase.
Genetic testing in the long QT syndrome: development and validation of an efficient approach to genotyping in clinical practice.
Leonardi et al., Pavia, Italy. In Jama, 2006
The entire coding regions of KCNQ1, KCNH2, SCN5A, KCNE1, and KCNE2 were screened by denaturing high-performance liquid chromatography and DNA sequencing.
KCNQ1 gain-of-function mutation in familial atrial fibrillation.
Huang et al., Shanghai, China. In Science, 2003
The KCNQ1 gene encodes the pore-forming alpha subunit of the cardiac I(Ks) channel (KCNQ1/KCNE1), the KCNQ1/KCNE2 and the KCNQ1/KCNE3 potassium channels.
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