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J Physiol
2011 Aug 01;589Pt 15:3709-20. doi: 10.1113/jphysiol.2011.210666.
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Alternative splicing determines mRNA translation initiation and function of human K(2P)10.1 K+ channels.
Staudacher K
,
Baldea I
,
Kisselbach J
,
Staudacher I
,
Rahm AK
,
Schweizer PA
,
Becker R
,
Katus HA
,
Thomas D
.
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Potassium-selective ion channels regulate cardiac and neuronal excitability by stabilizing the resting membrane potential and by modulating shape and frequency of action potentials. The delicate control of membrane voltage requires structural and functional diversity of K+ channel subunits expressed in a given cell. Here we reveal a previously unrecognized biological mechanism. Tissue-specific mRNA splicing regulates alternative translation initiation (ATI) of human K(2P)10.1 K+ background channels via recombination of 5 nucleotide motifs. ATI-dependent expression of full-length protein or truncated subunits initiated from two downstream start codons determines macroscopic current amplitudes and biophysical properties of hK(2P)10.1 channels. The interaction between hK(2P)10.1 mRNA splicing, translation and function increases K+ channel complexity and is expected to contribute to electrophysiological plasticity of excitable cells.
Bockenhauer,
KCNK2: reversible conversion of a hippocampal potassium leak into a voltage-dependent channel.
2001, Pubmed,
Xenbase
Bockenhauer,
KCNK2: reversible conversion of a hippocampal potassium leak into a voltage-dependent channel.
2001,
Pubmed
,
Xenbase
Cai,
Alteration of protein subcellular location and domain formation by alternative translational initiation.
2006,
Pubmed
Drummond,
Reporting ethical matters in the Journal of Physiology: standards and advice.
2009,
Pubmed
Goldstein,
Potassium leak channels and the KCNK family of two-P-domain subunits.
2001,
Pubmed
Gu,
Expression pattern and functional characteristics of two novel splice variants of the two-pore-domain potassium channel TREK-2.
2002,
Pubmed
Hann,
A non-AUG translational initiation in c-myc exon 1 generates an N-terminally distinct protein whose synthesis is disrupted in Burkitt's lymphomas.
1988,
Pubmed
,
Xenbase
Honoré,
Alternative translation initiation further increases the molecular and functional diversity of ion channels.
2008,
Pubmed
Kang,
Expression of thermosensitive two-pore domain K+ channels in human keratinocytes cell line HaCaT cells.
2007,
Pubmed
Kozak,
The scanning model for translation: an update.
1989,
Pubmed
Kozak,
Initiation of translation in prokaryotes and eukaryotes.
1999,
Pubmed
Lesage,
Human TREK2, a 2P domain mechano-sensitive K+ channel with multiple regulations by polyunsaturated fatty acids, lysophospholipids, and Gs, Gi, and Gq protein-coupled receptors.
2000,
Pubmed
Lu,
Translational regulatory mechanisms generate N-terminal glucocorticoid receptor isoforms with unique transcriptional target genes.
2005,
Pubmed
Mellentin,
lyl-1, a novel gene altered by chromosomal translocation in T cell leukemia, codes for a protein with a helix-loop-helix DNA binding motif.
1989,
Pubmed
Prats,
High molecular mass forms of basic fibroblast growth factor are initiated by alternative CUG codons.
1989,
Pubmed
Rhen,
Antiinflammatory action of glucocorticoids--new mechanisms for old drugs.
2005,
Pubmed
Simkin,
Control of the single channel conductance of K2P10.1 (TREK-2) by the amino-terminus: role of alternative translation initiation.
2008,
Pubmed
Sánchez-Sánchez,
Attenuation of disease phenotype through alternative translation initiation in low-penetrance retinoblastoma.
2007,
Pubmed
Thomas,
Alternative translation initiation in rat brain yields K2P2.1 potassium channels permeable to sodium.
2008,
Pubmed
,
Xenbase
Veale,
Dominant negative effects of a non-conducting TREK1 splice variant expressed in brain.
2010,
Pubmed
Yang,
Thrilling moment of an inhibitory channel.
2008,
Pubmed
