9677360

Source:http://linkedlifedata.com/resource/pubmed/id/9677360

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Predicate	Object
rdf:type	pubmed:Citation
lifeskim:mentions	umls-concept:C0014544, umls-concept:C0017262, umls-concept:C0032824, umls-concept:C0185117, umls-concept:C0205245, umls-concept:C0332240, umls-concept:C0439660, umls-concept:C1273518, umls-concept:C2911684
pubmed:issue	31
pubmed:dateCreated	1998-9-10
pubmed:abstractText	Benign familial neonatal convulsions (BFNC), a class of idiopathic generalized epilepsy, is an autosomal dominantly inherited disorder of newborns. BFNC has been linked to mutations in two putative K+ channel genes, KCNQ2 and KCNQ3. Amino acid sequence comparison reveals that both genes share strong homology to KvLQT1, the potassium channel encoded by KCNQ1, which is responsible for over 50% of inherited long QT syndrome. Here we describe the cloning, functional expression, and characterization of K+ channels encoded by KCNQ2 and KCNQ3 cDNAs. Individually, expression of KCNQ2 or KCNQ3 in Xenopus oocytes elicits voltage-gated, rapidly activating K+-selective currents similar to KCNQ1. However, unlike KCNQ1, KCNQ2 and KCNQ3 currents are not augmented by coexpression with the KCNQ1 beta subunit, KCNE1 (minK, IsK). Northern blot analyses reveal that KCNQ2 and KCNQ3 exhibit similar expression patterns in different regions within the brain. Interestingly, coexpression of KCNQ2 and KCNQ3 results in a substantial synergistic increase in current amplitude. Coexpression of KCNE1 with the two channels strongly suppressed current amplitude and slowed kinetics of activation. The pharmacological and biophysical properties of the K+ currents observed in the coinjected oocytes differ somewhat from those observed after injecting either KCNQ2 or KCNQ3 by itself. The functional interaction between KCNQ2 and KCNQ3 provides a framework for understanding how mutations in either channel can cause a form of idiopathic generalized epilepsy.
pubmed:language	eng
pubmed:journal	http://linkedlifedata.com/resource/pubmed/journal/2985121R
pubmed:citationSubset	IM
pubmed:chemical	http://linkedlifedata.com/resource/pubmed/chemical/KCNQ Potassium Channels, http://linkedlifedata.com/resource/pubmed/chemical/KCNQ1 Potassium Channel, http://linkedlifedata.com/resource/pubmed/chemical/KCNQ1 protein, human, http://linkedlifedata.com/resource/pubmed/chemical/KCNQ2 Potassium Channel, http://linkedlifedata.com/resource/pubmed/chemical/KCNQ2 protein, human, http://linkedlifedata.com/resource/pubmed/chemical/KCNQ3 Potassium Channel, http://linkedlifedata.com/resource/pubmed/chemical/KCNQ3 protein, human, http://linkedlifedata.com/resource/pubmed/chemical/Potassium Channels, http://linkedlifedata.com/resource/pubmed/chemical/Potassium Channels, Voltage-Gated, http://linkedlifedata.com/resource/pubmed/chemical/RNA, Messenger, http://linkedlifedata.com/resource/pubmed/chemical/potassium channel protein I(sk)
pubmed:status	MEDLINE
pubmed:month	Jul
pubmed:issn	0021-9258
pubmed:author	pubmed-author:BlanarM AMA, pubmed-author:ConderM LML, pubmed-author:LevesqueP CPC, pubmed-author:LittleW AWA, pubmed-author:NeubauerM GMG, pubmed-author:RamakrishnanPP, pubmed-author:YangW PWP
pubmed:issnType	Print
pubmed:day	31
pubmed:volume	273
pubmed:owner	NLM
pubmed:authorsComplete	Y
pubmed:pagination	19419-23
pubmed:dateRevised	2006-11-15
pubmed:meshHeading	pubmed-meshheading:9677360-Animals, pubmed-meshheading:9677360-Brain, pubmed-meshheading:9677360-Cloning, Molecular, pubmed-meshheading:9677360-Electrophysiology, pubmed-meshheading:9677360-Epilepsy, Generalized, pubmed-meshheading:9677360-Gene Expression Regulation, pubmed-meshheading:9677360-Humans, pubmed-meshheading:9677360-Ion Channel Gating, pubmed-meshheading:9677360-KCNQ Potassium Channels, pubmed-meshheading:9677360-KCNQ1 Potassium Channel, pubmed-meshheading:9677360-KCNQ2 Potassium Channel, pubmed-meshheading:9677360-KCNQ3 Potassium Channel, pubmed-meshheading:9677360-Microinjections, pubmed-meshheading:9677360-Oocytes, pubmed-meshheading:9677360-Potassium Channels, pubmed-meshheading:9677360-Potassium Channels, Voltage-Gated, pubmed-meshheading:9677360-RNA, Messenger, pubmed-meshheading:9677360-Xenopus
pubmed:year	1998
pubmed:articleTitle	Functional expression of two KvLQT1-related potassium channels responsible for an inherited idiopathic epilepsy.
pubmed:affiliation	Department of Cardiovascular Drug Discovery, Bristol-Myers Squibb Pharmaceutical Research Institute, Princeton, New Jersey 08543-4000, USA.
pubmed:publicationType	Journal Article, Research Support, Non-U.S. Gov't