| pubmed-article:11684073 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:11684073 | lifeskim:mentions | umls-concept:C0009015 | lld:lifeskim |
| pubmed-article:11684073 | lifeskim:mentions | umls-concept:C0032824 | lld:lifeskim |
| pubmed-article:11684073 | lifeskim:mentions | umls-concept:C0205245 | lld:lifeskim |
| pubmed-article:11684073 | lifeskim:mentions | umls-concept:C0205419 | lld:lifeskim |
| pubmed-article:11684073 | lifeskim:mentions | umls-concept:C0017262 | lld:lifeskim |
| pubmed-article:11684073 | lifeskim:mentions | umls-concept:C1516451 | lld:lifeskim |
| pubmed-article:11684073 | lifeskim:mentions | umls-concept:C1514623 | lld:lifeskim |
| pubmed-article:11684073 | lifeskim:mentions | umls-concept:C2911684 | lld:lifeskim |
| pubmed-article:11684073 | lifeskim:mentions | umls-concept:C0185117 | lld:lifeskim |
| pubmed-article:11684073 | pubmed:issue | 2 | lld:pubmed |
| pubmed-article:11684073 | pubmed:dateCreated | 2001-10-30 | lld:pubmed |
| pubmed-article:11684073 | pubmed:abstractText | The Ca(2+) independent transient outward K(+) current (I(to1)) in the heart is responsible for the initial phase of repolarization. The hKv4.3 K(+) channel alpha-subunit contributes to the I(to1) current in many regions of the human heart. Consistently, downregulation of hKv4.3 transcripts in heart failure and atrial fibrillation is linked to reduction in I(to1) conductance. The recently cloned KChIP family of calcium sensors has been shown to modulate A-type potassium channels of the Kv4 K(+) channel subfamily. | lld:pubmed |
| pubmed-article:11684073 | pubmed:language | eng | lld:pubmed |
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| pubmed-article:11684073 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:11684073 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:11684073 | pubmed:month | Nov | lld:pubmed |
| pubmed-article:11684073 | pubmed:issn | 0008-6363 | lld:pubmed |
| pubmed-article:11684073 | pubmed:author | pubmed-author:BuschA EAE | lld:pubmed |
| pubmed-article:11684073 | pubmed:author | pubmed-author:SteinmeyerKK | lld:pubmed |
| pubmed-article:11684073 | pubmed:author | pubmed-author:KaramanBB | lld:pubmed |
| pubmed-article:11684073 | pubmed:author | pubmed-author:Yüksel-ApakMM | lld:pubmed |
| pubmed-article:11684073 | pubmed:author | pubmed-author:WollnikBB | lld:pubmed |
| pubmed-article:11684073 | pubmed:author | pubmed-author:SchererC RCR | lld:pubmed |
| pubmed-article:11684073 | pubmed:author | pubmed-author:DecherNN | lld:pubmed |
| pubmed-article:11684073 | pubmed:author | pubmed-author:UygunerOO | lld:pubmed |
| pubmed-article:11684073 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:11684073 | pubmed:volume | 52 | lld:pubmed |
| pubmed-article:11684073 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:11684073 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:11684073 | pubmed:pagination | 255-64 | lld:pubmed |
| pubmed-article:11684073 | pubmed:dateRevised | 2007-11-15 | lld:pubmed |
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| pubmed-article:11684073 | pubmed:year | 2001 | lld:pubmed |
| pubmed-article:11684073 | pubmed:articleTitle | hKChIP2 is a functional modifier of hKv4.3 potassium channels: cloning and expression of a short hKChIP2 splice variant. | lld:pubmed |
| pubmed-article:11684073 | pubmed:affiliation | Aventis Pharma Deutschland GmbH, DG Cardiovascular Diseases, D-65926, Frankfurt am Main, Germany. | lld:pubmed |
| pubmed-article:11684073 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:11684073 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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