| pubmed-article:12271142 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:12271142 | lifeskim:mentions | umls-concept:C0038435 | lld:lifeskim |
| pubmed-article:12271142 | lifeskim:mentions | umls-concept:C1416578 | lld:lifeskim |
| pubmed-article:12271142 | lifeskim:mentions | umls-concept:C0392673 | lld:lifeskim |
| pubmed-article:12271142 | lifeskim:mentions | umls-concept:C1546857 | lld:lifeskim |
| pubmed-article:12271142 | lifeskim:mentions | umls-concept:C1556066 | lld:lifeskim |
| pubmed-article:12271142 | lifeskim:mentions | umls-concept:C1619636 | lld:lifeskim |
| pubmed-article:12271142 | lifeskim:mentions | umls-concept:C1514873 | lld:lifeskim |
| pubmed-article:12271142 | pubmed:issue | 20 | lld:pubmed |
| pubmed-article:12271142 | pubmed:dateCreated | 2002-10-2 | lld:pubmed |
| pubmed-article:12271142 | pubmed:abstractText | Reaction to stress requires feedback adaptation of cellular functions to secure a response without distress, but the molecular order of this process is only partially understood. Here, we report a previously unrecognized regulatory element in the general adaptation syndrome. Kir6.2, the ion-conducting subunit of the metabolically responsive ATP-sensitive potassium (K(ATP)) channel, was mandatory for optimal adaptation capacity under stress. Genetic deletion of Kir6.2 disrupted K(ATP) channel-dependent adjustment of membrane excitability and calcium handling, compromising the enhancement of cardiac performance driven by sympathetic stimulation, a key mediator of the adaptation response. In the absence of Kir6.2, vigorous sympathetic challenge caused arrhythmia and sudden death, preventable by calcium-channel blockade. Thus, this vital function identifies a physiological role for K(ATP) channels in the heart. | lld:pubmed |
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| pubmed-article:12271142 | pubmed:language | eng | lld:pubmed |
| pubmed-article:12271142 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:12271142 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:12271142 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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| pubmed-article:12271142 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:12271142 | pubmed:month | Oct | lld:pubmed |
| pubmed-article:12271142 | pubmed:issn | 0027-8424 | lld:pubmed |
| pubmed-article:12271142 | pubmed:author | pubmed-author:MikiTakashiT | lld:pubmed |
| pubmed-article:12271142 | pubmed:author | pubmed-author:Bienengraeber... | lld:pubmed |
| pubmed-article:12271142 | pubmed:author | pubmed-author:DzejaPetras... | lld:pubmed |
| pubmed-article:12271142 | pubmed:author | pubmed-author:TerzicAndreA | lld:pubmed |
| pubmed-article:12271142 | pubmed:author | pubmed-author:ZingmanLeonid... | lld:pubmed |
| pubmed-article:12271142 | pubmed:author | pubmed-author:HodgsonDenice... | lld:pubmed |
| pubmed-article:12271142 | pubmed:author | pubmed-author:AlekseevAlexe... | lld:pubmed |
| pubmed-article:12271142 | pubmed:author | pubmed-author:SeinoSusumuS | lld:pubmed |
| pubmed-article:12271142 | pubmed:author | pubmed-author:PucarDarkoD | lld:pubmed |
| pubmed-article:12271142 | pubmed:author | pubmed-author:KaneGarvan... | lld:pubmed |
| pubmed-article:12271142 | pubmed:author | pubmed-author:Perez-TerzicC... | lld:pubmed |
| pubmed-article:12271142 | pubmed:author | pubmed-author:GuminaRichard... | lld:pubmed |
| pubmed-article:12271142 | pubmed:author | pubmed-author:BastPeter HPH | lld:pubmed |
| pubmed-article:12271142 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:12271142 | pubmed:day | 1 | lld:pubmed |
| pubmed-article:12271142 | pubmed:volume | 99 | lld:pubmed |
| pubmed-article:12271142 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:12271142 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:12271142 | pubmed:pagination | 13278-83 | lld:pubmed |
| pubmed-article:12271142 | pubmed:dateRevised | 2009-11-18 | lld:pubmed |
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