pubmed-article:2206531 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:2206531 | lifeskim:mentions | umls-concept:C0542341 | lld:lifeskim |
pubmed-article:2206531 | lifeskim:mentions | umls-concept:C1442161 | lld:lifeskim |
pubmed-article:2206531 | lifeskim:mentions | umls-concept:C0439799 | lld:lifeskim |
pubmed-article:2206531 | lifeskim:mentions | umls-concept:C1515926 | lld:lifeskim |
pubmed-article:2206531 | pubmed:issue | 4 | lld:pubmed |
pubmed-article:2206531 | pubmed:dateCreated | 1990-11-21 | lld:pubmed |
pubmed-article:2206531 | pubmed:abstractText | Voltage-dependent ion channels are thought to consist of a highly conserved repeated core of six transmembrane segments, flanked by more variable cytoplasmic domains. Significant functional differences exist among related types of K+ channels. These differences have been attributed to the variable domains, most prominently the N- and C-termini. We have therefore investigated the functional importance of both termini for the delayed rectifier K+ channel from rat brain encoded by the drk1 gene. This channel has an unusually long C-terminus. Deletions in either terminus affected both activation and inactivation, in some cases profoundly. Unexpectedly, more extensive deletions in both termini restored gating. We could therefore define a core region only slightly longer than the six transmembrane segments that is sufficient for the formation of channels with the kinetics of a delayed rectifier. | lld:pubmed |
pubmed-article:2206531 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:2206531 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:2206531 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:2206531 | pubmed:language | eng | lld:pubmed |
pubmed-article:2206531 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:2206531 | pubmed:citationSubset | IM | lld:pubmed |
pubmed-article:2206531 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:2206531 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:2206531 | pubmed:month | Oct | lld:pubmed |
pubmed-article:2206531 | pubmed:issn | 0896-6273 | lld:pubmed |
pubmed-article:2206531 | pubmed:author | pubmed-author:BrownA MAM | lld:pubmed |
pubmed-article:2206531 | pubmed:author | pubmed-author:JohoR HRH | lld:pubmed |
pubmed-article:2206531 | pubmed:author | pubmed-author:DreweJ AJA | lld:pubmed |
pubmed-article:2206531 | pubmed:author | pubmed-author:VanDongenA... | lld:pubmed |
pubmed-article:2206531 | pubmed:author | pubmed-author:FrechG CGC | lld:pubmed |
pubmed-article:2206531 | pubmed:issnType | Print | lld:pubmed |
pubmed-article:2206531 | pubmed:volume | 5 | lld:pubmed |
pubmed-article:2206531 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:2206531 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:2206531 | pubmed:pagination | 433-43 | lld:pubmed |
pubmed-article:2206531 | pubmed:dateRevised | 2007-11-14 | lld:pubmed |
pubmed-article:2206531 | pubmed:meshHeading | pubmed-meshheading:2206531-... | lld:pubmed |
pubmed-article:2206531 | pubmed:meshHeading | pubmed-meshheading:2206531-... | lld:pubmed |
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pubmed-article:2206531 | pubmed:meshHeading | pubmed-meshheading:2206531-... | lld:pubmed |
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pubmed-article:2206531 | pubmed:meshHeading | pubmed-meshheading:2206531-... | lld:pubmed |
pubmed-article:2206531 | pubmed:year | 1990 | lld:pubmed |
pubmed-article:2206531 | pubmed:articleTitle | Alteration and restoration of K+ channel function by deletions at the N- and C-termini. | lld:pubmed |
pubmed-article:2206531 | pubmed:affiliation | Department of Molecular Physiology and Biophysics, Baylor College of Medicine, Houston, Texas 77030. | lld:pubmed |
pubmed-article:2206531 | pubmed:publicationType | Journal Article | lld:pubmed |
pubmed-article:2206531 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
pubmed-article:2206531 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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