| pubmed-article:9058603 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:9058603 | lifeskim:mentions | umls-concept:C0005100 | lld:lifeskim |
| pubmed-article:9058603 | lifeskim:mentions | umls-concept:C0070570 | lld:lifeskim |
| pubmed-article:9058603 | lifeskim:mentions | umls-concept:C0021467 | lld:lifeskim |
| pubmed-article:9058603 | lifeskim:mentions | umls-concept:C0048212 | lld:lifeskim |
| pubmed-article:9058603 | lifeskim:mentions | umls-concept:C0021469 | lld:lifeskim |
| pubmed-article:9058603 | lifeskim:mentions | umls-concept:C0439799 | lld:lifeskim |
| pubmed-article:9058603 | pubmed:issue | 3 | lld:pubmed |
| pubmed-article:9058603 | pubmed:dateCreated | 1997-3-28 | lld:pubmed |
| pubmed-article:9058603 | pubmed:abstractText | Phenol has various medical applications but can cause convulsions and cardiac arrhythmia suggestive of K+ channel block. We examined phenol inhibition of the delayed-rectifier RCK1 (Kv1.1) K+ channel cloned from rat brain and expressed in Xenopus laevis oocytes. Phenol (2.5 mM) caused a 43 +/- 5 mV depolarizing shift in the RCK1 half-activation voltage (Vg) but only a 10 +/- 3% decrease in the peak conductance at 80 mV. The 10-90% rise time was slightly increased, but this was not simply the result of the activation shift. By contrast, deactivation kinetics at -40 mV were greatly accelerated. The importance of the phenolic hydroxyl group was assessed by comparing the effects of p-cresol (a phenol) and its structural isomer benzyl alcohol (an aryl alcohol). p-Cresol (1.5 mM) produced a 53 +/- 2 mV depolarizing shift in Vg, but benzyl alcohol was much less effective--20 mM caused a depolarizing shift of only 23 +/- 1 mV. Both isomers also accelerated channel deactivation. Phenol and p-cresol are better hydrogen bond donors than acceptors, whereas benzyl alcohol is a better acceptor than donor. A hydrogen bond between the phenolic hydroxyl and a presently unknown acceptor group may therefore underlie some aspects of K+ channel inhibition. Depolarizing shifts in Vg and accelerated tail kinetics are consistent with 1) preferential phenol binding to resting channels, causing the shift in Vg, and 2) a conducting phenol-bound open state with faster deactivation kinetics than the unbound open state. | lld:pubmed |
| pubmed-article:9058603 | pubmed:language | eng | lld:pubmed |
| pubmed-article:9058603 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:9058603 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:9058603 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:9058603 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:9058603 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:9058603 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:9058603 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:9058603 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:9058603 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:9058603 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:9058603 | pubmed:month | Mar | lld:pubmed |
| pubmed-article:9058603 | pubmed:issn | 0026-895X | lld:pubmed |
| pubmed-article:9058603 | pubmed:author | pubmed-author:ElliottJ RJR | lld:pubmed |
| pubmed-article:9058603 | pubmed:author | pubmed-author:ElliottA AAA | lld:pubmed |
| pubmed-article:9058603 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:9058603 | pubmed:volume | 51 | lld:pubmed |
| pubmed-article:9058603 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:9058603 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:9058603 | pubmed:pagination | 475-83 | lld:pubmed |
| pubmed-article:9058603 | pubmed:dateRevised | 2006-11-15 | lld:pubmed |
| pubmed-article:9058603 | pubmed:meshHeading | pubmed-meshheading:9058603-... | lld:pubmed |
| pubmed-article:9058603 | pubmed:meshHeading | pubmed-meshheading:9058603-... | lld:pubmed |
| pubmed-article:9058603 | pubmed:meshHeading | pubmed-meshheading:9058603-... | lld:pubmed |
| pubmed-article:9058603 | pubmed:meshHeading | pubmed-meshheading:9058603-... | lld:pubmed |
| pubmed-article:9058603 | pubmed:meshHeading | pubmed-meshheading:9058603-... | lld:pubmed |
| pubmed-article:9058603 | pubmed:meshHeading | pubmed-meshheading:9058603-... | lld:pubmed |
| pubmed-article:9058603 | pubmed:meshHeading | pubmed-meshheading:9058603-... | lld:pubmed |
| pubmed-article:9058603 | pubmed:meshHeading | pubmed-meshheading:9058603-... | lld:pubmed |
| pubmed-article:9058603 | pubmed:meshHeading | pubmed-meshheading:9058603-... | lld:pubmed |
| pubmed-article:9058603 | pubmed:meshHeading | pubmed-meshheading:9058603-... | lld:pubmed |
| pubmed-article:9058603 | pubmed:meshHeading | pubmed-meshheading:9058603-... | lld:pubmed |
| pubmed-article:9058603 | pubmed:meshHeading | pubmed-meshheading:9058603-... | lld:pubmed |
| pubmed-article:9058603 | pubmed:meshHeading | pubmed-meshheading:9058603-... | lld:pubmed |
| pubmed-article:9058603 | pubmed:meshHeading | pubmed-meshheading:9058603-... | lld:pubmed |
| pubmed-article:9058603 | pubmed:year | 1997 | lld:pubmed |
| pubmed-article:9058603 | pubmed:articleTitle | Voltage-dependent inhibition of RCK1 K+ channels by phenol, p-cresol, and benzyl alcohol. | lld:pubmed |
| pubmed-article:9058603 | pubmed:affiliation | Department of Anatomy and Physiology, University of Dundee, Scotland. | lld:pubmed |
| pubmed-article:9058603 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:9058603 | pubmed:publicationType | Comparative Study | lld:pubmed |
| pubmed-article:9058603 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
| http://linkedlifedata.com/r... | pubmed:referesTo | pubmed-article:9058603 | lld:pubmed |
| http://linkedlifedata.com/r... | pubmed:referesTo | pubmed-article:9058603 | lld:pubmed |
