| pubmed-article:21421849 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:21421849 | lifeskim:mentions | umls-concept:C0036536 | lld:lifeskim |
| pubmed-article:21421849 | lifeskim:mentions | umls-concept:C0036537 | lld:lifeskim |
| pubmed-article:21421849 | lifeskim:mentions | umls-concept:C0024432 | lld:lifeskim |
| pubmed-article:21421849 | lifeskim:mentions | umls-concept:C0021755 | lld:lifeskim |
| pubmed-article:21421849 | lifeskim:mentions | umls-concept:C1515877 | lld:lifeskim |
| pubmed-article:21421849 | lifeskim:mentions | umls-concept:C0205263 | lld:lifeskim |
| pubmed-article:21421849 | lifeskim:mentions | umls-concept:C0439799 | lld:lifeskim |
| pubmed-article:21421849 | lifeskim:mentions | umls-concept:C1879547 | lld:lifeskim |
| pubmed-article:21421849 | lifeskim:mentions | umls-concept:C0964849 | lld:lifeskim |
| pubmed-article:21421849 | pubmed:issue | 9 | lld:pubmed |
| pubmed-article:21421849 | pubmed:dateCreated | 2011-4-20 | lld:pubmed |
| pubmed-article:21421849 | pubmed:abstractText | Anthrax lethal toxin (LeTx) is a virulence factor of Bacilillus anthracis that is a bivalent toxin, containing lethal factor (LF) and protective Ag proteins, which causes cytotoxicity and altered macrophage function. LeTx exposure results in early K(+) efflux from macrophages associated with caspase-1 activation and increased IL-1? release. The mechanism of this toxin-induced K(+) efflux is unknown. The goals of the current study were to determine whether LeTx-induced K(+) efflux from macrophages is mediated by toxin effects on specific K(+) channels and whether altered K(+)-channel activity is involved in LeTx-induced IL-1? release. Exposure of macrophages to LeTx induced a significant increase in the activities of two types of K(+) channels that have been identified in mouse macrophages: Ba(2+)-sensitive inwardly rectifying K(+) (Kir) channels and 4-aminopyridine-sensitive outwardly rectifying voltage-gated K(+) (Kv) channels. LeTx enhancement of both Kir and Kv required the proteolytic activity of LF, because exposure of macrophages to a mutant LF-protein (LF(E687C)) combined with protective Ag protein had no effect on the currents. Furthermore, blocking Kir and Kv channels significantly decreased LeTx-induced release of IL-1?. In addition, retroviral transduction of macrophages with wild-type Kir enhanced LeTx-induced release of IL-1?, whereas transduction of dominant-negative Kir blocked LeTx-induced release of IL-1?. Activation of caspase-1 was not required for LeTx-induced activation of either of the K(+) channels. These data indicate that a major mechanism through which LeTx stimulates macrophages to release IL-1? involves an LF-protease effect that enhances Kir and Kv channel function during toxin stimulation. | lld:pubmed |
| pubmed-article:21421849 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:21421849 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:21421849 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:21421849 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:21421849 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:21421849 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:21421849 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:21421849 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:21421849 | pubmed:language | eng | lld:pubmed |
| pubmed-article:21421849 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:21421849 | pubmed:citationSubset | AIM | lld:pubmed |
| pubmed-article:21421849 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:21421849 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:21421849 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:21421849 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:21421849 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:21421849 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:21421849 | pubmed:month | May | lld:pubmed |
| pubmed-article:21421849 | pubmed:issn | 1550-6606 | lld:pubmed |
| pubmed-article:21421849 | pubmed:author | pubmed-author:NattelStanley... | lld:pubmed |
| pubmed-article:21421849 | pubmed:author | pubmed-author:CookJames LJL | lld:pubmed |
| pubmed-article:21421849 | pubmed:author | pubmed-author:LevitanIrenaI | lld:pubmed |
| pubmed-article:21421849 | pubmed:author | pubmed-author:ChristmanJohn... | lld:pubmed |
| pubmed-article:21421849 | pubmed:author | pubmed-author:JohnsonThomas... | lld:pubmed |
| pubmed-article:21421849 | pubmed:author | pubmed-author:ChopraArunA | lld:pubmed |
| pubmed-article:21421849 | pubmed:author | pubmed-author:GhassemiMahmo... | lld:pubmed |
| pubmed-article:21421849 | pubmed:author | pubmed-author:EpshteinYulia... | lld:pubmed |
| pubmed-article:21421849 | pubmed:author | pubmed-author:OrdogBalazsB | lld:pubmed |
| pubmed-article:21421849 | pubmed:issnType | Electronic | lld:pubmed |
| pubmed-article:21421849 | pubmed:day | 1 | lld:pubmed |
| pubmed-article:21421849 | pubmed:volume | 186 | lld:pubmed |
| pubmed-article:21421849 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:21421849 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:21421849 | pubmed:pagination | 5236-43 | lld:pubmed |
| pubmed-article:21421849 | pubmed:meshHeading | pubmed-meshheading:21421849... | lld:pubmed |
| pubmed-article:21421849 | pubmed:meshHeading | pubmed-meshheading:21421849... | lld:pubmed |
| pubmed-article:21421849 | pubmed:meshHeading | pubmed-meshheading:21421849... | lld:pubmed |
| pubmed-article:21421849 | pubmed:meshHeading | pubmed-meshheading:21421849... | lld:pubmed |
| pubmed-article:21421849 | pubmed:meshHeading | pubmed-meshheading:21421849... | lld:pubmed |
| pubmed-article:21421849 | pubmed:meshHeading | pubmed-meshheading:21421849... | lld:pubmed |
| pubmed-article:21421849 | pubmed:meshHeading | pubmed-meshheading:21421849... | lld:pubmed |
| pubmed-article:21421849 | pubmed:meshHeading | pubmed-meshheading:21421849... | lld:pubmed |
| pubmed-article:21421849 | pubmed:meshHeading | pubmed-meshheading:21421849... | lld:pubmed |
| pubmed-article:21421849 | pubmed:meshHeading | pubmed-meshheading:21421849... | lld:pubmed |
| pubmed-article:21421849 | pubmed:year | 2011 | lld:pubmed |
| pubmed-article:21421849 | pubmed:articleTitle | Anthrax lethal factor activates K(+) channels to induce IL-1? secretion in macrophages. | lld:pubmed |
| pubmed-article:21421849 | pubmed:affiliation | Section of Pulmonary, Critical Care, Sleep and Allergy, Department of Medicine, University of Illinois at Chicago, Chicago, IL 60612, USA. | lld:pubmed |
| pubmed-article:21421849 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:21421849 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
| pubmed-article:21421849 | pubmed:publicationType | Research Support, N.I.H., Extramural | lld:pubmed |
