pubmed-article:15770697 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:15770697 | lifeskim:mentions | umls-concept:C1457887 | lld:lifeskim |
pubmed-article:15770697 | lifeskim:mentions | umls-concept:C0026809 | lld:lifeskim |
pubmed-article:15770697 | lifeskim:mentions | umls-concept:C0022009 | lld:lifeskim |
pubmed-article:15770697 | lifeskim:mentions | umls-concept:C0014072 | lld:lifeskim |
pubmed-article:15770697 | lifeskim:mentions | umls-concept:C1416611 | lld:lifeskim |
pubmed-article:15770697 | lifeskim:mentions | umls-concept:C0332206 | lld:lifeskim |
pubmed-article:15770697 | pubmed:issue | 4 | lld:pubmed |
pubmed-article:15770697 | pubmed:dateCreated | 2005-4-5 | lld:pubmed |
pubmed-article:15770697 | pubmed:abstractText | The KCNN4 potassium-ion channel has been reported to play an important role in regulating antigen-induced T cell effector functions in vitro. This study presents the first evidence that a selective KCNN4 blocker, TRAM-34, confers protection against experimental autoimmune encephalomyelitis (EAE) in the mouse model. Treatment with the KCNN4 blocker did not prevent infiltration of T cells in the spinal cord, but resulted in the reduction of both the protein and the message levels of TNF-alpha and IFN-gamma as well as the message levels of several other pro-inflammatory molecules in the spinal cord. Plasma concentrations of TRAM-34 within a 24-h period were between the in vitro IC(50) and IC(90) values for the KCNN4 channel. The effect of TRAM-34 was reversible, as indicated by the development of clinical EAE symptoms within 48 h after withdrawal of treatment. In summary, our data support the idea that KCNN4 channels play a critical role in the immune response during the development of MOG-induced EAE in C57BL/6 mice. | lld:pubmed |
pubmed-article:15770697 | pubmed:language | eng | lld:pubmed |
pubmed-article:15770697 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:15770697 | pubmed:citationSubset | IM | lld:pubmed |
pubmed-article:15770697 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:15770697 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:15770697 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:15770697 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:15770697 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:15770697 | pubmed:month | Apr | lld:pubmed |
pubmed-article:15770697 | pubmed:issn | 0014-2980 | lld:pubmed |
pubmed-article:15770697 | pubmed:author | pubmed-author:NomeirAmin... | lld:pubmed |
pubmed-article:15770697 | pubmed:author | pubmed-author:VassilevaGaly... | lld:pubmed |
pubmed-article:15770697 | pubmed:author | pubmed-author:KozlowskiJose... | lld:pubmed |
pubmed-article:15770697 | pubmed:author | pubmed-author:YangLilyL | lld:pubmed |
pubmed-article:15770697 | pubmed:author | pubmed-author:ChuInhouI | lld:pubmed |
pubmed-article:15770697 | pubmed:author | pubmed-author:CuiLongL | lld:pubmed |
pubmed-article:15770697 | pubmed:author | pubmed-author:ChouChuan-Chu... | lld:pubmed |
pubmed-article:15770697 | pubmed:author | pubmed-author:Pugliese-Sivo... | lld:pubmed |
pubmed-article:15770697 | pubmed:author | pubmed-author:PetroMaryM | lld:pubmed |
pubmed-article:15770697 | pubmed:author | pubmed-author:ZavodnyPaul... | lld:pubmed |
pubmed-article:15770697 | pubmed:author | pubmed-author:NarulaSatwant... | lld:pubmed |
pubmed-article:15770697 | pubmed:author | pubmed-author:ZhangLi-KangL... | lld:pubmed |
pubmed-article:15770697 | pubmed:author | pubmed-author:XianLiangL | lld:pubmed |
pubmed-article:15770697 | pubmed:author | pubmed-author:GolovkoAndrei... | lld:pubmed |
pubmed-article:15770697 | pubmed:author | pubmed-author:ReichEva-PiaE... | lld:pubmed |
pubmed-article:15770697 | pubmed:issnType | Print | lld:pubmed |
pubmed-article:15770697 | pubmed:volume | 35 | lld:pubmed |
pubmed-article:15770697 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:15770697 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:15770697 | pubmed:pagination | 1027-36 | lld:pubmed |
pubmed-article:15770697 | pubmed:dateRevised | 2005-11-17 | lld:pubmed |
pubmed-article:15770697 | pubmed:meshHeading | pubmed-meshheading:15770697... | lld:pubmed |
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pubmed-article:15770697 | pubmed:meshHeading | pubmed-meshheading:15770697... | lld:pubmed |
pubmed-article:15770697 | pubmed:meshHeading | pubmed-meshheading:15770697... | lld:pubmed |
pubmed-article:15770697 | pubmed:meshHeading | pubmed-meshheading:15770697... | lld:pubmed |
pubmed-article:15770697 | pubmed:meshHeading | pubmed-meshheading:15770697... | lld:pubmed |
pubmed-article:15770697 | pubmed:year | 2005 | lld:pubmed |
pubmed-article:15770697 | pubmed:articleTitle | Blocking ion channel KCNN4 alleviates the symptoms of experimental autoimmune encephalomyelitis in mice. | lld:pubmed |
pubmed-article:15770697 | pubmed:affiliation | Schering-Plough Research Institute, Kenilworth, New Jersey 07033, USA. | lld:pubmed |
pubmed-article:15770697 | pubmed:publicationType | Journal Article | lld:pubmed |
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