| pubmed-article:19592641 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:19592641 | lifeskim:mentions | umls-concept:C1335877 | lld:lifeskim |
| pubmed-article:19592641 | lifeskim:mentions | umls-concept:C0031715 | lld:lifeskim |
| pubmed-article:19592641 | lifeskim:mentions | umls-concept:C0546816 | lld:lifeskim |
| pubmed-article:19592641 | lifeskim:mentions | umls-concept:C2003941 | lld:lifeskim |
| pubmed-article:19592641 | lifeskim:mentions | umls-concept:C1524075 | lld:lifeskim |
| pubmed-article:19592641 | lifeskim:mentions | umls-concept:C1149207 | lld:lifeskim |
| pubmed-article:19592641 | lifeskim:mentions | umls-concept:C1882417 | lld:lifeskim |
| pubmed-article:19592641 | lifeskim:mentions | umls-concept:C0851285 | lld:lifeskim |
| pubmed-article:19592641 | lifeskim:mentions | umls-concept:C0337112 | lld:lifeskim |
| pubmed-article:19592641 | pubmed:issue | 3 | lld:pubmed |
| pubmed-article:19592641 | pubmed:dateCreated | 2009-7-21 | lld:pubmed |
| pubmed-article:19592641 | pubmed:abstractText | Several commonly occurring polymorphisms in the IL-4R(alpha) have been associated with atopy in humans; the Q576R and the S503P polymorphisms reside in the cytoplasmic domain, whereas the I50 to V50 polymorphism resides in the extracellular domain of the IL-4R(alpha). The effects of these polymorphisms on signaling remain controversial. To determine the effect of the polymorphisms on IL-4 signaling in human cells, we stably transfected the human monocytic cell line U937 with murine IL-4R(alpha) cDNA bearing the I or V at position 50 and the P503/R576 double mutant. Each form of the murine IL-4R(alpha) mediated tyrosine phosphorylation of STAT6 in response to murine IL-4 treatment similar to the induction of tyrosine phosphorylation by human IL-4 signaling through the endogenous human IL-4R(alpha). After IL-4 removal, tyrosine-phosphorylated STAT6 rapidly decayed in cells expressing I50 or P503R576 murine IL-4Ralpha. In contrast, STAT6 remained significantly phosphorylated for several hours after murine IL-4 withdrawal in cells expressing the V50 polymorphism. This persistence in tyrosine-phosphorylated STAT6 was associated with persistence in CIS mRNA expression. Blocking IL-4 signaling during the decay phase using the JAK inhibitor AG490 or the anti-IL-4R(alpha) Ab M1 abrogated the persistence of phosphorylated STAT6 observed in the V50-IL-4R(alpha)-expressing cells. These results indicate that the V50 polymorphism promotes sustained STAT6 phosphorylation and that this process is mediated by continued engagement of IL-4R(alpha), suggesting enhanced responses of V50 IL-4R when IL-4 is limiting. | lld:pubmed |
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| pubmed-article:19592641 | pubmed:language | eng | lld:pubmed |
| pubmed-article:19592641 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:19592641 | pubmed:citationSubset | AIM | lld:pubmed |
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| pubmed-article:19592641 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:19592641 | pubmed:month | Aug | lld:pubmed |
| pubmed-article:19592641 | pubmed:issn | 1550-6606 | lld:pubmed |
| pubmed-article:19592641 | pubmed:author | pubmed-author:KeeganAchsah... | lld:pubmed |
| pubmed-article:19592641 | pubmed:author | pubmed-author:BoothbyMark... | lld:pubmed |
| pubmed-article:19592641 | pubmed:author | pubmed-author:StephensonLin... | lld:pubmed |
| pubmed-article:19592641 | pubmed:author | pubmed-author:HellerNicola... | lld:pubmed |
| pubmed-article:19592641 | pubmed:author | pubmed-author:FordAndrew... | lld:pubmed |
| pubmed-article:19592641 | pubmed:issnType | Electronic | lld:pubmed |
| pubmed-article:19592641 | pubmed:day | 1 | lld:pubmed |
| pubmed-article:19592641 | pubmed:volume | 183 | lld:pubmed |
| pubmed-article:19592641 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:19592641 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:19592641 | pubmed:pagination | 1607-16 | lld:pubmed |
| pubmed-article:19592641 | pubmed:dateRevised | 2011-9-26 | lld:pubmed |
| pubmed-article:19592641 | pubmed:meshHeading | pubmed-meshheading:19592641... | lld:pubmed |
| pubmed-article:19592641 | pubmed:meshHeading | pubmed-meshheading:19592641... | lld:pubmed |
| pubmed-article:19592641 | pubmed:meshHeading | pubmed-meshheading:19592641... | lld:pubmed |
| pubmed-article:19592641 | pubmed:meshHeading | pubmed-meshheading:19592641... | lld:pubmed |
| pubmed-article:19592641 | pubmed:meshHeading | pubmed-meshheading:19592641... | lld:pubmed |
| pubmed-article:19592641 | pubmed:meshHeading | pubmed-meshheading:19592641... | lld:pubmed |
| pubmed-article:19592641 | pubmed:meshHeading | pubmed-meshheading:19592641... | lld:pubmed |
| pubmed-article:19592641 | pubmed:meshHeading | pubmed-meshheading:19592641... | lld:pubmed |
| pubmed-article:19592641 | pubmed:meshHeading | pubmed-meshheading:19592641... | lld:pubmed |
| pubmed-article:19592641 | pubmed:meshHeading | pubmed-meshheading:19592641... | lld:pubmed |
| pubmed-article:19592641 | pubmed:year | 2009 | lld:pubmed |
| pubmed-article:19592641 | pubmed:articleTitle | An atopy-associated polymorphism in the ectodomain of the IL-4R(alpha) chain (V50) regulates the persistence of STAT6 phosphorylation. | lld:pubmed |
