pubmed-article:14678266 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:14678266 | lifeskim:mentions | umls-concept:C0035820 | lld:lifeskim |
pubmed-article:14678266 | lifeskim:mentions | umls-concept:C0079904 | lld:lifeskim |
pubmed-article:14678266 | lifeskim:mentions | umls-concept:C0021467 | lld:lifeskim |
pubmed-article:14678266 | lifeskim:mentions | umls-concept:C0441655 | lld:lifeskim |
pubmed-article:14678266 | lifeskim:mentions | umls-concept:C1521991 | lld:lifeskim |
pubmed-article:14678266 | lifeskim:mentions | umls-concept:C1539081 | lld:lifeskim |
pubmed-article:14678266 | lifeskim:mentions | umls-concept:C1705525 | lld:lifeskim |
pubmed-article:14678266 | lifeskim:mentions | umls-concept:C1417708 | lld:lifeskim |
pubmed-article:14678266 | lifeskim:mentions | umls-concept:C1423613 | lld:lifeskim |
pubmed-article:14678266 | lifeskim:mentions | umls-concept:C0021469 | lld:lifeskim |
pubmed-article:14678266 | lifeskim:mentions | umls-concept:C0441712 | lld:lifeskim |
pubmed-article:14678266 | lifeskim:mentions | umls-concept:C0429403 | lld:lifeskim |
pubmed-article:14678266 | pubmed:issue | 1 | lld:pubmed |
pubmed-article:14678266 | pubmed:dateCreated | 2003-12-17 | lld:pubmed |
pubmed-article:14678266 | pubmed:abstractText | Nuclear factor kappa B (NF-kappaB) is a transcription factor pivotal for the development of inflammation. A dysregulation of NF-kappaB has been shown to play an important role in many chronic inflammatory diseases including rheumatoid arthritis, inflammatory bowel disease and psoriasis. Although classical NF-kappaB, a heterodimer composed of the p50 and p65 subunits, has been well studied, little is known about gene regulation by other hetero- and homodimeric forms of NF-kappaB. While p65 possesses a transactivation domain, p50 does not. Indeed, p50/p50 homodimers have been shown to inhibit transcriptional activity. We have recently shown that Interleukin-10 exerts its anti-inflammatory activity in part through the inhibition of NF-kappaB by blocking IkappaB kinase activity and by inhibiting NF-kappaB already found in the nucleus. Since the inhibition of nuclear NF-kappaB could not be explained by an increase of nuclear IkappaB, we sought to further investigate the mechanisms involved in the inhibition of NF-kappaB by IL-10. We show here that IL-10 selectively induced nuclear translocation and DNA-binding of p50/p50 homodimers in human monocytic cells. TNF-alpha treatment led to a strong translocation of p65 and p50, whereas pretreatment with IL-10 followed by TNF-alpha blocked p65 translocation but did not alter the strong translocation of p50. Furthermore, macrophages of p105/p50-deficient mice exhibited a significantly decreased constitutive production of MIP-2alpha and IL-6 in comparison to wild type controls. Surprisingly, IL-10 inhibited high constitutive levels of these cytokines in wt macrophages but not in p105/p50 deficient cells. Our findings suggest that the selective induction of nuclear translocation and DNA-binding of the repressive p50/p50 homodimer is an important anti-inflammatory mechanism utilized by IL-10 to repress inflammatory gene transcription. | lld:pubmed |
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pubmed-article:14678266 | pubmed:language | eng | lld:pubmed |
pubmed-article:14678266 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:14678266 | pubmed:citationSubset | IM | lld:pubmed |
pubmed-article:14678266 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:14678266 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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pubmed-article:14678266 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:14678266 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:14678266 | pubmed:month | Jan | lld:pubmed |
pubmed-article:14678266 | pubmed:issn | 0009-9104 | lld:pubmed |
pubmed-article:14678266 | pubmed:author | pubmed-author:SabbaFF | lld:pubmed |
pubmed-article:14678266 | pubmed:author | pubmed-author:VenstromKK | lld:pubmed |
pubmed-article:14678266 | pubmed:author | pubmed-author:AsadullahKK | lld:pubmed |
pubmed-article:14678266 | pubmed:author | pubmed-author:SchotteliusA... | lld:pubmed |
pubmed-article:14678266 | pubmed:author | pubmed-author:DriesslerFF | lld:pubmed |
pubmed-article:14678266 | pubmed:issnType | Print | lld:pubmed |
pubmed-article:14678266 | pubmed:volume | 135 | lld:pubmed |
pubmed-article:14678266 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:14678266 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:14678266 | pubmed:pagination | 64-73 | lld:pubmed |
pubmed-article:14678266 | pubmed:dateRevised | 2009-11-18 | lld:pubmed |
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pubmed-article:14678266 | pubmed:year | 2004 | lld:pubmed |