pubmed-article:19917682 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:19917682 | lifeskim:mentions | umls-concept:C0024501 | lld:lifeskim |
pubmed-article:19917682 | lifeskim:mentions | umls-concept:C0011306 | lld:lifeskim |
pubmed-article:19917682 | lifeskim:mentions | umls-concept:C0024518 | lld:lifeskim |
pubmed-article:19917682 | lifeskim:mentions | umls-concept:C1306235 | lld:lifeskim |
pubmed-article:19917682 | lifeskim:mentions | umls-concept:C1519751 | lld:lifeskim |
pubmed-article:19917682 | lifeskim:mentions | umls-concept:C0152060 | lld:lifeskim |
pubmed-article:19917682 | lifeskim:mentions | umls-concept:C0439858 | lld:lifeskim |
pubmed-article:19917682 | lifeskim:mentions | umls-concept:C1514873 | lld:lifeskim |
pubmed-article:19917682 | lifeskim:mentions | umls-concept:C0205154 | lld:lifeskim |
pubmed-article:19917682 | pubmed:issue | 11 | lld:pubmed |
pubmed-article:19917682 | pubmed:dateCreated | 2009-11-20 | lld:pubmed |
pubmed-article:19917682 | pubmed:abstractText | MARCH-I (membrane-associated RING-CH I) has been suggested as a physiological E3 ubiquitin ligase for both MHC class II (MHC II) and B7-2. In this study, we show that MARCH-I-mediated MHC II ubiquitination is necessary for the maintenance of conventional dendritic cell (cDC) functions in the steady state. MARCH-I-deficient cDCs accumulated MHC II and B7-2 and exhibited low Ag-presenting ability for exogenous Ags and low cytokine-producing ability upon stimulation in vivo. Importantly, MHC II, but not B7-2, was required for impaired cDC function induced by loss of MARCH-I in vivo. Moreover, MHC II knockin mice whose MHC II was not ubiquitinated showed dysfunction of cDC similar to that of MARCH-I knockout mice. These results suggest that the accumulation of MHC II resulting from loss of ubiquitination caused cDC abnormality; therefore, MARCH-I may function as a housekeeper of cDC in the steady state. | lld:pubmed |
pubmed-article:19917682 | pubmed:language | eng | lld:pubmed |
pubmed-article:19917682 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:19917682 | pubmed:citationSubset | AIM | lld:pubmed |
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pubmed-article:19917682 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:19917682 | pubmed:month | Dec | lld:pubmed |
pubmed-article:19917682 | pubmed:issn | 1550-6606 | lld:pubmed |
pubmed-article:19917682 | pubmed:author | pubmed-author:AbéHH | lld:pubmed |
pubmed-article:19917682 | pubmed:author | pubmed-author:OharaOsamuO | lld:pubmed |
pubmed-article:19917682 | pubmed:author | pubmed-author:NakayamaManab... | lld:pubmed |
pubmed-article:19917682 | pubmed:author | pubmed-author:IshidoSatoshi... | lld:pubmed |
pubmed-article:19917682 | pubmed:author | pubmed-author:Ohmura-Hoshin... | lld:pubmed |
pubmed-article:19917682 | pubmed:author | pubmed-author:MatsukiYoheiY | lld:pubmed |
pubmed-article:19917682 | pubmed:author | pubmed-author:Mito-YoshidaM... | lld:pubmed |
pubmed-article:19917682 | pubmed:author | pubmed-author:Aoki-Kawasumi... | lld:pubmed |
pubmed-article:19917682 | pubmed:issnType | Electronic | lld:pubmed |
pubmed-article:19917682 | pubmed:day | 1 | lld:pubmed |
pubmed-article:19917682 | pubmed:volume | 183 | lld:pubmed |
pubmed-article:19917682 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:19917682 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:19917682 | pubmed:pagination | 6893-7 | lld:pubmed |
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pubmed-article:19917682 | pubmed:year | 2009 | lld:pubmed |
pubmed-article:19917682 | pubmed:articleTitle | Cutting edge: requirement of MARCH-I-mediated MHC II ubiquitination for the maintenance of conventional dendritic cells. | lld:pubmed |
pubmed-article:19917682 | pubmed:affiliation | Laboratory for Infectious Immunity, RIKENResearch Center for Allergy and Immunology, Tsurumi-ku, Yokohama, Kanagawa, Japan. | lld:pubmed |
pubmed-article:19917682 | pubmed:publicationType | Journal Article | lld:pubmed |
pubmed-article:19917682 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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