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| pubmed-article:20421522 | lifeskim:mentions | umls-concept:C1449799 | lld:lifeskim |
| pubmed-article:20421522 | pubmed:issue | 18 | lld:pubmed |
| pubmed-article:20421522 | pubmed:dateCreated | 2010-5-11 | lld:pubmed |
| pubmed-article:20421522 | pubmed:abstractText | Members of the tumor necrosis factor superfamily, such as tumor necrosis factor-alpha, potently promote atherogenesis in mice and humans. Tumor necrosis factor receptor-associated factors (TRAFs) are cytoplasmic adaptor proteins for this group of cytokines. | lld:pubmed |
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| pubmed-article:20421522 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:20421522 | pubmed:month | May | lld:pubmed |
| pubmed-article:20421522 | pubmed:issn | 1524-4539 | lld:pubmed |
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| pubmed-article:20421522 | pubmed:issnType | Electronic | lld:pubmed |
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| pubmed-article:20421522 | pubmed:year | 2010 | lld:pubmed |
| pubmed-article:20421522 | pubmed:articleTitle | Tumor necrosis factor receptor-associated factor 1 (TRAF1) deficiency attenuates atherosclerosis in mice by impairing monocyte recruitment to the vessel wall. | lld:pubmed |
| pubmed-article:20421522 | pubmed:affiliation | Department of Cardiology, University of Freiburg, Germany. | lld:pubmed |
| pubmed-article:20421522 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:20421522 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
| pubmed-article:20421522 | pubmed:publicationType | Research Support, N.I.H., Extramural | lld:pubmed |
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