| pubmed-article:20177146 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:20177146 | lifeskim:mentions | umls-concept:C0020731 | lld:lifeskim |
| pubmed-article:20177146 | lifeskim:mentions | umls-concept:C0229671 | lld:lifeskim |
| pubmed-article:20177146 | lifeskim:mentions | umls-concept:C0118022 | lld:lifeskim |
| pubmed-article:20177146 | lifeskim:mentions | umls-concept:C0002716 | lld:lifeskim |
| pubmed-article:20177146 | lifeskim:mentions | umls-concept:C1704259 | lld:lifeskim |
| pubmed-article:20177146 | lifeskim:mentions | umls-concept:C2754810 | lld:lifeskim |
| pubmed-article:20177146 | lifeskim:mentions | umls-concept:C1705987 | lld:lifeskim |
| pubmed-article:20177146 | lifeskim:mentions | umls-concept:C1314939 | lld:lifeskim |
| pubmed-article:20177146 | lifeskim:mentions | umls-concept:C0332324 | lld:lifeskim |
| pubmed-article:20177146 | pubmed:issue | 4 | lld:pubmed |
| pubmed-article:20177146 | pubmed:dateCreated | 2010-4-29 | lld:pubmed |
| pubmed-article:20177146 | pubmed:abstractText | Serum amyloid A (SAA) induced CCL2 production via a pertussis toxin (PTX)-insensitive pathway in human umbilical vein endothelial cells (HUVECs). SAA induced the activation of three MAPKs (ERK, p38 MAPK, and JNK), which were completely inhibited by knock-down of formyl peptide receptor 2 (FPR2). Inhibition of p38 MAPK and JNK by their specific inhibitors (SB203580 and SP600125), or inhibition by a dominant negative mutant of p38 MAPK dramatically decreased SAA-induced CCL2 production. Inactivation of G((i)) protein(s) by PTX inhibited the activation of SAA-induced ERK, but not p38 MAPK or JNK. The results indicate that SAA stimulates FPR2-mediated activation of p38 MAPK and JNK, which are independent of a PTX-sensitive G-protein and are essential for SAA-induced CCL2 production. | lld:pubmed |
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| pubmed-article:20177146 | pubmed:language | eng | lld:pubmed |
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| pubmed-article:20177146 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:20177146 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:20177146 | pubmed:month | Apr | lld:pubmed |
| pubmed-article:20177146 | pubmed:issn | 1226-3613 | lld:pubmed |
| pubmed-article:20177146 | pubmed:author | pubmed-author:BaeYoe-SikYS | lld:pubmed |
| pubmed-article:20177146 | pubmed:author | pubmed-author:BaekSuk-HwanS... | lld:pubmed |
| pubmed-article:20177146 | pubmed:author | pubmed-author:KimKoanhoiK | lld:pubmed |
| pubmed-article:20177146 | pubmed:author | pubmed-author:YunJeanhoJ | lld:pubmed |
| pubmed-article:20177146 | pubmed:author | pubmed-author:LeeHa YoungHY | lld:pubmed |
| pubmed-article:20177146 | pubmed:author | pubmed-author:KimSang DooSD | lld:pubmed |
| pubmed-article:20177146 | pubmed:author | pubmed-author:ShimJae... | lld:pubmed |
| pubmed-article:20177146 | pubmed:author | pubmed-author:KimHak JungHJ | lld:pubmed |
| pubmed-article:20177146 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:20177146 | pubmed:day | 30 | lld:pubmed |
| pubmed-article:20177146 | pubmed:volume | 42 | lld:pubmed |
| pubmed-article:20177146 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:20177146 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:20177146 | pubmed:pagination | 302-9 | lld:pubmed |
| pubmed-article:20177146 | pubmed:dateRevised | 2010-9-28 | lld:pubmed |
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| pubmed-article:20177146 | pubmed:year | 2010 | lld:pubmed |
| pubmed-article:20177146 | pubmed:articleTitle | A pertussis toxin sensitive G-protein-independent pathway is involved in serum amyloid A-induced formyl peptide receptor 2-mediated CCL2 production. | lld:pubmed |
| pubmed-article:20177146 | pubmed:affiliation | Department of Biological Science, Sungkyunkwan University, Suwon 440-746, Korea. | lld:pubmed |
| pubmed-article:20177146 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:20177146 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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