| pubmed-article:16633358 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:16633358 | lifeskim:mentions | umls-concept:C0024432 | lld:lifeskim |
| pubmed-article:16633358 | lifeskim:mentions | umls-concept:C0221099 | lld:lifeskim |
| pubmed-article:16633358 | lifeskim:mentions | umls-concept:C2361980 | lld:lifeskim |
| pubmed-article:16633358 | lifeskim:mentions | umls-concept:C0456148 | lld:lifeskim |
| pubmed-article:16633358 | lifeskim:mentions | umls-concept:C0441712 | lld:lifeskim |
| pubmed-article:16633358 | pubmed:issue | 4 | lld:pubmed |
| pubmed-article:16633358 | pubmed:dateCreated | 2006-6-12 | lld:pubmed |
| pubmed-article:16633358 | pubmed:abstractText | The role of the anti-inflammatory protein annexin-A1 (Anx-A1) in the phagocytic process has been investigated using a murine bone marrow culture-derived macrophage model from Anx-A1(+/+) and Anx-A1(-/-) mice. Macrophages prepared from Anx-A1(-/-) mice exhibited a reduced ingestion of zymosan, Neisseria meningitidis or sheep red blood cells, when compared to Anx-A1(+/+) cells and in the case of zymosan this effect was also mirrored by a reduced clearance in vivo when particles were injected into the peritoneal cavity of Anx-A1(-/-) mice. The ablation of the Anx-A1 gene did not cause any apparent cytoskeletal defects associated with particle ingestion but the cell surface expression of the key adhesion molecule CD11b was depressed in the Anx-A1(-/-) cells providing a possible explanation for the attenuated phagocytic potential of these cells. The production of the cytokines TNFalpha and IL-6 was increased in Anx-A1(-/-) macrophages following phagocytosis of all types of particle. | lld:pubmed |
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| pubmed-article:16633358 | pubmed:language | eng | lld:pubmed |
| pubmed-article:16633358 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:16633358 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:16633358 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:16633358 | pubmed:month | Jun | lld:pubmed |
| pubmed-article:16633358 | pubmed:issn | 0007-1188 | lld:pubmed |
| pubmed-article:16633358 | pubmed:author | pubmed-author:PeiserLeanneL | lld:pubmed |
| pubmed-article:16633358 | pubmed:author | pubmed-author:GordonSiamonS | lld:pubmed |
| pubmed-article:16633358 | pubmed:author | pubmed-author:FlowerRoderic... | lld:pubmed |
| pubmed-article:16633358 | pubmed:author | pubmed-author:PerrettiMauro... | lld:pubmed |
| pubmed-article:16633358 | pubmed:author | pubmed-author:YonaSimonS | lld:pubmed |
| pubmed-article:16633358 | pubmed:author | pubmed-author:HeinsbroekSig... | lld:pubmed |
| pubmed-article:16633358 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:16633358 | pubmed:volume | 148 | lld:pubmed |
| pubmed-article:16633358 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:16633358 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:16633358 | pubmed:pagination | 469-77 | lld:pubmed |
| pubmed-article:16633358 | pubmed:dateRevised | 2009-11-18 | lld:pubmed |
| pubmed-article:16633358 | pubmed:meshHeading | pubmed-meshheading:16633358... | lld:pubmed |
| pubmed-article:16633358 | pubmed:meshHeading | pubmed-meshheading:16633358... | lld:pubmed |
| pubmed-article:16633358 | pubmed:meshHeading | pubmed-meshheading:16633358... | lld:pubmed |
| pubmed-article:16633358 | pubmed:meshHeading | pubmed-meshheading:16633358... | lld:pubmed |
| pubmed-article:16633358 | pubmed:meshHeading | pubmed-meshheading:16633358... | lld:pubmed |
| pubmed-article:16633358 | pubmed:meshHeading | pubmed-meshheading:16633358... | lld:pubmed |
| pubmed-article:16633358 | pubmed:meshHeading | pubmed-meshheading:16633358... | lld:pubmed |
| pubmed-article:16633358 | pubmed:meshHeading | pubmed-meshheading:16633358... | lld:pubmed |
| pubmed-article:16633358 | pubmed:meshHeading | pubmed-meshheading:16633358... | lld:pubmed |
| pubmed-article:16633358 | pubmed:meshHeading | pubmed-meshheading:16633358... | lld:pubmed |
| pubmed-article:16633358 | pubmed:year | 2006 | lld:pubmed |
| pubmed-article:16633358 | pubmed:articleTitle | Impaired phagocytic mechanism in annexin 1 null macrophages. | lld:pubmed |
| pubmed-article:16633358 | pubmed:affiliation | Department of Biochemical Pharmacology, The William Harvey Research Institute, St Bartholomew's and the Royal London School of Medicine, University of London. | lld:pubmed |
| pubmed-article:16633358 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:16633358 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
| http://linkedlifedata.com/r... | pubmed:referesTo | pubmed-article:16633358 | lld:pubmed |
