| pubmed-article:2551036 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:2551036 | lifeskim:mentions | umls-concept:C0027950 | lld:lifeskim |
| pubmed-article:2551036 | lifeskim:mentions | umls-concept:C0001511 | lld:lifeskim |
| pubmed-article:2551036 | lifeskim:mentions | umls-concept:C0033684 | lld:lifeskim |
| pubmed-article:2551036 | lifeskim:mentions | umls-concept:C0008013 | lld:lifeskim |
| pubmed-article:2551036 | lifeskim:mentions | umls-concept:C1334146 | lld:lifeskim |
| pubmed-article:2551036 | lifeskim:mentions | umls-concept:C1366562 | lld:lifeskim |
| pubmed-article:2551036 | lifeskim:mentions | umls-concept:C1706439 | lld:lifeskim |
| pubmed-article:2551036 | lifeskim:mentions | umls-concept:C0851285 | lld:lifeskim |
| pubmed-article:2551036 | pubmed:issue | 4923 | lld:pubmed |
| pubmed-article:2551036 | pubmed:dateCreated | 1989-10-13 | lld:pubmed |
| pubmed-article:2551036 | pubmed:abstractText | The neutrophil Mac-1 and gp100MEL-14 adhesion proteins are involved in neutrophil extravasation during inflammation. Both the expression and activity of Mac-1 are greatly increased after neutrophil activation. In contrast, neutrophils shed gp100MEL-14 from the cell surface within 4 minutes after activation with chemotactic factors or phorbol esters, releasing a 96-kilodalton fragment of the antigen into the supernatant. Immunohistology showed that gp100MEL-14 was downregulated on neutrophils that had extravasated into inflamed tissue. The gp100MEL-14 adhesion protein may participate in the binding of unactivated neutrophils to the endothelium; rapid shedding of gp100MEL-14 may prevent extravasation into and damage of normal tissues by activated neutrophils. | lld:pubmed |
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| pubmed-article:2551036 | pubmed:language | eng | lld:pubmed |
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| pubmed-article:2551036 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:2551036 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:2551036 | pubmed:month | Sep | lld:pubmed |
| pubmed-article:2551036 | pubmed:issn | 0036-8075 | lld:pubmed |
| pubmed-article:2551036 | pubmed:author | pubmed-author:ButcherE CEC | lld:pubmed |
| pubmed-article:2551036 | pubmed:author | pubmed-author:KishimotoT... | lld:pubmed |
| pubmed-article:2551036 | pubmed:author | pubmed-author:JutilaM AMA | lld:pubmed |
| pubmed-article:2551036 | pubmed:author | pubmed-author:BergE LEL | lld:pubmed |
| pubmed-article:2551036 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:2551036 | pubmed:day | 15 | lld:pubmed |
| pubmed-article:2551036 | pubmed:volume | 245 | lld:pubmed |
| pubmed-article:2551036 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:2551036 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:2551036 | pubmed:pagination | 1238-41 | lld:pubmed |
| pubmed-article:2551036 | pubmed:dateRevised | 2007-11-14 | lld:pubmed |
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| pubmed-article:2551036 | pubmed:year | 1989 | lld:pubmed |
| pubmed-article:2551036 | pubmed:articleTitle | Neutrophil Mac-1 and MEL-14 adhesion proteins inversely regulated by chemotactic factors. | lld:pubmed |
| pubmed-article:2551036 | pubmed:affiliation | Department of Pathology, Stanford University, CA 94305. | lld:pubmed |
| pubmed-article:2551036 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:2551036 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
| pubmed-article:2551036 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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