| pubmed-article:16138188 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:16138188 | lifeskim:mentions | umls-concept:C0521009 | lld:lifeskim |
| pubmed-article:16138188 | lifeskim:mentions | umls-concept:C1819995 | lld:lifeskim |
| pubmed-article:16138188 | lifeskim:mentions | umls-concept:C0017950 | lld:lifeskim |
| pubmed-article:16138188 | lifeskim:mentions | umls-concept:C1656970 | lld:lifeskim |
| pubmed-article:16138188 | lifeskim:mentions | umls-concept:C1880177 | lld:lifeskim |
| pubmed-article:16138188 | pubmed:issue | 9 | lld:pubmed |
| pubmed-article:16138188 | pubmed:dateCreated | 2005-9-2 | lld:pubmed |
| pubmed-article:16138188 | pubmed:abstractText | Group B Streptococcus (GBS) is an important cause of infections, including meningitis. The molecular events underlying its pathogenesis are poorly understood. A study in this issue of the JCI reports that the GBS invasion-associated gene (iagA) contributes to meningeal infection and virulence by facilitating invasion of the cells that compose the blood-brain barrier and of other host cells. The mechanism involved most likely relates to the gene product's role in synthesis of a glycolipid anchor for a bacterial cell-surface entity that interacts directly with host cells. | lld:pubmed |
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| pubmed-article:16138188 | pubmed:language | eng | lld:pubmed |
| pubmed-article:16138188 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:16138188 | pubmed:citationSubset | AIM | lld:pubmed |
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| pubmed-article:16138188 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:16138188 | pubmed:month | Sep | lld:pubmed |
| pubmed-article:16138188 | pubmed:issn | 0021-9738 | lld:pubmed |
| pubmed-article:16138188 | pubmed:author | pubmed-author:BaronMiriam... | lld:pubmed |
| pubmed-article:16138188 | pubmed:author | pubmed-author:KasperDennis... | lld:pubmed |
| pubmed-article:16138188 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:16138188 | pubmed:volume | 115 | lld:pubmed |
| pubmed-article:16138188 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:16138188 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:16138188 | pubmed:pagination | 2325-7 | lld:pubmed |
| pubmed-article:16138188 | pubmed:dateRevised | 2009-11-18 | lld:pubmed |
| pubmed-article:16138188 | pubmed:meshHeading | pubmed-meshheading:16138188... | lld:pubmed |
| pubmed-article:16138188 | pubmed:meshHeading | pubmed-meshheading:16138188... | lld:pubmed |
| pubmed-article:16138188 | pubmed:meshHeading | pubmed-meshheading:16138188... | lld:pubmed |
| pubmed-article:16138188 | pubmed:meshHeading | pubmed-meshheading:16138188... | lld:pubmed |
| pubmed-article:16138188 | pubmed:meshHeading | pubmed-meshheading:16138188... | lld:pubmed |
| pubmed-article:16138188 | pubmed:meshHeading | pubmed-meshheading:16138188... | lld:pubmed |
| pubmed-article:16138188 | pubmed:meshHeading | pubmed-meshheading:16138188... | lld:pubmed |
| pubmed-article:16138188 | pubmed:meshHeading | pubmed-meshheading:16138188... | lld:pubmed |
| pubmed-article:16138188 | pubmed:meshHeading | pubmed-meshheading:16138188... | lld:pubmed |
| pubmed-article:16138188 | pubmed:year | 2005 | lld:pubmed |
| pubmed-article:16138188 | pubmed:articleTitle | Anchors away: contribution of a glycolipid anchor to bacterial invasion of host cells. | lld:pubmed |
| pubmed-article:16138188 | pubmed:affiliation | The Channing Laboratory and the Division of Infectious Diseases, Department of Medicine, Brigham and Women's Hospital, Boston, Massachusetts 02115, USA. | lld:pubmed |
| pubmed-article:16138188 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:16138188 | pubmed:publicationType | Comment | lld:pubmed |
| pubmed-article:16138188 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
| pubmed-article:16138188 | pubmed:publicationType | Research Support, N.I.H., Extramural | lld:pubmed |
| http://linkedlifedata.com/r... | pubmed:referesTo | pubmed-article:16138188 | lld:pubmed |
