| pubmed-article:10734131 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:10734131 | lifeskim:mentions | umls-concept:C0376298 | lld:lifeskim |
| pubmed-article:10734131 | lifeskim:mentions | umls-concept:C0919490 | lld:lifeskim |
| pubmed-article:10734131 | lifeskim:mentions | umls-concept:C0033684 | lld:lifeskim |
| pubmed-article:10734131 | lifeskim:mentions | umls-concept:C1321919 | lld:lifeskim |
| pubmed-article:10734131 | lifeskim:mentions | umls-concept:C0021747 | lld:lifeskim |
| pubmed-article:10734131 | lifeskim:mentions | umls-concept:C1336636 | lld:lifeskim |
| pubmed-article:10734131 | lifeskim:mentions | umls-concept:C0017262 | lld:lifeskim |
| pubmed-article:10734131 | lifeskim:mentions | umls-concept:C0439677 | lld:lifeskim |
| pubmed-article:10734131 | lifeskim:mentions | umls-concept:C0851285 | lld:lifeskim |
| pubmed-article:10734131 | lifeskim:mentions | umls-concept:C2911684 | lld:lifeskim |
| pubmed-article:10734131 | lifeskim:mentions | umls-concept:C0185117 | lld:lifeskim |
| pubmed-article:10734131 | pubmed:issue | 13 | lld:pubmed |
| pubmed-article:10734131 | pubmed:dateCreated | 2000-5-4 | lld:pubmed |
| pubmed-article:10734131 | pubmed:abstractText | The protein product of the Toll-like receptor (TLR) 4 gene has been implicated in the signal transduction events induced by lipopolysaccharide (LPS). In mice, destructive mutations of Tlr4 impede the normal response to LPS and cause a high susceptibility to Gram-negative infection. Expression of TLR4 mRNA in humans is restricted to a small number of cell types, including LPS-responsive myeloid cells, B-cells, and endothelial cells. To investigate the molecular basis for TLR4 expression in cells of myeloid origin, we cloned the human TLR4 gene and analyzed its putative 5'-proximal promoter. In transient transfections a region of only 75 base pairs upstream of the major transcription initiation site was sufficient to induce maximal luciferase activity in THP-1 cells. The sequence of this region is similar in human and mouse TLR4 genes and lacks a TATA box, typical Sp1-sites or CCAAT box sequences. Instead, it contains consensus-binding sites for Ets family transcription factors, octamer-binding factors, and a composite interferon response factor/Ets motif. The activity of the promoter in macrophages was strictly dependent on the integrity of both half sites of the composite interferon response factor/Ets motif, which was constitutively bound by the myeloid and B-cell-specific transcription factor PU.1 and interferon consensus sequence-binding protein. These results indicate that the two tissue-restricted transcription factors PU.1 and interferon consensus sequence-binding protein participate in the basal regulation of human TLR4 in myeloid cells. Cloning of the human TLR4 gene provides a basis for further investigation of the possible impact of genetic variations on the susceptibility to infection and sepsis. | lld:pubmed |
| pubmed-article:10734131 | pubmed:language | eng | lld:pubmed |
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| pubmed-article:10734131 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:10734131 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:10734131 | pubmed:month | Mar | lld:pubmed |
| pubmed-article:10734131 | pubmed:issn | 0021-9258 | lld:pubmed |
| pubmed-article:10734131 | pubmed:author | pubmed-author:BeutlerBB | lld:pubmed |
| pubmed-article:10734131 | pubmed:author | pubmed-author:AndreesenRR | lld:pubmed |
| pubmed-article:10734131 | pubmed:author | pubmed-author:KrauseS WSW | lld:pubmed |
| pubmed-article:10734131 | pubmed:author | pubmed-author:PoltorakAA | lld:pubmed |
| pubmed-article:10734131 | pubmed:author | pubmed-author:RehliMM | lld:pubmed |
| pubmed-article:10734131 | pubmed:author | pubmed-author:Schwarzfische... | lld:pubmed |
| pubmed-article:10734131 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:10734131 | pubmed:day | 31 | lld:pubmed |
| pubmed-article:10734131 | pubmed:volume | 275 | lld:pubmed |
| pubmed-article:10734131 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:10734131 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:10734131 | pubmed:pagination | 9773-81 | lld:pubmed |
| pubmed-article:10734131 | pubmed:dateRevised | 2008-11-21 | lld:pubmed |
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| pubmed-article:10734131 | pubmed:year | 2000 | lld:pubmed |
| pubmed-article:10734131 | pubmed:articleTitle | PU.1 and interferon consensus sequence-binding protein regulate the myeloid expression of the human Toll-like receptor 4 gene. | lld:pubmed |
| pubmed-article:10734131 | pubmed:affiliation | Department of Hematology and Oncology, University of Regensburg, 93042 Regensburg, Germany. Michael.Rehli@klinik.uni-regensburg.de | lld:pubmed |
| pubmed-article:10734131 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:10734131 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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