| pubmed-article:17075044 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:17075044 | lifeskim:mentions | umls-concept:C0024264 | lld:lifeskim |
| pubmed-article:17075044 | lifeskim:mentions | umls-concept:C0597357 | lld:lifeskim |
| pubmed-article:17075044 | lifeskim:mentions | umls-concept:C1704675 | lld:lifeskim |
| pubmed-article:17075044 | lifeskim:mentions | umls-concept:C0017262 | lld:lifeskim |
| pubmed-article:17075044 | lifeskim:mentions | umls-concept:C1423842 | lld:lifeskim |
| pubmed-article:17075044 | lifeskim:mentions | umls-concept:C0851285 | lld:lifeskim |
| pubmed-article:17075044 | lifeskim:mentions | umls-concept:C2911684 | lld:lifeskim |
| pubmed-article:17075044 | lifeskim:mentions | umls-concept:C0913648 | lld:lifeskim |
| pubmed-article:17075044 | lifeskim:mentions | umls-concept:C0253307 | lld:lifeskim |
| pubmed-article:17075044 | lifeskim:mentions | umls-concept:C0185117 | lld:lifeskim |
| pubmed-article:17075044 | pubmed:issue | 45 | lld:pubmed |
| pubmed-article:17075044 | pubmed:dateCreated | 2006-11-8 | lld:pubmed |
| pubmed-article:17075044 | pubmed:abstractText | Selectin-dependent cell adhesion mediates inflammatory extravasation and routine homing of lymphocytes. Most resting peripheral T lymphocytes lack expression of sialyl Lewis X, the carbohydrate ligand for selectins, and are induced to strongly express it upon activation. T helper 1 (Th1) cells are known to more preferentially express sialyl Lewis X as compared with T helper 2 (Th2) cells upon activation. The molecular basis for this preferential expression, however, has not been elucidated to date. Here we show that the gene for fucosyltransferase VII (FUT7), the rate-limiting enzyme for sialyl Lewis X synthesis, is a unique example of the human genes with binding sites for both GATA-3 and T-bet, two opposing factors for Th1 and Th2 development, and is regulated transcriptionally by a balance of the two interacting transcription factors. T-bet promotes and GATA-3 represses FUT7 transcription. Our results indicated that T-bet interferes with the binding of GATA-3 to its target DNA, and also that GATA-3 significantly interferes with the binding of T-bet to the FUT7 promoter. T-bet has a binding ability to GATA-3, CBP/P300, and Sp1 to form a transcription factor complex, and GATA-3 regulates FUT7 transcription by phosphorylation-dependently recruiting histone deacetylase (HDAC)-3/HDAC-5 and by competing with CBP/P300 in binding to the N terminus of T-bet. Suppression of GATA-3 activity by dominant-negative GATA-3 or repressor of GATA (ROG) was necessary to attain a maximum expression of FUT7 and sialyl Lewis X in human T lymphoid cells. These results indicate that the GATA-3/T-bet transcription factor complex regulates the cell-lineage-specific expression of the lymphocyte homing receptors. | lld:pubmed |
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| pubmed-article:17075044 | pubmed:language | eng | lld:pubmed |
| pubmed-article:17075044 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:17075044 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:17075044 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:17075044 | pubmed:month | Nov | lld:pubmed |
| pubmed-article:17075044 | pubmed:issn | 0027-8424 | lld:pubmed |
| pubmed-article:17075044 | pubmed:author | pubmed-author:KannagiReijiR | lld:pubmed |
| pubmed-article:17075044 | pubmed:author | pubmed-author:OsadaHirotaka... | lld:pubmed |
| pubmed-article:17075044 | pubmed:author | pubmed-author:ChenGuo-YunGY | lld:pubmed |
| pubmed-article:17075044 | pubmed:author | pubmed-author:Santamaria-Ba... | lld:pubmed |
| pubmed-article:17075044 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:17075044 | pubmed:day | 7 | lld:pubmed |
| pubmed-article:17075044 | pubmed:volume | 103 | lld:pubmed |
| pubmed-article:17075044 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:17075044 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:17075044 | pubmed:pagination | 16894-9 | lld:pubmed |
| pubmed-article:17075044 | pubmed:dateRevised | 2009-11-18 | lld:pubmed |
| pubmed-article:17075044 | pubmed:meshHeading | pubmed-meshheading:17075044... | lld:pubmed |
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| pubmed-article:17075044 | pubmed:meshHeading | pubmed-meshheading:17075044... | lld:pubmed |
| pubmed-article:17075044 | pubmed:meshHeading | pubmed-meshheading:17075044... | lld:pubmed |
| pubmed-article:17075044 | pubmed:meshHeading | pubmed-meshheading:17075044... | lld:pubmed |
| pubmed-article:17075044 | pubmed:meshHeading | pubmed-meshheading:17075044... | lld:pubmed |
| pubmed-article:17075044 | pubmed:meshHeading | pubmed-meshheading:17075044... | lld:pubmed |
| pubmed-article:17075044 | pubmed:meshHeading | pubmed-meshheading:17075044... | lld:pubmed |
| pubmed-article:17075044 | pubmed:meshHeading | pubmed-meshheading:17075044... | lld:pubmed |
| pubmed-article:17075044 | pubmed:year | 2006 | lld:pubmed |
| pubmed-article:17075044 | pubmed:articleTitle | Interaction of GATA-3/T-bet transcription factors regulates expression of sialyl Lewis X homing receptors on Th1/Th2 lymphocytes. | lld:pubmed |
| pubmed-article:17075044 | pubmed:affiliation | Department of Molecular Pathology, Aichi Cancer Center, 1-1 Kanokoden, Chikusaku, Nagoya 464-8681, Japan. | lld:pubmed |
