| pubmed-article:9110977 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:9110977 | lifeskim:mentions | umls-concept:C0021368 | lld:lifeskim |
| pubmed-article:9110977 | lifeskim:mentions | umls-concept:C0079189 | lld:lifeskim |
| pubmed-article:9110977 | lifeskim:mentions | umls-concept:C0017262 | lld:lifeskim |
| pubmed-article:9110977 | lifeskim:mentions | umls-concept:C1817919 | lld:lifeskim |
| pubmed-article:9110977 | lifeskim:mentions | umls-concept:C2587213 | lld:lifeskim |
| pubmed-article:9110977 | lifeskim:mentions | umls-concept:C2911684 | lld:lifeskim |
| pubmed-article:9110977 | lifeskim:mentions | umls-concept:C0185117 | lld:lifeskim |
| pubmed-article:9110977 | pubmed:issue | 5312 | lld:pubmed |
| pubmed-article:9110977 | pubmed:dateCreated | 1997-5-9 | lld:pubmed |
| pubmed-article:9110977 | pubmed:abstractText | The gene encoding the BCL-6 transcriptional repressor is frequently translocated and mutated in diffuse large cell lymphoma. Mice with a disrupted BCL-6 gene developed myocarditis and pulmonary vasculitis, had no germinal centers, and had increased expression of T helper cell type 2 cytokines. The BCL-6 DNA recognition motif resembled sites bound by the STAT (signal transducers and activators of transcription) transcription factors, which mediate cytokine signaling. BCL-6 could repress interleukin-4 (IL-4)-induced transcription when bound to a site recognized by the IL-4-responsive transcription factor Stat6. Thus, dysregulation of STAT-responsive genes may underlie the inflammatory disease in BCL-6-deficient mice and participate in lymphoid malignancies. | lld:pubmed |
| pubmed-article:9110977 | pubmed:language | eng | lld:pubmed |
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| pubmed-article:9110977 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:9110977 | pubmed:month | Apr | lld:pubmed |
| pubmed-article:9110977 | pubmed:issn | 0036-8075 | lld:pubmed |
| pubmed-article:9110977 | pubmed:author | pubmed-author:YuXX | lld:pubmed |
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| pubmed-article:9110977 | pubmed:author | pubmed-author:DentA LAL | lld:pubmed |
| pubmed-article:9110977 | pubmed:author | pubmed-author:AllmanDD | lld:pubmed |
| pubmed-article:9110977 | pubmed:issnType | Print | lld:pubmed |
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| pubmed-article:9110977 | pubmed:volume | 276 | lld:pubmed |
| pubmed-article:9110977 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:9110977 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:9110977 | pubmed:pagination | 589-92 | lld:pubmed |
| pubmed-article:9110977 | pubmed:dateRevised | 2008-11-21 | lld:pubmed |
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| pubmed-article:9110977 | pubmed:year | 1997 | lld:pubmed |
| pubmed-article:9110977 | pubmed:articleTitle | Control of inflammation, cytokine expression, and germinal center formation by BCL-6. | lld:pubmed |
| pubmed-article:9110977 | pubmed:affiliation | Metabolism Branch, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USA. | lld:pubmed |
| pubmed-article:9110977 | pubmed:publicationType | Journal Article | lld:pubmed |
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