| pubmed-article:12810720 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:12810720 | lifeskim:mentions | umls-concept:C0035820 | lld:lifeskim |
| pubmed-article:12810720 | lifeskim:mentions | umls-concept:C0034809 | lld:lifeskim |
| pubmed-article:12810720 | lifeskim:mentions | umls-concept:C0017262 | lld:lifeskim |
| pubmed-article:12810720 | lifeskim:mentions | umls-concept:C0851285 | lld:lifeskim |
| pubmed-article:12810720 | pubmed:issue | 35 | lld:pubmed |
| pubmed-article:12810720 | pubmed:dateCreated | 2003-8-25 | lld:pubmed |
| pubmed-article:12810720 | pubmed:abstractText | Glucocorticoids are secreted from the adrenal glands and act as a peripheral effector of the hypothalamic-pituitary-adrenal axis, playing an essential role in stress response and homeostatic regulation. In target cells, however, it remains unknown how glucocorticoids fine-tune the cellular pathways mediating tissue and systemic adaptation. Recently, considerable evidence indicates that adaptation to hypoxic environments is influenced by glucocorticoids and there is cross-talk between hypoxia-dependent signals and glucocorticoid-mediated regulation of gene expression. We therefore investigated the interaction between these important stress-responsive pathways, focusing on the glucocorticoid receptor (GR) and hypoxia-inducible transcription factor HIF-1. Here we show that, under hypoxic conditions, HIF-1-dependent gene expression is further up-regulated by glucocorticoids via the GR. This up-regulation cannot be substituted by the other steroid receptors and is suggested to result from the interaction between the GR and the transactivation domain of HIF-1 alpha. Moreover, our results also indicate that the ligand binding domain of the GR is essential for this interaction, and the critical requirement for GR agonists suggests the importance of the ligand-mediated conformational change of the GR. Because these proteins are shown to colocalize in the distinct compartments of the nucleus, we suggest that these stress-responsive transcription factors have intimate communication in close proximity to each other, thereby enabling the fine-tuning of cellular responses for adaptation. | lld:pubmed |
| pubmed-article:12810720 | pubmed:language | eng | lld:pubmed |
| pubmed-article:12810720 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:12810720 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:12810720 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:12810720 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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| pubmed-article:12810720 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:12810720 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:12810720 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:12810720 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:12810720 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:12810720 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:12810720 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:12810720 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:12810720 | pubmed:month | Aug | lld:pubmed |
| pubmed-article:12810720 | pubmed:issn | 0021-9258 | lld:pubmed |
| pubmed-article:12810720 | pubmed:author | pubmed-author:MorimotoChika... | lld:pubmed |
| pubmed-article:12810720 | pubmed:author | pubmed-author:YoshikawaNori... | lld:pubmed |
| pubmed-article:12810720 | pubmed:author | pubmed-author:MakinoYuichiY | lld:pubmed |
| pubmed-article:12810720 | pubmed:author | pubmed-author:TanakaHirotos... | lld:pubmed |
| pubmed-article:12810720 | pubmed:author | pubmed-author:OuchidaRikaR | lld:pubmed |
| pubmed-article:12810720 | pubmed:author | pubmed-author:KodamaTsuneno... | lld:pubmed |
| pubmed-article:12810720 | pubmed:author | pubmed-author:OkamotoKensak... | lld:pubmed |
| pubmed-article:12810720 | pubmed:author | pubmed-author:NakamuraHiros... | lld:pubmed |
| pubmed-article:12810720 | pubmed:author | pubmed-author:HisadaTetsuya... | lld:pubmed |
| pubmed-article:12810720 | pubmed:author | pubmed-author:ShimizuNoriak... | lld:pubmed |
| pubmed-article:12810720 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:12810720 | pubmed:day | 29 | lld:pubmed |
| pubmed-article:12810720 | pubmed:volume | 278 | lld:pubmed |
| pubmed-article:12810720 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:12810720 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:12810720 | pubmed:pagination | 33384-91 | lld:pubmed |
| pubmed-article:12810720 | pubmed:dateRevised | 2008-11-21 | lld:pubmed |
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| pubmed-article:12810720 | pubmed:year | 2003 | lld:pubmed |
| pubmed-article:12810720 | pubmed:articleTitle | Role of the glucocorticoid receptor for regulation of hypoxia-dependent gene expression. | lld:pubmed |
| pubmed-article:12810720 | pubmed:affiliation | Division of Clinical Immunology, Advanced Clinical Research Center, Institute of Medical Science, University of Tokyo, 4-6-1 Shirokanedai, Minato-ku, Tokyo 08-8639, Japan. | lld:pubmed |
| pubmed-article:12810720 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:12810720 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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