| pubmed-article:17255940 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:17255940 | lifeskim:mentions | umls-concept:C0035820 | lld:lifeskim |
| pubmed-article:17255940 | lifeskim:mentions | umls-concept:C0078058 | lld:lifeskim |
| pubmed-article:17255940 | lifeskim:mentions | umls-concept:C1519670 | lld:lifeskim |
| pubmed-article:17255940 | lifeskim:mentions | umls-concept:C1256770 | lld:lifeskim |
| pubmed-article:17255940 | lifeskim:mentions | umls-concept:C0851285 | lld:lifeskim |
| pubmed-article:17255940 | lifeskim:mentions | umls-concept:C1511545 | lld:lifeskim |
| pubmed-article:17255940 | pubmed:issue | 3 | lld:pubmed |
| pubmed-article:17255940 | pubmed:dateCreated | 2007-2-8 | lld:pubmed |
| pubmed-article:17255940 | pubmed:abstractText | Regulation of vascular endothelial growth factor (VEGF) expression is a complex process involving a plethora of transcriptional regulators. The AP-1 transcription factor is considered as facilitator of hypoxia-induced VEGF expression through interaction with hypoxia-inducible factor (HIF) which plays a major role in mediating the cellular hypoxia response. As yet, both the decisive AP-1 subunit leading to VEGF induction and the molecular mechanism by which this subunit is activated have not been deciphered. Here, we demonstrate that the AP-1 subunit junB is a target gene of hypoxia-induced signaling via NF-kappaB. Loss of JunB in various cell types results in severely impaired hypoxia-induced VEGF expression, although HIF is present and becomes stabilized. Thus, we identify JunB as a critical independent regulator of VEGF transcription and provide a mechanistic explanation for the inherent vascular phenotypes seen in JunB-deficient embryos, ex vivo allantois explants and in vitro differentiated embryoid bodies. In support of these findings, tumor angiogenesis was impaired in junB(-/-) teratocarcinomas because of severely impaired paracrine-acting VEGF and the subsequent inability to efficiently recruit host-derived vessels. | lld:pubmed |
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| pubmed-article:17255940 | pubmed:language | eng | lld:pubmed |
| pubmed-article:17255940 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:17255940 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:17255940 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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| pubmed-article:17255940 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:17255940 | pubmed:month | Feb | lld:pubmed |
| pubmed-article:17255940 | pubmed:issn | 0261-4189 | lld:pubmed |
| pubmed-article:17255940 | pubmed:author | pubmed-author:AngelPeterP | lld:pubmed |
| pubmed-article:17255940 | pubmed:author | pubmed-author:AndrechtSvenS | lld:pubmed |
| pubmed-article:17255940 | pubmed:author | pubmed-author:Schorpp-Kistn... | lld:pubmed |
| pubmed-article:17255940 | pubmed:author | pubmed-author:FusenigNorber... | lld:pubmed |
| pubmed-article:17255940 | pubmed:author | pubmed-author:SchmidtDirkD | lld:pubmed |
| pubmed-article:17255940 | pubmed:author | pubmed-author:LichtAlexande... | lld:pubmed |
| pubmed-article:17255940 | pubmed:author | pubmed-author:PeinOliver... | lld:pubmed |
| pubmed-article:17255940 | pubmed:author | pubmed-author:TextorBjörnB | lld:pubmed |
| pubmed-article:17255940 | pubmed:author | pubmed-author:Sator-Schmitt... | lld:pubmed |
| pubmed-article:17255940 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:17255940 | pubmed:day | 7 | lld:pubmed |
| pubmed-article:17255940 | pubmed:volume | 26 | lld:pubmed |
| pubmed-article:17255940 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:17255940 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:17255940 | pubmed:pagination | 710-9 | lld:pubmed |
| pubmed-article:17255940 | pubmed:dateRevised | 2009-11-18 | lld:pubmed |
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