| http://purl.uniprot.org/citations/16432214 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/16432214 | http://www.w3.org/2000/01/rdf-schema#comment | "The VEGF system is essential for angiogenesis. VEGF overexpression frequently correlates with increased microvascularity and metastasis and decreased spontaneous apoptosis. Although a precise mechanism has not been established, studies suggest that VEGF expression is negatively regulated by p53, a master regulator and tumor suppressor. There are no reports of additional components of the VEGF signal transduction pathway being part of the p53 transcriptional network. A target of VEGF, the VEGF receptor 1/flt-1, can regulate growth and migration of endothelial cells and modulate angiogenesis. VEGF appears to be up-regulated in various cancers in which flt-1 may have a role in tumor progression and metastasis. We identified a C-to-T SNP upstream of the transcriptional start site in approximately 6% of the people examined. The SNP is located within a putative p53 response element. Only the promoter with the T SNP (FLT1-T) was responsive to p53 when examined with reporter assays or by endogenous gene expression analysis in cell lines with different SNP status. In response to doxorubicin-induced DNA damage, there was clear allele discrimination based on p53 binding at the FLT1-T but not FLT1-C promoters as well as p53-dependent induction of flt-1 mRNA, which required the presence of FLT1-T. Our results establish that p53 can differentially stimulate transcription at a polymorphic variant of the flt-1 promoter and directly places the VEGF system in the p53 stress-response network via flt-1 in a significant fraction of the human population. We suggest that the p53-VEGF-flt-1 interaction is relevant to risks in angiogenesis-associated diseases, including cancer."xsd:string |
| http://purl.uniprot.org/citations/16432214 | http://purl.org/dc/terms/identifier | "doi:10.1073/pnas.0508103103"xsd:string |
| http://purl.uniprot.org/citations/16432214 | http://purl.uniprot.org/core/author | "Resnick M.A."xsd:string |
| http://purl.uniprot.org/citations/16432214 | http://purl.uniprot.org/core/author | "Menendez D."xsd:string |
| http://purl.uniprot.org/citations/16432214 | http://purl.uniprot.org/core/author | "Inga A."xsd:string |
| http://purl.uniprot.org/citations/16432214 | http://purl.uniprot.org/core/author | "Krysiak B."xsd:string |
| http://purl.uniprot.org/citations/16432214 | http://purl.uniprot.org/core/author | "Krysiak O."xsd:string |
| http://purl.uniprot.org/citations/16432214 | http://purl.uniprot.org/core/author | "Schonfelder G."xsd:string |
| http://purl.uniprot.org/citations/16432214 | http://purl.uniprot.org/core/date | "2006"xsd:gYear |
| http://purl.uniprot.org/citations/16432214 | http://purl.uniprot.org/core/name | "Proc Natl Acad Sci U S A"xsd:string |
| http://purl.uniprot.org/citations/16432214 | http://purl.uniprot.org/core/pages | "1406-1411"xsd:string |
| http://purl.uniprot.org/citations/16432214 | http://purl.uniprot.org/core/title | "A SNP in the flt-1 promoter integrates the VEGF system into the p53 transcriptional network."xsd:string |
| http://purl.uniprot.org/citations/16432214 | http://purl.uniprot.org/core/volume | "103"xsd:string |
| http://purl.uniprot.org/citations/16432214 | http://www.w3.org/2004/02/skos/core#exactMatch | http://purl.uniprot.org/pubmed/16432214 |
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