ArticleOncotarget2013
p53 regulates the transcription of the anti-inflammatory molecule developmental endothelial locus-1 (Del-1).
Article in Oncotarget, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 16 citations in OpenAlex.
- Developmental endothelial locus-1 in cardiovascular and metabolic diseases: A promising biomarker and therapeutic target.Frontiers in immunology · 2022Review
- P53 in the impaired lungs.DNA repair · 2020Review
- Potential miRNAs for miRNA-Based Therapeutics in Breast Cancer.Non-coding RNA · 2020Review
- MicroRNA-137 Inhibits Cancer Progression by Targeting Del-1 in Triple-Negative Breast Cancer Cells.International journal of molecular sciences · 2019Article
- Transcriptome analysis of inflammation-related gene expression in endothelial cells activated by complement MASP-1.Scientific reports · 2017Article
- Inhibition of CDK9 as a therapeutic strategy for inflammatory arthritis.Scientific reports · 2016Article
- Overexpressed EDIL3 predicts poor prognosis and promotes anchorage-independent tumor growth in human pancreatic cancer.Oncotarget · 2016Article
- TAp73 promotes anabolism.Oncotarget · 2014Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Developmental endothelial locus-1 (Del-1) is an endothelium-derived anti-inflammatory molecule that is downregulated by inflammatory stimuli. Little is known about the molecular mechanisms by which Del-1 transcription is regulated. In the present study, a DNA sequence upstream of the Del-1 gene was analyzed and putative p53 response elements (p53REs) were identified. An approximately 2 kb fragment upstream of the translation start site displayed the highest Del-1 transcriptional activity, and the transcriptional activity of this fragment was enhanced by overexpression of p53. Chemical activation of endogenous p53 elevated the levels of Del-1 mRNA. Site-directed mutagenesis of CATG in the consensus sequences of the 2 kb fragment to TATA significantly reduced the transcription of Del-1. Chromatin immunoprecipitation revealed recruitment of p53 to the p53REs of the Del-1 promoter, resulting in increased Del-1 transcription. Finally, primary endothelial cells isolated from mice with reduced levels of p53 showed a decrease in Del-1 mRNA compared to wild-type endothelial cells. Moreover, Del-1 reciprocally enhanced p53 expression in primary endothelial cells. Thus, these findings suggest that Del-1 is a novel transcriptional target gene of p53.
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