ArticleNucleic acids research2002
A novel mechanism of repression of the vascular endothelial growth factor promoter, by single strand DNA binding cold shock domain (Y-box) proteins in normoxic fibroblasts.
Article in Nucleic acids research, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 35 citations in OpenAlex.
- Article
- Cold shock proteins: from cellular mechanisms to pathophysiology and disease.Cell communication and signaling : CCS · 2018Review
- Expression and network analysis of YBX1 interactors for identification of new drug targets in lung adenocarcinoma.Journal of genomics · 2018Article
- Overexpression of YB1 C-terminal domain inhibits proliferation, angiogenesis and tumorigenicity in a SK-BR-3 breast cancer xenograft mouse model.FEBS open bio · 2016Article
- Brain-derived neurotrophic factor gene-modified bone marrow mesenchymal stem cells.Experimental and therapeutic medicine · 2015Article
- The role of cold shock domain proteins in inflammatory diseases.Journal of molecular medicine (Berlin, Germany) · 2014Review
- Cold-shock-domain protein A (CSDA) contributes posttranscriptionally to gonadotropin-releasing hormone-regulated expression of Egr1 and indirectly to Lhb.Biology of reproduction · 2012Article
- Cold shock domain protein A (CSDA) overexpression inhibits tumor growth and lymph node metastasis in a mouse model of squamous cell carcinoma.Clinical & experimental metastasis · 2010Article
- Cold shock domain protein A represses angiogenesis and lymphangiogenesis via inhibition of serum response element.Oncogene · 2008Article
- Expression of Y-box-binding protein dbpC/contrin, a potentially new cancer/testis antigen.British journal of cancer · 2006Article
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Overexpression of vascular endothelial growth factor (VEGF) is implicated in a number of diseases. It is therefore critical that mechanisms exist to strictly regulate VEGF expression. A hypoxia-responsive (HR) region of the VEGF promoter which binds the HIF-1 transcription factor is a target for many signals that up-regulate VEGF transcription. Repressors targeting the HIF-1 transcription factor have been identified but no repressors directly binding the HR promoter region had been reported. We now report a novel mechanism of repression of the VEGF HR region involving DNA binding. We find that single strand DNA-specific cold shock domain (CSD or Y-box) proteins repress the HR region via a binding site downstream of the HIF-1 site. The repressor site is functional in unstimulated, normoxic fibroblasts and represents a novel means to prevent expression of VEGF in the absence of appropriate stimuli. We characterized complexes forming on the VEGF repressor site and identified a previously unreported nuclear CSD protein complex containing dbpA. Nuclear dbpA appears to bind as a dimer and we determined a means by which nuclear CSD proteins may enter double strand DNA to bind to their single strand sites to bring about repression of the VEGF HR region.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.