ArticleThe HUGO journal2010
Genome-wide identification and annotation of HIF-1α binding sites in two cell lines using massively parallel sequencing.
Article in The HUGO journal, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 36 citations in OpenAlex.
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- Systems approaches to understand oxygen sensing: how multi-omics has driven advances in understanding oxygen-based signalling.The Biochemical journal · 2022Review
- A functional map of genomic HIF1α-DNA complexes in the eye lens revealed through multiomics analysis.BMC genomics · 2021Article
- Now a Nobel gas: oxygen.Pflugers Archiv : European journal of physiology · 2019Review
- Mechanisms of hypoxia signalling: new implications for nephrology.Nature reviews. Nephrology · 2019Review
- Article
- The Transcription Factor Hif-1 Enhances the Radio-Resistance of Mouse MSCs.Frontiers in physiology · 2018Article
- Sexual dimorphism of the pulmonary transcriptome in neonatal hyperoxic lung injury: identification of angiogenesis as a key pathway.American journal of physiology. Lung cellular and molecular physiology · 2017Article
- Hypoxia inducible factors regulate the transcription of the sprouty2 gene and expression of the sprouty2 protein.PloS one · 2017Article
- Genome-wide analysis of HIF-2α chromatin binding sites under normoxia in human bronchial epithelial cells (BEAS-2B) suggests its diverse functions.Scientific reports · 2016Article
- Hypoxia, Hypoxia-inducible Transcription Factors, and Renal Cancer.European urology · 2016Review
- Spatial Interplay between Polycomb and Trithorax Complexes Controls Transcriptional Activity in T Lymphocytes.Molecular and cellular biology · 2015Article
- Destruction of a distal hypoxia response element abolishes trans-activation of the PAG1 gene mediated by HIF-independent chromatin looping.Nucleic acids research · 2015Article
- HIF1α Represses Cell Stress Pathways to Allow Proliferation of Hypoxic Fetal Cardiomyocytes.Developmental cell · 2015Article
- Analysis of RNA decay factor mediated RNA stability contributions on RNA abundance.BMC genomics · 2015Article
- Article
- Aberrant transcriptional regulations in cancers: genome, transcriptome and epigenome analysis of lung adenocarcinoma cell lines.Nucleic acids research · 2014Article
- Molecular responses to hypoxia-inducible factor 1α and beyond.Molecular pharmacology · 2014Review
- Construction of mate pair full-length cDNAs libraries and characterization of transcriptional start sites and termination sites.Nucleic acids research · 2014Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
unlabelledWe identified 531 and 616 putative HIF-1α target sites by ChIP-Seq in the cancerous cell line DLD-1 and the non-cancerous cell line TIG-3, respectively. We also examined the positions and expression levels of transcriptional start sites (TSSs) in these cell lines using our TSS-Seq method. We observed that 121 and 48 genes in DLD-1 and TIG-3 cells, respectively, had HIF-1α binding sites in proximal regions of the previously reported TSSs that were up-regulated at the transcriptional level. In addition, 193 and 123 of the HIF-1α target sites, respectively, were located in proximal regions of previously uncharacterized TSSs, namely, TSSs of putative alternative promoters of protein-coding genes or promoters of putative non-protein-coding transcripts. The hypoxic response of DLD-1 cells was more significant than that of TIG-3 cells with respect to both the number of target sites and the degree of induced changes in transcript expression. The Nucleosome-Seq and ChIP-Seq analyses of histone modifications revealed that the chromatin formed an open structure in regions surrounding the HIF-1α binding sites, but this event occurred prior to the actual binding of HIF-1α. Different cellular histories may be encoded by chromatin structures and determine the activation of specific genes in response to hypoxic shock. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (doi:10.1007/s11568-011-9150-9) contains supplementary material, which is available to authorized users.
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