High resolution genome-wide mapping of HIF binding sites by ChIP-seq
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE28352 | GEO | 2011/04/05
SECONDARY ACCESSION(S): PRJNA139281
REPOSITORIES: GEO
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Project description:We report ChIP-Seq analysis of HIF-1 alpha, HIF-2 alpha, and HIF-1 beta binding in MCF-7 breast cancer cells Sample analysis compared to pre-immune serum chromatin immunoprecipitation
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Project description:Kidney cancer accounts for more than 100,000 deaths per year world-wide. More than 80% are clear cell tumors (ccRCCs) and the majority are associated with loss of function of the von Hippel Lindau (pVHL) tumor suppressor resulting in upregulation of HIF-{alpha} subunits, and activation of HIF-dependent transcriptional pathways. Recent GWAS studies have discovered RCC-susceptibility loci both within EPAS1 (HIF-2{alpha}) and in an intergenic region of unknown function on 11q13.3. As part of an ongoing study to define the direct transcriptional targets of HIF-2 in renal cancer, we undertook a genome-wide analysis of HIF-2-binding sites in pVHL-defective 786-O cells (that lack functional HIF-1{alpha} due to a truncated transcript) using chromatin immunoprecipitation with antibodies directed against HIF-2{alpha} and its dimerization partner HIF-1{beta}, coupled to high-throughput sequencing (ChIP-seq). Amongst approximately 600 pangenomic HIF-2{beta} ChIP signals, we observed strong binding (ranked 12th by peak height) almost precisely coinciding with the RCC predisposition SNP rs7105934 on 11q13.3. We report binding of HIF-2{alpha} and HIF-1{beta} in 786-O clear cell renal carcinoma cells. 3 samples examined, HIF-2{alpha}, HIF-1{beta} and pre-immune control ChIP.
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Project description:Kidney cancer accounts for more than 100,000 deaths per year world-wide. More than 80% are clear cell tumors (ccRCCs) and the majority are associated with loss of function of the von Hippel Lindau (pVHL) tumor suppressor resulting in upregulation of HIF-{alpha} subunits, and activation of HIF-dependent transcriptional pathways. Recent GWAS studies have discovered RCC-susceptibility loci both within EPAS1 (HIF-2{alpha}) and in an intergenic region of unknown function on 11q13.3. As part of an ongoing study to define the direct transcriptional targets of HIF-2 in renal cancer, we undertook a genome-wide analysis of HIF-2-binding sites in pVHL-defective 786-O cells (that lack functional HIF-1{alpha} due to a truncated transcript) using chromatin immunoprecipitation with antibodies directed against HIF-2{alpha} and its dimerization partner HIF-1{beta}, coupled to high-throughput sequencing (ChIP-seq). Amongst approximately 600 pangenomic HIF-2{beta} ChIP signals, we observed strong binding (ranked 12th by peak height) almost precisely coinciding with the RCC predisposition SNP rs7105934 on 11q13.3.
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Project description:Analysis of the binding sites of Hif-1α in both wild-type and von Hippel Lindau mutant zebrafish lines at 4dpf by ChIP linked next generation sequencing. The von Hippel Lindau mutant displays a systemic hypoxic response under normoxic conditions. Results show the extent of Hif-1α binding to the genome, and provide a basis for analysis of the transcriptional response to genetically induced hypoxia in zebrafish. Analysis of the DNA binding sites of Hif-1α in both wild-type and von Hippel Lindau mutant zebrafish lines at 4dpf. The von Hippel Lindau mutant displays a systemic hypoxic response under normoxic conditions. Results show the extent of Hif-1α binding to the genome, and provide a basis for analysis of the dependency of the transcriptional response on Hif-1α in conditions of genetically induced hypoxia in zebrafish.
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Project description:Analysis of gene expression changes in the von Hippel Lindau when mutant compared to wild-type at 4dpf using a whole genome microarray expression profiling. The von Hippel Lindau mutant displays a systemic hypoxic response under normoxic conditions. We performed single-colour microarrays to identify the gene expression changes which underpin the hypoxic phenotype. We used 3 biological replicates from both mutant and control, followed by analysis using Limma to identify significant gene expression changes. This work, together with ChIP-seq data for the Hif-1α in von Hippel Lindau mutants, should allow for the Hif-1α dependency of these gene expression changes to be assessed. The changes in gene expression between von Hippel Lindau mutants and wild-type controls was measured at 4 days post fertilisation. For both wild-type and mutant, 3 biological replicates, each of 30 embryos were used.
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Project description:Analysis of the binding sites of Hif-1α in both wild-type and von Hippel Lindau mutant zebrafish lines at 4dpf by ChIP linked next generation sequencing. The von Hippel Lindau mutant displays a systemic hypoxic response under normoxic conditions. Results show the extent of Hif-1α binding to the genome, and provide a basis for analysis of the transcriptional response to genetically induced hypoxia in zebrafish.
2016-03-22 | GSE70727 | GEO
Project description:Analysis of gene expression changes in the von Hippel Lindau when mutant compared to wild-type at 4dpf using a whole genome microarray expression profiling. The von Hippel Lindau mutant displays a systemic hypoxic response under normoxic conditions. We performed single-colour microarrays to identify the gene expression changes which underpin the hypoxic phenotype. We used 3 biological replicates from both mutant and control, followed by analysis using Limma to identify significant gene expression changes. This work, together with ChIP-seq data for the Hif-1α in von Hippel Lindau mutants, should allow for the Hif-1α dependency of these gene expression changes to be assessed.
2016-03-22 | GSE70885 | GEO
Project description:Intestinal epithelia exist in a uniquely dynamic oxygen tension microenvironment. Adaptive responses to hypoxia in mammalian cells are regulated largely by hypoxia inducible factor (HIF) transcriptional complexes. Functional HIF exists as an obligate alpha/beta heterodimer, comprising both a constitutive subunit (HIF-1beta), and an oxygen-labile regulatory (alpha) component. To date, three regulatory subunits have been identified, namely HIF-1alpha, HIF-2alpha, and HIF-3alpha, with the highest level of sequence homology conserved between HIF-1alpha and HIF-2alpha. Despite their concurrent expression in intestinal epithelial cells, HIF-1 and HIF-2 play non-redundant roles in the regulation of an overlapping but distinct set of gene targets. In this study, we performed ChIP-on-chip analysis of chromatin isolated from hypoxic intestinal epithelia to delineate HIF-1 and HIF-2 specific loci.
2013-11-05 | GSE43108 | GEO