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E-GEOD-34871 - Genome-wide mapping of HIF-2 binding in 786-O clear cell renal carcinoma cells

Released on 1 February 2012, last updated on 11 March 2013
Homo sapiens
Samples (3)
Protocols (6)
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.
Experiment type
David Robert Mole <>, David R Mole, Johannes Schoedel
Common genetic variants at the 11q13.3 renal cancer susceptibility locus influence binding of HIF to an enhancer of cyclin D1 expression. Sch�del J, Bardella C, Sciesielski LK, Brown JM, Pugh CW, Buckle V, Tomlinson IP, Ratcliffe PJ, Mole DR. , PMID:22406644
Exp. designProtocolsVariablesProcessedSeq. reads
Investigation descriptionE-GEOD-34871.idf.txt
Sample and data relationshipE-GEOD-34871.sdrf.txt
Processed data (1)