ChIP-chip from human liver cancer cells with HIF-2a
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
SUBMITTER: Haixiang Sun
PROVIDER: E-GEOD-37167 | biostudies-arrayexpress |
REPOSITORIES: biostudies-arrayexpress
Similar Datasets
Project description:Chromatin immunoprecipitation on microarrays (ChIP-chip) has been widely used to investigate the DNA binding sites for a variety of proteins such as histone and transcription factors on a genome-wide scale. The purpose of this study is to evaluate the status of histone H3 lysine 9 trimethylation in salivary gland adenoid cystic carcinoma.
2014-11-04 | E-MTAB-3053 | biostudies-arrayexpress
Project description:The H3K27me3 is a repressive histone mark associated with repressive chromatin and is important for X chromosome inactivation. ChIP-chip of H3K27me3 along the mouse X chromosome in male and female livers and p12.5 embryos demonstrated that H3K27me3 is absent at the genes that escape X inactivation. Comparison of H3K27me3 enrichment along the X chromosome in male and female adult livers and P12.5 embryos
2010-03-04 | E-GEOD-20617 | biostudies-arrayexpress
Project description:Emerging evidences indicate that microRNAs (miRNAs) are often deregulated and have fundamental roles in hepatocellular carcinoma (HCC). However, the mechanism underlying miRNA dysregulation in HCC is still elusive. In this report, we used an integrated analysis strategy combining methylated DNA immunoprecipitation chip (MeDIP-chip) and miRNA expression microarray data to study the correlation between aberrant methylation and dysregulation of miRNA in HCC. In all, we showed that global miRNA methylation profiles were significantly different between cancerous and normal hepatocytes, and abnormal methylation was an important mechanism governing miRNA expression in HCC. MeDIP-chip was processed in cancerous hepatocytes SK-HEP-1, HepG2, MHCC97-H and normal hepatocytes PHHC-4-1, PHHC-4-2, PHHC-4-3 (3 technical repeat of PHHC-4). MiRNA microarray were processed for cancerous hepatocytes SK-HEP-1, HepG2, Hep3B, Huh7, MHCC97-H, MHCC97-L, SMMC-7721 and normal hepatocytes PHHC-1, PHHC-2, PHHC-3. Then an integrated analysis strategy combining MeDIP-chip and miRNA expression microarray [GSE20077] were used to study the correlation of aberrant DNA methylation and dysregulation of miRNAs.
2015-08-05 | E-GEOD-49554 | biostudies-arrayexpress
Project description:Changes in gene expression contribute to the long-lasting regulation of the brain's reward circuitry seen in drug addiction, however, the specific genes regulated and the transcriptional mechanisms underlying such regulation remain poorly understood. Here, we used chromatin immunoprecipitation coupled with promoter microarray analysis to characterize genome-wide epigenetic changes in the mouse nucleus accumbens, a crucial brain reward region, after repeated cocaine administration. Our findings reveal several interesting principles of gene regulation by cocaine and of the role of Î?FosB and CREB, two prominent cocaine-induced transcription factors, in this brain region. Mice were treated with cocaine or saline. Chromatin immunoprecipitation was performed for acetylated histone H3 and H4 as described previously (Kumar et al., 2005) with minor modifications. Immunoprecipitated DNA was amplified via ligation-mediated PCR and hybridized to Nimblgen mouse MM5 promoter arrays. 2 biological replicates per condition.
2010-05-18 | E-GEOD-16183 | biostudies-arrayexpress
Project description:Changes in gene expression contribute to the long-lasting regulation of the brain's reward circuitry seen in drug addiction, however, the specific genes regulated and the transcriptional mechanisms underlying such regulation remain poorly understood. Here, we used chromatin immunoprecipitation coupled with promoter microarray analysis to characterize genome-wide epigenetic changes in the mouse nucleus accumbens, a crucial brain reward region, after repeated cocaine administration. Our findings reveal several interesting principles of gene regulation by cocaine and of the role of Î?FosB and CREB, two prominent cocaine-induced transcription factors, in this brain region. Mice were treated with cocaine or saline. Chromatin immunoprecipitation was performed for methylated histone H3 lysine 9 and 27, â??FosB, and phospho-CREB as described previously (Kumar et al., 2005) with minor modifications. Immunoprecipitated DNA was amplified via ligation-mediated PCR and hybridized to Nimblgen mouse MM8 promoter arrays. 2-3 biological replicates per condition.
2010-05-18 | E-GEOD-16184 | biostudies-arrayexpress
Project description:This SuperSeries is composed of the following subset Series: GSE16183: Genome-Wide Promoter Analysis of Epigenetic Regulation by Cocaine (MM5 data) GSE16184: Genome-Wide Promoter Analysis of Epigenetic Regulation by Cocaine (MM8 data) Refer to individual Series
2010-05-19 | E-GEOD-15968 | biostudies-arrayexpress
Project description:The Polycomb repressive complex 2 (PRC2) is important for the maintenance of stem cell pluripotency and suppression of cell differentiation by promoting histone H3 lysine 27 trimethylation (H3K27me3) and silencing expression of genes regulating differentiation. Here we show decreased expression of BRCA1 promotes EZH2 re-targeting genome wide and enhances H3K27me3 levels at PRC2 target loci in mouse ES cells. R1 mouse ES cells were transfected with control siRNA and Brca1 specific siRNA. At 48h after transfection, cells were harvested and subjected to ChIP assay with Ezh2 antibody. Brca1 wild-type (AB2.2) and Brca1 deficient (PL2F8) mouse ES cells were harvested and subjected to ChIP assay with Ezh2 antibody. Fragmented DNA obtained from ChIP assay was repaired by DNA Terminator End Repair Kit (Lucigen Corporation, Middleton, WI) and purified by QIAquick PCR purification kit. Then two unidirectional linkers JW102 and JW103 were annealed and ligated to the blunt ends DNA at 16M-BM-0C overnight. The purified products were amplified to 2 M-NM-<g by LM-PCR. NimbleGen Mouse ChIP 3x720K RefSeq Promoter Array (Roche) were used for the hybridization. Relative enrichments were calculated by dividing the normalized level of ChIP DNA to that of input DNA at corresponding locus. Labeling, hybridization and washing were carried out according to manufacturerM-bM-^@M-^Ys instructions. Experiments in AB2.2 and PL2F8 cells were performed in duplicate.
2013-07-01 | E-GEOD-37321 | biostudies-arrayexpress
Project description:The transcription factor HIF-2a play an important role in the tumor progress, the aim is to explore the target genes of HIF-2a in liver cancer cell line. Chromatin immunoprecipitation (ChIP) of HIF-2a together with chromatin profiling by ChIP-on-chip analysis demonstrated that HIF-2a directly activates many target genes.
2012-04-12 | GSE37167 | GEO
Project description:HIF-1A and HIF-2A regulate both overlapping and unique target genes in response to hypoxia. In this dataset, we identify specific HIF-1A and HIF-2A target genes in glioblastoma cells. 12 samples were analysed comprising 4 experimental conditions (normoxia scr, hypoxia scr, hypoxia siHIF1, hypoxia siHIF2) in triplicate. We made pairwise comparisons between the averages of each triplicate set to normoxia scr using the Partek suite.
2012-02-25 | E-GEOD-27523 | biostudies-arrayexpress
Project description:GSK3b signaling has been implicated in the pathophysiology of bipolar affective disorder based on the inhibitory effect of lithium salts on this pathway. This has been supported by a recent genome wide association study. In addition, GSK3b signaling may also play a role in schizophrenia, an idea that is based on the finding that the protein encoded by the schizophrenia candidate gene DISC1 inhibits GSK3b. Gene expression is affected by GSK3b signaling through the activation of the transcription factor b-catenin, which modulates expression through a protein-protein binding interaction with members of the TCF/LEF family. To identify genes targeted by GSK3b/b-catenin, investigators have used expression profiling in lithium treated cells and animals. Gene knockdown and transfection are other experimental methodologies one can employ. However, these approaches are not possible using human brain tissue. Consequently, we used ChIP-chip to identify promoters bound by b-catenin as an indirect method for identifying genes targeted by GSK3b. Fetal brain was used because schizophrenia is viewed as a neurodevelopmental disorder. In addition, fetal brain tissue is not affected by the confounding factors associated with postmortem tissue (postmortem delay, cause of death, brain pH, use of medication and other environmental factors). We carried out two complete promoter array hybridizations on different biological isolates using the 385K two-Array Human Promoter Set developed by Nimblegen/Roche. Significant enrichment for b-catenin immunoprecipitates was determined in each experiment if the log2 ratio of signal obtained for the b-catenin antibody compared with control was below an FDR<0.2 using NimbleScan. NimbleScan reports three different levels of enrichment (peaks) based on the FDR score, as described in methods. Since whole brain tissue was used in these experiments, we chose the least conservative FDR (<0.2) to reduce the type II error (false negative) rate, which could be caused by enrichment at some promoters in a subset of cells being diluted by the absence of b-catenin immunoprecipitates at those loci in other cells. A total of 640 gene promoters showed evidence for b-catenin binding on two arrays. We validated enrichment at 9 gene promoters using real time PCR. The 640 genes are analyzed using SLEP (Sullivan Lab Evidence Project, http://slep.unc.edu). Analysis of the SLEP database was restricted to genome wide association studies (GWAS) and copy number variants (CNVs) in ASD, BD and SZ. In addition, a gene was scored as a potential candidate if it fell within a linkage peak or if multiple positive association studies were found upon a candidate gene analysis. Promoters for 24 genes implicated in these disorders were targeted by b-catenin. Of these, a total of 16 genes are very strong candidates based on unbiased genome-wide surveys (GWAS and CNV screening). The other 8 have been implicated by linkage analysis and candidate gene analysis, which are the least robust genetic methods for targeting specific genes in psychiatric disorders. We carried out a similar analysis on 640 genes that did not show evidence for enrichment in the b-catenin ChIP-chip. Only 5 genes were found, none of which are GWAS or CNV targets. Based on the finding that five candidate genes were found in a group of 640 randomly selected genes, while 24 were identified in the ChIP-chip experiment, the binding of b-catenin to schizophrenia and bipolar disorder candidate gene promoters is highly significant (p = 6.5 x 10-12). The findings suggest that many seemingly disparate candidate genes for psychiatric disorders can be grouped into the GSK3b/b-catenin signaling pathway. The results could also have therapeutic implications in helping to identify bipolar patients who respond best to lithium, as well as identify patients with schizophrenia who might benefit from the drug. Immunoprecipitates were generated with an antibody to b-Catenin
2010-04-01 | E-GEOD-21151 | biostudies-arrayexpress