ENCODE: HisH4 ChIP-chip of retinoic acid-stimulated HL60 cells at 4 timepoints (NCBIv35) - strict analysis parameters
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
SUBMITTER: Dione Kampa
PROVIDER: E-GEOD-3659 | biostudies-arrayexpress |
REPOSITORIES: biostudies-arrayexpress
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Project description:H3K9K14D ChIP-chip of retinoic acid-stimulated HL60 cells at 0, 2, 8, or 32 hours using Affymetrix ENCODE tiling chip with NCBI build 35 annotation. H3K9K14D ChIP-chip of retinoic acid-stimulated HL60 cells at 0, 2, 8, or 32 hours.
2010-06-05 | E-GEOD-3658 | biostudies-arrayexpress
Project description:Pol2 ChIP-chip of retinoic acid-stimulated HL60 cells at 0, 2, 8, or 32 hours using Affymetrix ENCODE tiling chip with NCBI build 35 annotation. Pol2 ChIP-chip of retinoic acid-stimulated HL60 cells at 0, 2, 8, or 32 hours.
2010-06-05 | E-GEOD-3660 | biostudies-arrayexpress
Project description:p63 with and without actinomycin D treatment ChIP from retinoic acid stimulated ME180 Cells at 0 hours using Affymetrix ENCODE tiling chip with NCBI build 35 annotation. p63_ActD and p63_mActD ChIP from retinoic acid stimulated ME180 Cells, 0 hours.
2010-06-05 | E-GEOD-3661 | biostudies-arrayexpress
Project description:Identifying the physiological functions of microRNAs (miRNAs) is often challenging because miRNAs commonly impact gene expression under specific physiological conditions through complex miRNA::mRNA interaction networks and in coordination with other means of gene regulation, such as transcriptional regulation and protein degradation. Such complexity creates difficulties in dissecting miRNA functions through traditional genetic methods using individual miRNA mutations. To investigate the physiological functions of miRNAs in neurons, we combined a genetic M-bM-^@M-^\enhancerM-bM-^@M-^] approach complemented by biochemical analysis of neuronal miRNA-induced silencing complexes (miRISCs) in C. elegans. Total miRNA function can be compromised by mutating one of the two GW182 proteins (AIN-1), an important component of miRISC. We found that combining an ain-1 mutation with a mutation in unc-3, a neuronal transcription factor, resulted in an inappropriate entrance into the stress-induced, alternative larval stage known as dauer, indicating a role of miRNAs in preventing aberrant dauer formation. Analysis of this genetic interaction suggests that neuronal miRNAs perform such a role partly by regulating endogenous cyclic guanosine monophosphate (cGMP) signaling, potentially influencing two other dauer-regulating pathways. Through tissue-specific immunoprecipitations of miRISC, we identified miRNAs and their likely target mRNAs within neuronal tissue. We verified the biological relevance of several of these miRNAs and found that many miRNAs likely regulate dauer formation through multiple dauer-related targets. Further analysis of target mRNAs suggests potential miRNA involvement in various neuronal processes, but the importance of these miRNA::mRNA interactions remains unclear. Finally, we found that neuronal genes may be more highly regulated by miRNAs than intestinal genes. Overall, our study identifies miRNAs and their targets, and a physiological function of these miRNAs in neurons. It also suggests that compromising other aspects of gene expression, along with miRISC, can be an effective approach to reveal miRNA functions in specific tissues under specific physiological conditions. Each array was used for one biological replicate, where the red channel is used for IP RNA and the green channel is used for Total RNA. IP RNA indicates the transcripts associated with a neuronally expressed, GFP-tagged, miRISC. Five biological replicates were done on asynchronous worms. Please note the two different microarray platforms that were used.
2014-01-01 | E-GEOD-45871 | biostudies-arrayexpress
Project description:Publication title: Distinct DNA methylation patterns characterize differentiated human embryonic stem cells and developing human fetal liver; To investigate the role of DNA methylation during human development, we developed Methyl-seq, a method that assays DNA methylation at more than 90,000 regions throughout the genome. Performing Methyl-seq on human embryonic stem cells (hESCs), their derivatives and human tissues allowed us to identify several trends during hESC and in vivo liver differentiation. First, differentiation results in DNA methylation changes at a minimal number of assayed regions, both in vitro and in vivo (2-11%). Second, in vitro hESC differentiation is characterized by both de novo methylation and demethylation, whereas in vivo fetal liver development is characterized predominantly by demethylation. Third, hESC differentiation is uniquely characterized by methylation changes specifically at H3K27me3-occupied regions, bivalent domains and low-density CpG promoters (LCPs) suggesting that these regions are more likely to be involved in transcriptional regulation during hESC differentiation. Although both H3K27me3-occupied domains and LCPs are also regions of high variability in DNA methylation state during human liver development, these regions become highly unmethylated, which is a distinct trend from that observed in hESCs. Taken together, our results indicate that hESC differentiation has a unique DNA methylation signature that may not be indicative of in vivo differentiation. Experiment Overall Design: lumina gene expression beadchips of human ES cell lines, ES-derived cells, and normal liver (15 samples). High-throughput sequencing of ES cell lines, ES-derived cells, and fetal and normal livers (17 samples). Raw data: SRA008154 http://www.ncbi.nlm.nih.gov/sites/entrez?db=sra&cmd=search&term=SRA008154
2009-08-29 | E-GEOD-14966 | biostudies-arrayexpress
Project description:To generate a high quality, annotated gene expression database of T. cruzi trypomastigotes(TRP), amastigotes (AMA), epimastigotes (EPI), and metacyclic trypomastigotes (MET). The global assessment of transcript abundances in each life-cycle stage of T. cruzi will identify stage-regulated genes and provide an essential element of an integrated database of T. cruzi genomic, proteomic, and transcriptomic data. RNAs from 3 biological replicates from a single time point in each stage will be subjected to DNA microarrays containing probes for the complete, annotated T. cruzi genome, as it is currently known. The arrays for this project will be provided by the Pathogen Functional Genomics Resource Center (PFGRC) at The Institute for Genomic Research (TIGR) sponsored by the National Institute of Allergy and Infectious Diseases (NIAID), and will contain long oligonucleotides complementary to every annotated gene in the newly sequenced T. cruzi genome. The resulting data and analysis results will be deposited in TcruziDB (http://TcruziDB.org). Keywords: Gene expression comparisons between the four life-cycle stages of T. cruzi Six hybridizations were performed for each life-cycle stage. The hybridizations consisted of three dye-swap experiments from three independent samples (biological replicates). In each case, the experimental sample was from a single life-cycle stage and the control sample was an equal mixture of all four life-cycle stages. A total of 24 hybridizations were preformed.
2010-05-15 | E-GEOD-14641 | biostudies-arrayexpress
Project description:The tumorigenesis of small intestinal neuroendocrine tumors (NETs) is poorly understood. Recent studies have associated alternative polyadenylation with proliferation, cell transformation and cancer. Polyadenylation is the process in which the pre-mRNA is cleaved at a polyA site and a polyA tail is added. Genes with two or more polyA sites can undergo alternative polyadenylation. This produces two or more distinct mRNA isoforms with different 3M-bM-^@M-^Y untranslated regions. Additionally, alternative polyadenylation can also produce mRNAs containing different 3M-bM-^@M-^Y-terminal coding regions. Therefore, alternative polyadenylation alters both the repertoire and the expression level of proteins. Here we used high-throughput sequencing data to map polyA sites and characterize polyadenylation genome-wide in three small intestinal neuroendocrine tumors and a reference sample. In the tumors sixteen genes showed significant changes of alternative polyadenylation pattern, which lead to either the 3M-bM-^@M-^Y truncation of mRNA coding regions or 3M-bM-^@M-^Y untranslated regions. Among these, 11 genes had been previously associated with cancer, with 4 genes being known tumor suppressors: DCC, PDZD2, MAGI1 and DACT2. We validated the alternative polyadenylation in 3 out of 3 cases with Q-RT-PCR. Our findings suggest that changes of alternative polyadenylation pattern in these 16 genes could be involved in the tumorigenesis of small intestinal neuroendocrine tumors. Furthermore, they also point to alternative polyadenylation as a new target for both diagnostic and treatment of small intestinal neuroendocrine tumors. The identified genes with alternative polyadenylation specific to the small intestinal neuroendocrine tumors could be further tested as diagnostic markers and drug targets for disease prevention and treatment. PolyA-seq profiling of 3 human neuroendocrine tumors compared and pituitary using Direct RNA Sequencing from Helicos Biosciences Technology
2014-04-10 | E-GEOD-56657 | biostudies-arrayexpress
Project description:The RNA editing enzyme ADAR chemically modifies adenosine (A) to inosine (I), which is interpreted by the ribosome as a guanosine. Here we assess cotranscriptional A-to-I editing in Drosophila, by isolating nascent RNA from adult fly heads and subjecting samples to high-throughput sequencing. There are a large number of edited sites within nascent exons. Nascent RNA from an ADAR null mutant strain was also sequenced, indicating that almost all A-to-I events require ADAR. Moreover, mRNA editing levels correlate with editing levels within the cognate nascent RNA sequence, indicating that the extent of editing is set cotranscriptionally. Surprisingly, the nascent data also identify an excess of intronic over exonic editing sites. These intronic sites occur preferentially within introns that are poorly spliced cotranscriptionally, suggesting a link between editing and splicing. We conclude that ADAR-mediated editing is more widespread than previously indicated and largely occurs cotranscriptionally. GSM914095: Fly genomic DNA sequencing. Sequenced on the Illumina GA II. GSM914102-GSM914113: Fly head nascent RNA profiles over 6 time points of a 12hr light:dark cycle in duplicate; sequenced on the Illumina GA II. GSM914114-GSM914119: Fly head nascent RNA profiles of yw, FM7, ADAR0 males in duplicate; sequenced on the HiSeq2000. GSM915213-GSM915214: Fly head mRNA profiles over 2 time points of a 12hr light:dark cycle; sequenced on the Illumina GA II. GSM915215-GSM915220: Fly head mRNA profiles over 6 time points of a 12hr light:dark cycle; paired-end sequenced on the Illumina GA II. GSM915221-GSM91526: Fly head mRNA profiles over 6 time points of a 12hr light:dark cycle; sequenced on the Illumina GA II.
2012-05-31 | E-GEOD-37232 | biostudies-arrayexpress
Project description:Gene regulation by microRNAs (miRNAs) under specific physiological conditions often involves complex interactions between multiple miRNAs and a large number of their targets, as well as coordination with other regulatory mechanisms, limiting the effectiveness of classical genetic methods to identify miRNA functions. We took a systematic approach to analyze the miRNA-induced silencing complex (miRISC) in individual tissues of C. elegans and found that mRNAs encoded by pathogen-responsive genes were dramatically over-represented in the intestinal miRISC, and that multiple miRNAs accumulated in the intestinal miRISCs upon infection. Inactivation of the miRISC or ablation of miRNAs from different families, resulted in over-expression of several pathogen-responsive genes under basal conditions and, surprisingly, enhanced worm survival on pathogenic Pseudomonas aeruginosa. These results indicate that much of the miRNA activity in the gut is dedicated to attenuating the activity of the pathogen response system, uncovering a novel and complex physiological function of the miRNA network. Each array was used for one biological replicate of a given experiment. One channel was used to probe Total RNA, the other was for IP RNA. Channels were swapped between biological replicates. 4 biological replicates for each asynchronous intestine IPs, 4 biological replicates for asynchronous muscle IP, 5 biolgoical replicates for L4 intestine IP, and two new biological replicates for the GFP control IP (previous biological replicates can be found in GSE9073: GSM230865-GSM2308657 and GSM230873-GSM230875).
2012-03-23 | E-GEOD-36419 | biostudies-arrayexpress
Project description:Synthetic DNA-binding proteins have found broad application in gene therapies and as tools for interrogating biology. Engineered proteins based on the CRISPR/Cas9 and TALE systems have been used to alter genomic DNA sequences, control transcription of endogenous genes, and modify epigenetic states. Although the activity of these proteins at their intended genomic target sites have been assessed, the genome-wide effects of their action have not been extensively characterized. Additionally, the role of chromatin structure in determining the binding of CRISPR/Cas9 and TALE proteins to their target sites and the regulation of nearby genes is poorly understood. Characterization of the activity these proteins using modern high-throughput genomic methods would provide valuable insight into the specificity and off-target effects of CRISPR- and TALE-based genome engineering tools. We have analyzed the genome-wide effects of TALE- and CRISPR-based transcriptional activators targeted to the promoters of two different endogenous human genes in HEK293T cells using a variety of high-throughput DNA sequencing methods. In particular, we assayed the DNA-binding specificity of these proteins and their effects on the epigenome. DNA-binding specificity was evaluated by ChIP-seq and RNA-seq was used to measure the specificity of these activators in perturbing the transcriptome. Additionally, DNase-seq was used to identify the chromatin state at target sites of the synthetic transcriptional activators and the genome-wide chromatin remodeling that occurs as a result of their action. Our results show that these genome engineering technologies are highly specific in both binding to their promoter target sites and inducing expression of downstream genes when multiple activators bind to a single promoter. Moreover, we show that these synthetic activators are able to induce the expression of silent genes in heterochromatic regions of the genome by opening regions of closed chromatin and decreasing DNA methylation. Interestingly, the transcriptional activation domain was not necessary for DNA-binding or chromatin remodeling in these regions, but was critical to inducing gene expression. This study shows that these CRISPR- and TALE-based transcriptional activators are exceptionally specific. Although we detected limited binding of off-target sites in the genome and changes to genome structure, these off-target event did not lead to any detectable changes in gene regulation. Collectively, these results underscore the potential for these technologies to make precise changes to gene expression for gene and cell therapies or fundamental studies of gene function. HEK293T cells were transfected in triplicate with plasmids expressing synthetic transcription factors. The synthetic TFs were either (a) dCas9-VP64 fusion protein and a targeting guide RNA (gRNA), or (b) a TALE-VP64 fusion protein engineered to bind to a specific target site in the genome. As a control, cells were transfected with plasmids expressing GFP. After transfection, ChIP-seq was used to identify both on-target and off-target binding sites for the synthetic TFs.
2015-04-24 | E-GEOD-57085 | biostudies-arrayexpress