Homo sapiens strain:K562
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ABSTRACT:
PROVIDER: PRJDB13680 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:We report the results of chromatin immunoprecipitation following by high-thoughput tag sequencing (ChIP-Seq) using the GA II platform from Illumina for the human RNA Polymerase III in K562 cells. We have also generated a sequenced input DNA datasets for K562 cells. For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODEDataReleasePolicyFinal2008.pdf Map binding sites of RNA Polymerase III in the genome of K562 cells. The K562 input data has been deposited in GEO as GSM325934.
2009-12-31 | E-GEOD-19548 | biostudies-arrayexpress
Project description:CLIP-seq analysis of Myc-tagged DDX41 on K562 leukemia cell-line.
| PRJDB11668 | ENA
Project description:Transcription profiling of two cancer cell lines: K562 and U937. It has recently been shown that nucleosome distribution, histone modifications and RNA polymerase II (Pol II) occupancy show preferential association with exons ("exon-intron marking"), linking chromatin structure and function to co- transcriptional splicing in a variety of eukaryotes. Previous ChIP-sequencing studies suggested that these marking patterns reflect the nucleosomal landscape. By analyzing ChIP-chip datasets across the human genome in three cell types, we have found that this marking system is far more complex than previously observed. We show here that a range of histone modifications and Pol II are preferentially associated with exons. However, there is noticeable cell-type specificity in the degree of exon marking by histone modifications and, surprisingly, this is also reflected in some histone modifications patterns showing biases towards introns. Exon-intron marking is laid down in the absence of transcription on silent genes, with some marking biases changing or becoming reversed for genes expressed at different levels. Furthermore, the relationship of this marking system with splicing is not simple, with only some histone modifications reflecting exon usage/inclusion, while others mirror patterns of exon exclusion. By examining nucleosomal distributions in all three cell types, we demonstrate that these histone modification patterns cannot solely be accounted for by differences in nucleosome levels between exons and introns. In addition, because of inherent differences between ChIP-chip array and ChIP-sequencing approaches, these platforms report different nucleosome distribution patterns across the human genome. Our findings confound existing views and point to active cellular mechanisms which dynamically regulate histone modification levels and account for exon-intron marking. We believe that these histone modification patterns provide links between chromatin accessibility, Pol II movement and co-transcriptional splicing.
2010-12-03 | E-MTAB-335 | biostudies-arrayexpress
Project description:As Integrator is tightly associated with RNAPII-CTD, it is critical to understand how the RNAPII engaged and conducted within the active gene promoter for divergent transcription. We thus employed RNAPII ChIP-seq (Chromatin Immuno-precipitation with RNAPII antibody) to determine the distribution of the total RNAPII and its phosphorylation isoforms. Total RNA polymerase II and its carbon terminal phosphorylation(RNA polymerase II-ctd-Tyr-1，RNA polymerase II-ctd-ser-2) before and after INTS11 knockdown in HCT116-INTS11-AID cells changes chromatin immunoprecipitation DNA sequencing (ChIP-seq).
2023-07-25 | GSE207269 | GEO
Project description:To investigate changes in the elongating form of RNA Polymerase II across different conditions, we peformed ChIP-seq using antibody against the Ser2P RNAPII of pTEFb in K562 cells at 4 days after modified allele expression We then performed coverage plot analyses using data obtained from ChIP-seq from IP and Input fractions to investigate Ser2P RNAPII distribution changes
2024-03-12 | GSE225995 | GEO
Project description:To investigate changes in the elongating form of RNA Polymerase II across different conditions, we peformed ChIP-seq using antibody against the Ser5P RNAPII of pTEFb in K562 cells at 4 days after modified allele expression We then performed coverage plot analyses using data obtained from ChIP-seq from IP and Input fractions to investigate Ser5P RNAPII distribution changes
2024-03-12 | GSE254791 | GEO
Project description:We report the results of chromatin immunoprecipitation following by high-thoughput tag sequencing (ChIP-Seq) using the GA II platform from Illumina for the human RNA Polymerase III in K562 cells. We have also generated a sequenced input DNA datasets for K562 cells. For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODEDataReleasePolicyFinal2008.pdf
2009-12-31 | GSE19548 | GEO
Project description:Chromatin immunoprecipitation microarray (ChIP-chip) study using 3 human cell lines (K562, U937, CD14+); of 19 histone modifications across 1% of the human genome used in the pilot phase of the ENCODE project.<br>paper abstract: It has recently been shown that nucleosome distribution, histone modifications and RNA polymerase II (Pol II) occupancy show preferential association with exons ("exon-intron marking"), linking chromatin structure and function to co- transcriptional splicing in a variety of eukaryotes. Previous ChIP-sequencing studies suggested that these marking patterns reflect the nucleosomal landscape. By analyzing ChIP-chip datasets across the human genome in three cell types, we have found that this marking system is far more complex than previously observed. We show here that a range of histone modifications and Pol II are preferentially associated with exons. However, there is noticeable cell-type specificity in the degree of exon marking by histone modifications and, surprisingly, this is also reflected in some histone modifications patterns showing biases towards introns. Exon-intron marking is laid down in the absence of transcription on silent genes, with some marking biases changing or becoming reversed for genes expressed at different levels. Furthermore, the relationship of this marking system with splicing is not simple, with only some histone modifications reflecting exon usage/inclusion, while others mirror patterns of exon exclusion. By examining nucleosomal distributions in all three cell types, we demonstrate that these histone modification patterns cannot solely be accounted for by differences in nucleosome levels between exons and introns. In addition, because of inherent differences between ChIP-chip array and ChIP-sequencing approaches, these platforms report different nucleosome distribution patterns across the human genome. Our findings confound existing views and point to active cellular mechanisms which dynamically regulate histone modification levels and account for exon-intron marking. We believe that these histone modification patterns provide links between chromatin accessibility, Pol II movement and co-transcriptional splicing.
2010-12-29 | E-MTAB-334 | biostudies-arrayexpress
Project description:We performed ChIP-Seq analysis with an antibody against RNA polymerase II (Pol II). We found that the distribution of Pol II signals was decreased at the transcription start sites (TSSs) and transcription end sites (TESs) upon depletion of NKAP.
2023-07-01 | GSE229412 | GEO