Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA187981 | ENA |
REPOSITORIES: ENA
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Project description:PcG and TrxG are important epigenetic regulators of genome expression. Here we have determined genomic distributions of TRX, ASH1, RNA Pol II, H3K4me3, H3K27ac, H3K9ac in cultured Drosophila Sg4 cells by hybridization of ChIP products with tiling microarrays.
2010-01-08 | GSE18176 | GEO
Project description:Release of promoter-proximal paused RNA polymerase II (Pol II) during early elongation is a critical step in transcriptional regulation in metazoan cells. Paused Pol II release is thought to require the kinase activity of cyclin-dependent kinase 9 (CDK9) for the phosphorylation of DRB sensitivity-inducing factor, negative elongation factor, and C-terminal domain (CTD) serine-2 of Pol II. We found that Pol II-associated factor 1 (PAF1) is a critical regulator of paused Pol II release, that positive transcription elongation factor b (P-TEFb) directly regulates the initial recruitment of PAF1 complex (PAF1C) to genes, and that the subsequent recruitment of CDK12 is dependent on PAF1C. These findings reveal cooperativity among P-TEFb, PAF1C, and CDK12 in pausing release and Pol II CTD phosphorylation. Comparison of the chromatin occupancy of [1] PAF1, CDC73, LEO1, CTR9, total Pol II, and CTD serine 2-phosphorylated Pol II by ChIP-seq in THP1 cells; [2] PAF1, Pol II, Pol II (ser-5p), CDK12, and CDK9 by ChIP-seq in control and PAF1 knockdown cells; [3] LEO1 and Pol II by ChIP-seq in control and flavopiridol treated THP1 cells.
2015-12-11 | E-GEOD-62171 | biostudies-arrayexpress
Project description:The transition from transcription initiation to elongation is a key regulatory step in gene expression, which requires RNA polymerase II (Pol II) to escape promoter proximal pausing on chromatin. While elongation factors promote pause release leading to transcription elongation, the role of epigenetic modifications during this critical transition step is poorly understood. Two histone marks on histone H3, lysine 4 trimethylation (H3K4me3) and lysine 9 acetylation (H3K9ac), co-localize on active gene promoters and are associated with active transcription. H3K4me3 can promote transcription initiation, yet the functional role of H3K9ac is much less understood. We hypothesized that H3K9ac may function downstream of transcription initiation by recruiting specific proteins important for the next step of transcription. Here, we describe a functional role for H3K9ac in promoting Pol II pause release by directly recruiting the super elongation complex (SEC) to chromatin. H3K9ac serves as a substrate for direct binding of the SEC, as does acetylation of histone H4 lysine 5 (H4K5ac), to a lesser extent. Furthermore, lysine 9 on histone H3 is necessary for maximal Pol II pause release through SEC action, and loss of H3K9ac increases the Pol II pausing index on a subset of genes in HeLa cells. At select gene promoters, loss of H3K9ac or depletion of the SEC reduces gene expression and increases paused Pol II occupancy. We therefore propose that an ordered histone code drives progression through the transcription cycle, providing new mechanistic insight that SEC recruitment to certain acetylated histones promotes the subsequent release of paused Pol II needed for transcription elongation.
2017-07-11 | GSE99998 | GEO
Project description:This SuperSeries is composed of the following subset Series: GSE36084: Gene expression data from human lymphocytes GSE36397: ChIP-chip of monocytes using H3K9Ac, H3K4me3, H3K9me2 and H4K16Ac antibodies GSE36402: ChIP-chip of lymphocytes using H3K9Ac, H3K4me3, H3K9me3, H3K27me3 and H4K16Ac antibodies Refer to individual Series
2012-05-31 | E-GEOD-36403 | biostudies-arrayexpress
Project description:We report ChIP-Seq analysis of the RNA polyemerase I trascription factor UBF1/2 in NIH3T3, HMEC and HMLER cell lines. NIH3T3* samples: We correlated UBF1/2 binding across the genome with that of RNA polemerase I (Pol I), RNA polemerase II (Pol II) and chromatin states in NIH3T3 cells We perfromed ChIP-seq of UBF1/2 (2 biological replicates), Pol I (POLR1A/RPA194), Pol II, H3K9me3, H3K4Me3, H3K9ac, H4 hyperacetylation and genomic DNA input as reference. HMEC* samples: We report ChIP-Seq analysis of UBF1/2 and Pol I (POLR1A/RPA194) in human mammary epithelial cells (HMEC). In addition we include UBF1/2 ChIP-seq in the tumourigenic epithelial cell line HMLER. In this study, we compared UBF1/2 binding in HMEC to UBF1/2 binding in in the tumorigenic HMLER cells, an isogenic HMEC-derived cell line expressing the SV40 large-T, TERT, and an oncogenic allele of the HRAS gene (expressing HRASV12G) that forms tumors in nude mice (Elenbaas et al., Gene & Development 2001) We sequenced UBF1/2 ChIP and Pol I(POLR1A/RPA194) ChIP and gDNA input from HMEC. We sequenced UBF1/2 ChIP and gDNA input from HMLER
2014-11-14 | E-GEOD-63255 | biostudies-arrayexpress
Project description:Alternative splicing is a promising therapeutic target in acute lymphoblastic leukemia. Here, we report the alternative splicing changes in B-ALL cell lines including NALM6 cells and MUTZ-5 cells treated with DYRK1 inhibitor, EHT 1610 and GNF 2133. Dysregulation of co-transcriptional splicing is a therapeutic target in acute lymphoblastic leukemia (ALL). Here, we detected the alternative splicing in NALM6 cells or MUTZ-5 cells treated with EHT 1610 or GNF2133. We detected the alternative splicing in NALM6 cells cells treated with THAL-SNS-032. We also determined the alternative splicing in MEF2D-BCL9 ALL and MEF2D-HNRNPUL1 ALL patient xenografted samples treated with E7820, a anticancer sulfamide, or DMSO. Furthermore, ChIP-seq for RNA polymerase II (Pol II), p-Ser2 Pol II, and p-Ser5 Pol II were performed after DMSO or EHT 1610 treatment in NALM6 cells. ChIP-seq for p-Ser2 Pol II, and p-Ser5 Pol II were performed after DMSO or THAL-SNS-032 treatment in NALM6 cells.PRO-seq in NALM6 cells treated with DMSO, EHT 1610, and THAL-SNS-032 were performed.
2024-09-09 | GSE252550 | GEO
Project description:We have discovered distinctive protein interactomes for Ser2 and Ser5 phosphorylation of the C-terminal domain (CTD) of RNA Pol II. Calcium Homeostasis Endoplasmic reticulum (CHERP) was identified in our pulldown to directly interact with Ser2 phosphomarks on the CTD of Pol II. As Pol II is a chromatin-associated protein, we sought to identify genomic regions that CHERP, a Pol II binding protein, occupy through ChIP-seq analysis.
2023-08-17 | GSE226908 | GEO
Project description:ChIP-chip of monocytes using H3K9Ac, H3K4me3, H3K9me2 and H4K16Ac antibodies
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Project description:pNET-seq (Pol II Ser5) in Arabidopsis
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Project description:Whole genome analysis of total RNA pol II, Ser2-, Ser5- and Ser7-phosphorylated RNA pol II, in WT and mutants of the C-terminal domain (CTD) kinases Ctk1 and Kin28, and localization of the termination factors Pcf11, Nrd1 and Rat1. ChIP-chip using ligation-mediated PCR-amplified material hybridized to NimbleGen 385K arrays (50mers, median probe spacing 32 bp, cat. No. C4214-00-01).
2010-09-15 | E-GEOD-23960 | biostudies-arrayexpress