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PARP-1, H3 and H3K4me3 ChIP-chip from MCF7 cells

ABSTRACT: We are examining the mechanisms by which the nuclear enzyme PARP-1 regulates gene expression. We performed ChIP-chip for PARP-1, histone H3 and H3K4me3 (lysine 4 trimethylation on histone H3) in MCF7 breast carcinoma cells, and looked at 23550 RefSeq genes to determine binding patterns of these factors at promoters. Each experiment was performed in duplicate. ChIP-chip biological replicates for PARP-1, H3 and H3K4me3 (2 replicates each) from MCF7 human breast carcinoma cells are included.

ORGANISM(S): Homo sapiens

SUBMITTER: Lee Kraus

PROVIDER: E-GEOD-19619 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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PARP-1 regulates chromatin structure and transcription through a KDM5B-dependent pathway.

Krishnakumar Raga R Kraus W Lee WL

Molecular cell 20100901 5

PARP-1 is an abundant nuclear enzyme that regulates gene expression, although the underlying mechanisms are unclear. We examined the interplay between PARP-1, histone 3 lysine 4 trimethylation (H3K4me3), and linker histone H1 in the chromatin-dependent control of transcription. We show that PARP-1 is required for a series of molecular outcomes at the promoters of PARP-1-regulated genes, leading to a permissive chromatin environment that allows loading of the RNA Pol II machinery. PARP-1 does so ...[more]

PMID: 20832725

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ERalpha ChIP-chip from HeLA-ER cells treated with E2

Project description:We are studying the mechanisms by which the estrogen receptor, ERalpha, is recruited to and regulates genes with a non-direct DNA binding. We performed ChIP-chip for ERalpha in E2 treated HeLa-ER cells, and looked at 19000 RefSeq genes to determine binding patterns of the receptor at promoters. The experiment was performed in duplicate. ChIP-chip biological replicates for Eralpha in E2 treated HeLa-ER cells are included.

2011-02-22 | E-GEOD-22099 | biostudies-arrayexpress

MacroH2A1 ChIP-chip

Project description:MacroH2A1 ChIP-chip was performed on custom Nimblegen genomic tiling arrays, to understand the genomic binding patterns of this histone variant and its relationship to gene expression Keywords: ChIP-chip Two macroH2A biological replicates are included. An H3 ChIP-chip sample is included as a control

2010-10-08 | E-GEOD-9607 | biostudies-arrayexpress

Homo sapiens

Project description:PARP-1, H3 and H3K4me3 ChIP-chip from MCF7 cells

| PRJNA122571 | ENA

PARP-1, H3 and H3K4me3 ChIP-chip from MCF7 cells

Project description:We are examining the mechanisms by which the nuclear enzyme PARP-1 regulates gene expression. We performed ChIP-chip for PARP-1, histone H3 and H3K4me3 (lysine 4 trimethylation on histone H3) in MCF7 breast carcinoma cells, and looked at 23550 RefSeq genes to determine binding patterns of these factors at promoters. Each experiment was performed in duplicate.

2010-09-20 | GSE19619 | GEO

MacroH2A1 ChIP-seq from IMR90 human primary lung fibroblasts

Project description:The histone variant macroH2A1 and the poly(ADP-ribose) polymerase PARP-1 both regulate gene transcription by modulating chromatin structure and function. Of the two macroH2A1 splice variants, macroH2A1.1 and macroH2A1.2, the former is often suppressed in cancer and has the unique ability to interact with poly(ADP-ribose). Using ChIP-seq in primary lung fibroblasts, we demonstrate that macroH2A1 is incorporated into either of two spatially and functionally distinct types of chromatin; the first is marked by H3 K27 trimethylation, while the second contains a set of nine histone acetylations. MacroH2A1-regulated genes are involved in cancer progression are specifically found in macroH2A1-containing acetylated chromatin. Through the recruitment of PARP-1, macroH2A1.1 promotes the acetylation of H2B K12 and K120 which plays a key role in the regulation of macroH2A1 target genes in primary cells. The macroH2A1/PARP-1 pathway regulating H2B K12 and K120 acetylation is disrupted in cancer cells, in part, explaining macroH2A1M-bM-^@M-^Ys role in cancer suppression. Two biological replicates of the macroH2A1 ChIP and two corresponding input samples were sequenced

2014-09-15 | E-GEOD-54845 | biostudies-arrayexpress

Examination of functional interplay between NMNAT-1 (a nuclear NAD+ synthase) and PARP-1 (a nuclear poly(ADP-ribose) polymerase)

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2012-02-15 | E-GEOD-35358 | biostudies-arrayexpress

Postrecruitment Regulation of RNA Pol II Directs Rapid Signaling Responses at the Promoters of Estrogen Target Genes

Project description:Under current models for signal-dependent transcription in eukaryotes, DNA-binding activator proteins regulate the recruitment of RNA polymerase II (Pol II) to a set of target promoters. Yet, recent studies, as well as our results herein, show that Pol II is widely distributed (i.e., "preloaded") at the promoters of many genes prior to specific signaling events. How Pol II recruitment and Pol II preloading fit within a unified model of gene regulation is unclear. In addition, the mechanisms through which cellular signals activate preloaded Pol II across mammalian genomes remain largely unknown. Here we show that the predominant genomic outcome of estrogen signaling is the post-recruitment regulation of Pol II activity through phosphorylation, rather than recruitment of Pol II. Furthermore, we show that negative elongation factor (NELF) binds to estrogen target promoters in conjunction with preloaded Pol II and represses gene expression until the appropriate signal is received. Finally, our studies reveal that the estrogen-dependent activation of preloaded Pol II facilitates rapid transcriptional and post-transcriptional responses which play important physiological roles in regulating estrogen signaling itself. Our results reveal a broad use of post-recruitment Pol II regulation by the estrogen signaling pathway, a mode of regulation that is likely to apply to a wide variety of signal-regulated pathways. ChIP-chip analysis for RNA Pol II, Ser5 phosphorylated RNA Pol II and NELF-A in MCF7 breast cancer cells.

2010-05-14 | E-GEOD-13051 | biostudies-arrayexpress

H3Cit26 ChIP-chip from MCF-7 cells

Project description:Estrogen receptor M-NM-1 (ER), a member of the nuclear hormone receptor superfamily, regulates transcriptional activity by ligand-dependent recruitment of cofactors which, in turn, locally alter chromatin structure. It is generally believed that co-factor activity at target promoters leads to a more open, transcriptionally permissive chromatin structure, however, these mechanisms remain to be fully established. Peptidylarginine deiminases (PADIs) catalyze the conversion of positively charged arginine and methylarginine residues to neutrally charged citrulline and this activity has been linked to the gene regulation. Here, we found that PADI2 citrullinate H3 Arginine 26 (H3R26) in vitro and, using a specific H3R26 citrulline (H3Cit26) antibody, we demonstrate that H3Cit26 occurs in vivo following 17M-NM-2-estradiol (E2) stimulation and this unique and pronounced global activation of H3Cit26 is ER-dependent. Using a mammalian-based promoter chromosomal array system, we observed that citrullination at H3R26 is robust and co-localizes with ER at decondensed chromatin loci. Additionally, this histone modification is specifically enriched at ER bound regions of target promoters, forming a permissive chromatin environment for gene transactivation. Interestingly, we have shown in a reciprocal way, that either depletion of PADI2 or inhibition of ER not only dramatically abolished E2-induced activation of H3Cit26 on gene promoters but also affect ER recruitment. Collectively, our results demonstrate that citrullination of H3R26 by PADI2 following estrogen stimulation plays a role in ER target gene activation, likely via decondensation of the local chromatin architecture. Two H3Cit26 ChIP-chip biological replicates under vehicle treatment and two H3Cit26 ChIP-chip biological replicates under E2 stimulation from MCF-7 human breast cancer cells are included.

2012-09-04 | E-GEOD-32599 | biostudies-arrayexpress

PELP1 ChIP-chip from MCF-7 cells

Project description:Proline-, glutamic acid-, and leucine-rich protein 1 (PELP1) is a transcriptional coactivator that has previously been shown to collaborate with nuclear receptors. Evidence from other groups suggest that PELP1 may stimulate transcription by displacing the linker histone H1 and/or by recruiting the lysine demethylase KDM1 to demethylate H3K9me2. Also known as modulator of the non-genomic activity of estrogen receptor (MNAR), PELP1 has also been implicated promoting estrogen receptor signaling from the plasma membrane. We recently identified PELP1 a factor that interacts with the macro domain of the histone variant macroH2A1. To determine if PELP1 interacts with macroH2A1 in cells, we performed PELP1 ChIP-chip from MCF-7 cells. The pattern of PELP1 bind across the genome strongly correlates with that previously determined for macroH2A1. This data combined with additional experiments allow us to conclude that macroH2A1 regulates target gene expression in part by recruiting the transcriptional coregulator PELP1. Two PELP1 ChIP-chip biological replicates from MCF-7 human breast cancer cells are included.

2014-04-24 | E-GEOD-22254 | biostudies-arrayexpress

Estrogen Regulates the JNK1 Genomic Localization Program in Breast Cancer Cells to Control Gene Expression and Cell Growth

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