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Chip-chip from Jurkat with p300 and pol II

ABSTRACT: We profiled the dynamic interaction of p300 with proximal promoters of human T cells identified a class of genes that rapidly coassemble p300 and RNA polymerase II following mitogen stimulation. We classified the genes that rapidly coassemble p300 and pol II following mitogen stimulation

ORGANISM(S): Homo sapiens

PROVIDER: GSE19311 | GEO | 2009/12/04

SECONDARY ACCESSION(S): PRJNA120907

REPOSITORIES: GEO

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Chip-chip from Jurkat with p300 and pol II

Project description:We profiled the dynamic interaction of p300 with proximal promoters of human T cells identified a class of genes that rapidly coassemble p300 and RNA polymerase II following mitogen stimulation. We classified the genes that rapidly coassemble p300 and pol II following mitogen stimulation Comparison the unstimulated to P/I stimulated pol II and p300 enrichment fold in Jurkat

2010-05-18 | E-GEOD-19311 | biostudies-arrayexpress

Expression data following mitogen stimulation from Jurkat Cell

Project description:Gene expression analysis identified 27 of these 744 p300 and pol II associated genes as significantly increased (p≤ 0.05) within the first hour following mitogen stimulation Keywords: time course

2009-12-04 | GSE11118 | GEO

Transcription profiling by array of human jurkat cells after mitogen stimulation

Project description:Gene expression analysis identified 27 of these 744 p300 and pol II associated genes as significantly increased (p? 0.05) within the first hour following mitogen stimulation Experiment Overall Design: Total RNA was purified from Jurkat T-cells treated 0, 30, and 60 min with phorbol ester and ionomycin. Antisense biotin-labeled RNA (aRNA) suitable for application to the Affymetrix microarray platform was generated using the Ambion MessageAmp 2-Biotin Enhanced kit as suggested by the manufacturer (www.Ambion.com). Purified biotin-labeled aRNA was fragmented and hybridized to U133 plus 2 GenechipsTM (Affymetrix), as recommended by the manufacturer. All samples were hybridized as technical replicates. Affymetrix U133 plus 2 GenechipsTM contain probe-sets corresponding to over 56,000 targets.

2009-12-11 | E-GEOD-11118 | biostudies-arrayexpress

Homo sapiens

Project description:Expression data following mitogen stimulation from Jurkat Cell

| PRJNA107015 | ENA

GR and Pol II interactions with regulatory elements in response to ultradian (pulsed) hormone stimulation [ChIP-seq]

Project description:We report changes in GR and Pol II binding profiles genome-wide upon treatment with corticosterone (Cort) for 20 minutes, treatment with Cort for 20 minutes followed by hormone withdrawal for 40 minutes, 60 minutes continuous stimulation with Cort, and 60 minutes continuous stimulation with Dexamethasone (Dex). We examine GR binding upon following treatments: 0' Cort, 20' Cort, 60' Cort Pulsed, 60' Cort Constant; Pol II binding upon following treatments: 0' Cort, 20' Cort, 60' Cort Pulsed, 60' Cort Constant, 60' Dex Constant; Pol II binding upon Mock treatments simulating 0' Cort, 20' Cort, 60' Cort Pulsed, 60' Cort Constant; CTCF binding profile of untreated cells.

2015-02-12 | E-GEOD-61234 | biostudies-arrayexpress

Genome-wide assessment of differential roles for p300 and CBP in transcription regulation

Project description:Through ChIP-Seq analysis with the Illumina Whole Genome Analyzer, we identify binding sites for P300 (EP300) and CBP (CREBBP) in Human glioblastoma T98G cells that were cell cycle synchronized before and after stimulation. In our analysis, we focused on the identification of genes differentially bound by P300 and CBP. ChIP-seq with P300 and CBP antibodies over 2 timepoints

2010-03-30 | E-GEOD-21026 | biostudies-arrayexpress

p300-mediated gene expression during muscle cell survival

Project description:Type of experiment: The primary focus of these studies is to define the transcriptional network regulated by ectopic expression of the transcriptional co-activator protein, p300, in order to define its mechanism(s) of action in promoting muscle cell survival. Experimental factors: Our laboratory has generated a murine C2-derived myoblast cell line stably expressing an IGF-II cDNA in antisense orientation (C2AS12 cells). These cells proliferate normally in serum-rich growth medium but progressively die in low-serum differentiation medium. Ectopic expression of p300 (a transcriptional co-coactivator with acetyltransferase activity) prevents the progressive cell death induced by serum withdrawal, however, the mechanism of this action is not understood. Further, over-expression of a mutated form of p300, lacking at protein interaction domain (deltaTAZ2), failed to maintain cell viability although it retains catalytic activity. Wild-type and mutant p300 are delivered using recombinant adenoviruses (Ad-p300 and Ad-p300deltaTAZ2) and their expression is regulated by a second recombinant adenovirus encoding the tetracycline transactivator protein (Ad-tTA), affording regulated expression of p300 forms (Tet-off system) and providing a control for viral load. Using these reagents the overall experiment was as follows: Three parallel series of C2AS12 cells were infected with (1) wt p300 + tTA, (2) p300deltaTAZ2 +tTA, (3) wt p300 +tTA +doxycycline. Infected cells were grown to confluence followed by transfer to low-serum differentiation medium (T0). Cell were isolated at this point and following 24 (T24) hours incubation for RNA isolation. Companion dishes of cells were included for analysis by immunocytochemistry to ensure regulated transgene expression and cell viabilities. Keywords: time course

2006-03-01 | GSE4224 | GEO

A UTX–MLL4–p300 Transcriptional Regulatory Network Coordinately Shapes Active Enhancer Landscapes for Eliciting Transcription (ChIP-Seq)

Project description:Enhancer activation is a critical step for gene activation. Here we report a novel epigenetic crosstalk at enhancers between the UTX (H3K27 demethylase)-MLL4 (H3K4 methyltransferase) complex and the histone acetyltransferase p300. We demonstrate that UTX, in a demethylase activity-independent manner, facilitates conversion of naïve (unmarked) enhancers in embryonic stem cells to an active (H3K4me1+/H3K27ac+) state by recruiting and coupling the enzymatic functions of MLL4 and p300. Loss of UTX leads to attenuated enhancer activity, characterized by reduced levels of H3K4me1 and H3K27ac as well as impaired transcription. The UTX-MLL4 complex enhances p300-dependent H3K27 acetylation through UTX-dependent stimulation of p300 recruitment while MLL4-mediated H3K4 monomethylation, reciprocally, requires p300 function. Importantly, MLL4-generated H3K4me1 further enhances p300-dependent transcription. This work reveals a previously unrecognized cooperativity among enhancer-associated chromatin modulators, including a unique function for UTX, in establishing an “active enhancer landscape” and defines a mechanism for the joint deposition of H3K4me1 and H3K27ac.

2017-07-06 | GSE97701 | GEO

Transcription profiling of mouse C2AS12 cells infected with (1) wt p300 + tTA, (2) p300deltaTAZ2 +tTA, (3) wt p300 +tTA +doxycycline to define the transcriptional network regulated by ectopic expression of the transcriptional co-activator protein, p300 and define its role in promoting muscle cell survival

Project description:The primary focus of these studies is to define the transcriptional network regulated by ectopic expression of the transcriptional co-activator protein, p300, in order to define its mechanism(s) of action in promoting muscle cell survival. Our laboratory has generated a murine C2-derived myoblast cell line stably expressing an IGF-II cDNA in antisense orientation (C2AS12 cells). These cells proliferate normally in serum-rich growth medium but progressively die in low-serum differentiation medium. Ectopic expression of p300 (a transcriptional co-coactivator with acetyltransferase activity) prevents the progressive cell death induced by serum withdrawal, however, the mechanism of this action is not understood. Further, over-expression of a mutated form of p300, lacking at protein interaction domain (deltaTAZ2), failed to maintain cell viability although it retains catalytic activity. Wild-type and mutant p300 are delivered using recombinant adenoviruses (Ad-p300 and Ad-p300deltaTAZ2) and their expression is regulated by a second recombinant adenovirus encoding the tetracycline transactivator protein (Ad-tTA), affording regulated expression of p300 forms (Tet-off system) and providing a control for viral load. Using these reagents the overall experiment was as follows: Three parallel series of C2AS12 cells were infected with (1) wt p300 + tTA, (2) p300deltaTAZ2 +tTA, (3) wt p300 +tTA +doxycycline. Infected cells were grown to confluence followed by transfer to low-serum differentiation medium (T0). Cell were isolated at this point and following 24 (T24) hours incubation for RNA isolation. Companion dishes of cells were included for analysis by immunocytochemistry to ensure regulated transgene expression and cell viabilities. 6 biological replicates, representing 3 treatment groups, two timepoints and 2 biological outcomes (cell survival with p300wt and apoptotic cell death with p300wt+Dox and p300mut)

2007-12-07 | E-GEOD-4224 | biostudies-arrayexpress

Genome-wide assessment of differential roles for p300 and CBP in transcription regulation

2010-03-30 | GSE21026 | GEO

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