Browse
Submit Data
Databases
API
Help

Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Genome-wide analysis distinguishes hyperglycemia regulated epigenetic signatures of primary vascular cells (gene expression)

ABSTRACT: We report that hyperglycemia-mediated induction of genes and pathways associated to endothelial dysfunction occur through modulation of acetylated H3K9/K14 inversely correlated with methyl-CpG content. Examination of H3K9/K14 histone acetylation and DNA methylation in hyperglycemic conditions. see GSE29251 for histone acetylation and DNA methylation

ORGANISM(S): Homo sapiens

SUBMITTER: Assam El-Osta

PROVIDER: E-GEOD-30780 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

ACCESS DATA

Json Xml

Similar Datasets

Genome-wide analysis distinguishes hyperglycemia regulated epigenetic signatures of primary vascular cells (ChIP-seq)

Project description:We report that hyperglycemia-mediated induction of genes and pathways associated to endothelial dysfunction occur through modulation of acetylated H3K9/K14 inversely correlated with methyl-CpG content. Examination of H3K9/K14 histone acetylation and DNA methylation in hyperglycemic conditions.

2011-06-01 | E-GEOD-29251 | biostudies-arrayexpress

Genome-wide analysis distinguishes hyperglycemia regulated epigenetic signatures of primary vascular cells (gene expression)

2011-07-20 | GSE30780 | GEO

Genome-wide analysis distinguishes hyperglycemia regulated epigenetic signatures of primary vascular cells (ChIP-seq)

2011-06-01 | GSE29251 | GEO

Genome-wide profiling of H3K9/K14 Acetylation and H3K27 trimethylation at promoters in the human lung embryonic fibroblast cell line MRC5

Project description:Genome-wide profiling of H3K9/K14 Acetylation and H3K27 trimethylation at promoters in the human lung embryonic fibroblast cell line MRC5

2013-11-11 | E-MTAB-2004 | biostudies-arrayexpress

Histone H3K9 and H3K14 acetylation mark active enhancers and promoters together with bivalent promoters in mouse embryonic stem cells

Project description:Transcription regulation in pluripotent embryonic stem (ES) cells is a complex process that involves multitude of regulatory layers, one of which is post-translational modification of histones. Here we have investigated the genome-wide occurrence of two histone marks, acetylation of histone H3K9 and K14 (H3K9ac and H3K14ac), in mouse ES cells. We demonstrate genome-wide that H3K9ac and H3K14ac show very high correlation. Examination of H3K9ac and H3K14ac in mES cells

2012-10-01 | E-GEOD-31284 | biostudies-arrayexpress

Histone H3K9 and H3K14 acetylation mark active enhancers and promoters together with bivalent promoters in mouse embryonic stem cells

2012-10-01 | GSE31284 | GEO

ChIP-Seq for cofactors in cancer

Project description:Critical drivers of cancer progression are likely controlled through the actions of transcription factors and cofactors that bind to the genome and form enhancers that stimulate gene expression. We present ChIP-seq analysis of key transcriptional regulators, cofactors and histone modifications that indicate transcriptional activity across a range of different cancer cells. ChIP-seq was performed against the cofactors Med1, Brd4 and CDK7 in MM1.S multiple myeloma cells; Brd4 in Sk-MEL-5 melanoma cells; and H3K9/K14 acetylation in MV4;11 leukemia cells,

2013-04-13 | E-GEOD-45984 | biostudies-arrayexpress

Vascular histone deacetylation by pharmacological HDAC inhibition [TSA, MBD-seq]

Project description:HDAC inhibitors are thought to regulate gene expression by post-translational modification of histone as well as non-histone proteins. Often studied at single loci, increased histone acetylation is the paradigmatic mechanism of action, however, little is known of the extent of genome-wide changes of the mammalian genome when stimulated by the hydroxamic acids, TSA and SAHA. In primary human vascular endothelial cells we map the chromatin modifications, histone H3 acetylation of lysine 9 and 14 (H3K9/14ac) using chromatin immunoprecipitation (ChIP) coupled with massive parallel sequencing (ChIP-seq). Since acetylation mediated gene expression is often associated with modification of other lysine residues we also examined H3K4me3 and H3K9me3 as well as changes in CpG methylation (CpG-seq). Genome-wide mRNA sequencing indicates the differential expression of about 30% of genes, with almost equal numbers being up- and down- regulated. We observe deacetylation conferred by TSA and SAHA that are associated with decreased gene expression. Histone deacetylation is associated with the loss of p300/CBP binding at gene promoters. This study provides an important framework for HDAC inhibitor function in vascular biology and a comprehensive description of genome-wide deacetylation. HAEC MethylMiner profiles of TSA treated and control samples were generated by deep sequencing, in triplicate, using Illumina GAIIx.

2014-02-23 | E-GEOD-54911 | biostudies-arrayexpress

Vascular histone deacetylation by pharmacological HDAC inhibition [TSA, RNA-seq]

Project description:HDAC inhibitors are thought to regulate gene expression by post-translational modification of histone as well as non-histone proteins. Often studied at single loci, increased histone acetylation is the paradigmatic mechanism of action, however, little is known of the extent of genome-wide changes of the mammalian genome when stimulated by the hydroxamic acids, TSA and SAHA. In primary human vascular endothelial cells we map the chromatin modifications, histone H3 acetylation of lysine 9 and 14 (H3K9/14ac) using chromatin immunoprecipitation (ChIP) coupled with massive parallel sequencing (ChIP-seq). Since acetylation mediated gene expression is often associated with modification of other lysine residues we also examined H3K4me3 and H3K9me3 as well as changes in CpG methylation (CpG-seq). Genome-wide mRNA sequencing indicates the differential expression of about 30% of genes, with almost equal numbers being up- and down- regulated. We observe deacetylation conferred by TSA and SAHA that are associated with decreased gene expression. Histone deacetylation is associated with the loss of p300/CBP binding at gene promoters. This study provides an important framework for HDAC inhibitor function in vascular biology and a comprehensive description of genome-wide deacetylation. HAEC mRNA profiles of TSA treated and control samples were generated by deep sequencing, in triplicate, using Illumina GAIIx.

2014-02-23 | E-GEOD-37376 | biostudies-arrayexpress

Vascular histone deacetylation by pharmacological HDAC inhibition [SAHA, RNA-seq]

Project description:HDAC inhibitors are thought to regulate gene expression by post-translational modification of histone as well as non-histone proteins. Often studied at single loci, increased histone acetylation is the paradigmatic mechanism of action, however, little is known of the extent of genome-wide changes of the mammalian genome when stimulated by the hydroxamic acids, TSA and SAHA. In primary human vascular endothelial cells we map the chromatin modifications, histone H3 acetylation of lysine 9 and 14 (H3K9/14ac) using chromatin immunoprecipitation (ChIP) coupled with massive parallel sequencing (ChIP-seq). Since acetylation mediated gene expression is often associated with modification of other lysine residues we also examined H3K4me3 and H3K9me3 as well as changes in CpG methylation (CpG-seq). Genome-wide mRNA sequencing indicates the differential expression of about 30% of genes, with almost equal numbers being up- and down- regulated. We observe deacetylation conferred by TSA and SAHA that are associated with decreased gene expression. Histone deacetylation is associated with the loss of p300/CBP binding at gene promoters. This study provides an important framework for HDAC inhibitor function in vascular biology and a comprehensive description of genome-wide deacetylation. HAEC mRNA profiles of SAHA treated and control samples were generated by deep sequencing, in triplicate, using Illumina GAIIx.

2014-02-23 | E-GEOD-54912 | biostudies-arrayexpress

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data