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Genome-wide analysis of human pluripotent cells after kd/oe of SNF5

ABSTRACT: Analysis of global gene expression by SNF5 level change in human pluripotent and differentiated cells. The core subunit of BAF complex SNF5 is at the nexus of the link between chromatin remodeling and tumor suppression. We demonstrated a role for the remodeler SNF5 as a key executor in regulating pluripotency gene networks during differentiation by using loss and gain of function experiments followed by gene-expression arrays. Total RNA obtained from pluripotent state, differentiated state, absense of SNF5 and overexpression of SNF5

ORGANISM(S): Homo sapiens

SUBMITTER: jueng soo You

PROVIDER: E-GEOD-35909 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Genome-wide analysis of human pluripotent cells after kd/oe of SNF5

Project description:Analysis of global gene expression by SNF5 level change in human pluripotent and differentiated cells. The core subunit of BAF complex SNF5 is at the nexus of the link between chromatin remodeling and tumor suppression. We demonstrated a role for the remodeler SNF5 as a key executor in regulating pluripotency gene networks during differentiation by using loss and gain of function experiments followed by gene-expression arrays.

2013-01-01 | GSE35909 | GEO

Genome-wide maps of chromatin remodeler SNF5 in human pluripotent cells.

Project description:We report the application of single-molecule-based sequencing technology for high-throughput profiling of SNF5 binding in human pluripotent embryonic carcinoma NCCIT and SNF5 overexpressed NCCIT cells. We generated genome-wide cSNF5 maps of NCCIT and SNF5 overexpressed NCCIT cells from chromatin immunoprecipitated DNA. SNF5 and OCT4 seem not to share their binding in OCT4 centered binding plot in control, while SNF5 overexpression directs SNF5 to OCT4 target genes.

2013-01-01 | GSE36134 | GEO

Genome-wide maps of chromatin remodeler SNF5 in human pluripotent cells.

2013-01-01 | E-GEOD-36134 | biostudies-arrayexpress

Elevated levels of H3K27me3 in Snf5-deficient cells

2010-10-19 | GSE23658 | GEO

Epigenetic antagonism between Snf5 and Ezh2 during oncogenic transformation

Project description:Epigenetic alterations have been increasingly implicated in oncogenesis. Analysis of Drosophila mutants suggests that Polycomb and SWI/SNF complexes can serve antagonistic developmental roles. However, the relevance of this relationship to human disease is unclear. Here we have investigated functional relationships between these epigenetic regulators in oncogenic transformation. Mechanistically, we show that loss of the SNF5 tumor suppressor leads to elevated expression of the Polycomb gene EZH2 and that Polycomb targets are broadly H3K27-trimethylated and repressed in SNF5-deficient fibroblasts and cancers. Further, we show antagonism between SNF5 and EZH2 in the regulation of stem cell-associated programs and that Snf5 loss activates those programs. Finally, using conditional mouse models, we show that inactivation of Ezh2 blocks tumor formation driven by Snf5 loss. Mouse Embryonic Fibroblasts (MEFs) conditionally inactivated for Ezh2, Snf5 and Ezh2, or from control WT MEFs were used to evaluated epigenetic antagonism between Snf5 and Ezh2 in the control of gene expression programs. Snf5-deficient lymphoma samples and control CD8+ WT T-cells were used to evaluate genetic programs misregulated by Snf5 inactivation during tumorigenesis. RNA was isolated from each of these samples and used for gene expression profiling on Affymetrix arrays.

2010-10-19 | E-GEOD-23656 | biostudies-arrayexpress

Epigenetic antagonism between Snf5 and Ezh2 during oncogenic transformation

2010-10-19 | GSE23656 | GEO

Transcription profiling of mouse SNF5 liver-specific inactivation in SNF5 flox/knockouts

Project description:Effect of liver-specific inactivation of SNF5 on liver transcriptome. Comparison of control and mutant livers.

2005-12-19 | E-MEXP-241 | biostudies-arrayexpress

Loss of Snf5 and the formation of an aberrant SWI/SNF complex

Project description:Aberrant forms of the SWI/SNF chromatin remodeling complex are associated with human disease. Loss of the Snf5 subunit of SWI/SNF is a driver mutation in pediatric rhabdoid cancers and forms aberrant sub-complexes that are not well characterized. We determined the effects of loss of Snf5 on the composition, nucleosome binding, recruitment and remodeling activities of yeast SWI/SNF. The Snf5 subunit interacts with the ATPase domain of Snf2 and forms a submodule consisting of Snf5, Swp82 and Taf14 as shown by mapping SWI/SNF subunit interactions by crosslinking-mass spectrometry and subunit deletion followed by immunoaffinity chromatography. Snf5 promoted binding of the Snf2 ATPase domain to nucleosomal DNA, enhanced its catalytic activity and facilitated nucleosome remodeling. Snf5 was required for acidic transcription factors to recruit SWI/SNF to chromatin. RNA-seq analysis suggested that both the recruitment and catalytic functions mediated by Snf5 are required for SWI/SNF regulation of gene expression.

2017-01-30 | GSE85460 | GEO

Localization of Snf5 in wild-type and knockout yeast

Project description:ChIP-chip assays to determine the localization of Snf5 in wild-type and knockout yeast.

2017-01-16 | GSE84065 | GEO

Epigenetic antagonism between Snf5 and Ezh2 during oncogenic transformation and elevated levels of H3K27me3 in Snf5-deficient cells

Project description:Epigenetic antagonism between Snf5 and Ezh2 during oncogenic transformation and elevated levels of H3K27me3 in Snf5-deficient cells

| PRJNA130857 | ENA

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