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Polycomb dysregulation in gliomagenesis targets a Zfp423-dependent differentiation network

ABSTRACT: Polycomb dysregulation in gliomagenesis targets a Zfp423-dependent differentiation network

PROVIDER: PRJNA306825 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR3050700.fastq.gz	Fastqsanger.gz
	SRR3050710_1.fastq.gz	Fastqsanger.gz
	SRR3050710_2.fastq.gz	Fastqsanger.gz
	SRR3050701_1.fastq.gz	Fastqsanger.gz
	SRR3050701_2.fastq.gz	Fastqsanger.gz

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Similar Datasets

Polycomb dysregulation in gliomagenesis targets a Zfp423-dependent differentiation network [ChIP-Seq]

Project description:Malignant gliomas constitute one of the most significant areas of unmet medical need, due to the invariable failure of surgical eradication and their marked molecular heterogeneity. Accumulating evidence has revealed a critical contribution by the Polycomb axis of epigenetic repression. However, a coherent understanding of the regulatory networks affected by Polycomb during gliomagenesis is still lacking. Here we integrate transcriptomic and epigenomic analyses to define Polycomb-dependent networks that promote gliomagenesis, validating them both in two independent mouse models and in a large cohort of human samples. We found that Polycomb dysregulation in gliomagenesis affects transcriptional networks associated to invasiveness and de-differentiation. The dissection of these networks uncovers Zfp423 as a crtitical Polycomb-dependent transcription factor whose silencing negatively impacts survival. The anti-gliomagenic activity of Zfp423 requires interaction with the SMAD proteins within the BMP signaling pathway, pointing to a novel synergic circuit through which Polycomb inhibits BMP signaling. Analysis of H3K27me3 distribition in two different stages of gliomagenesis

2016-03-02 | E-GEOD-76289 | biostudies-arrayexpress

Polycomb dysregulation in gliomagenesis targets a Zfp423-dependent differentiation network [RNA-Seq]

Project description:Malignant gliomas constitute one of the most significant areas of unmet medical need, due to the invariable failure of surgical eradication and their marked molecular heterogeneity. Accumulating evidence has revealed a critical contribution by the Polycomb axis of epigenetic repression. However, a coherent understanding of the regulatory networks affected by Polycomb during gliomagenesis is still lacking. Here we integrate transcriptomic and epigenomic analyses to define Polycomb-dependent networks that promote gliomagenesis, validating them both in two independent mouse models and in a large cohort of human samples. We found that Polycomb dysregulation in gliomagenesis affects transcriptional networks associated to invasiveness and de-differentiation. The dissection of these networks uncovers Zfp423 as a crtitical Polycomb-dependent transcription factor whose silencing negatively impacts survival. The anti-gliomagenic activity of Zfp423 requires interaction with the SMAD proteins within the BMP signaling pathway, pointing to a novel synergic circuit through which Polycomb inhibits BMP signaling. Transcriptomic analysis of two different stages of gliomagenesis

2016-03-02 | E-GEOD-76291 | biostudies-arrayexpress

Polycomb dysregulation in gliomagenesis targets a Zfp423-dependent differentiation network [RNA-Seq]

2016-03-02 | GSE76291 | GEO

Polycomb dysregulation in gliomagenesis targets a Zfp423-dependent differentiation network [ChIP-Seq]

2016-03-02 | GSE76289 | GEO

Polycomb dysregulation in gliomagenesis targets a Zfp423-dependent differentiation network.

Project description:Malignant gliomas constitute one of the most significant areas of unmet medical need, owing to the invariable failure of surgical eradication and their marked molecular heterogeneity. Accumulating evidence has revealed a critical contribution by the Polycomb axis of epigenetic repression. However, a coherent understanding of the regulatory networks affected by Polycomb during gliomagenesis is still lacking. Here we integrate transcriptomic and epigenomic analyses to define Polycomb-dependent networks that promote gliomagenesis, validating them both in two independent mouse models and in a large cohort of human samples. We find that Polycomb dysregulation in gliomagenesis affects transcriptional networks associated with invasiveness and de-differentiation. The dissection of these networks uncovers Zfp423 as a critical Polycomb-dependent transcription factor whose silencing negatively impacts survival. The anti-gliomagenic activity of Zfp423 requires interaction with the SMAD proteins within the BMP signalling pathway, pointing to a novel synergic circuit through which Polycomb inhibits BMP signalling.

| S-EPMC4773478 | biostudies-literature

Polycomb dysregulation in gliomagenesis targets a Zfp423-dependent differentiation network

Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

2016-03-02 | E-GEOD-76292 | biostudies-arrayexpress

Polycomb dysregulation in gliomagenesis targets a Zfp423-dependent differentiation network

Project description:This SuperSeries is composed of the SubSeries listed below.

2016-03-02 | GSE76292 | GEO

Mus musculus

Project description:Polycomb dysregulation in gliomagenesis targets a Zfp423-dependent differentiation network [ChIP-Seq]

| PRJNA306831 | ENA

Mus musculus

Project description:Polycomb dysregulation in gliomagenesis targets a Zfp423-dependent differentiation network [RNA-Seq]

| PRJNA306830 | ENA

Identification of Zfp423-dependent genes in adult inguinal white adipocytes

Project description:We derived a model that allows for doxycycline-inducible deletion of Zfp423 in mature adipocytes of adult mice (Adiponectin-rtTA; TRE-CRE; Zfp423 loxP/loxP). In these animals deletion of Zfp423 results in a spontaneous conversion of white adipocytes into beige-like adipocytes at room temperature. The goal of this expression analysis was to 1) determine the gene programs dependent on adipocyte Zfp423 in inguinal WAT, and 2) determine the similarity between the converted beige-like cells to normal beige adipose tissue that accumulates upon cold exppsure.

2016-02-10 | GSE74899 | GEO

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