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Genome wide targeting of the epigenetic regulatory protein CTCF to gene promoters by the transcription factor TFII-I [gene expression]

ABSTRACT: Analysis of the effect of TFII-I depletion on gene expression Wehi-231 cell lines. Total RNA were extract from shCT and shTFII-I Wehi-231 cells.

ORGANISM(S): Mus musculus

SUBMITTER: Michael Witcher

PROVIDER: E-GEOD-60915 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Genome wide targeting of the epigenetic regulatory protein CTCF to gene promoters by the transcription factor TFII-I [ChIP-Seq]

Project description:Analysis of CTCF binding in Wehi-231 with TFII-I knockdown compare to Wehi-231 wt. ChIP experiment of CTCF in Wehi-231-CT and Wehi-231-shTFII-I

2014-08-29 | E-GEOD-60917 | biostudies-arrayexpress

Genome wide targeting of the epigenetic regulatory protein CTCF to gene promoters by the transcription factor TFII-I [ChIP-Seq]

Project description:Analysis of CTCF binding in Wehi-231 with TFII-I knockdown compare to Wehi-231 wt.

2014-08-29 | GSE60917 | GEO

Genome wide targeting of the epigenetic regulatory protein CTCF to gene promoters by the transcription factor TFII-I [gene expression]

Project description:Analysis of the effect of TFII-I depletion on gene expression Wehi-231 cell lines.

2014-08-29 | GSE60915 | GEO

Genome-wide targeting of the epigenetic regulatory protein CTCF to gene promoters by the transcription factor TFII-I.

Project description:CCCTC-binding factor (CTCF) is a key regulator of nuclear chromatin structure and gene regulation. The impact of CTCF on transcriptional output is highly varied, ranging from repression to transcriptional pausing and transactivation. The multifunctional nature of CTCF may be directed solely through remodeling chromatin architecture. However, another hypothesis is that the multifunctional nature of CTCF is mediated, in part, through differential association with protein partners having unique functions. Consistent with this hypothesis, our mass spectrometry analyses of CTCF interacting partners reveal a previously undefined association with the transcription factor general transcription factor II-I (TFII-I). Biochemical fractionation of CTCF indicates that a distinct CTCF complex incorporating TFII-I is assembled on DNA. Unexpectedly, we found that the interaction between CTCF and TFII-I is essential for directing CTCF to the promoter proximal regulatory regions of target genes across the genome, particularly at genes involved in metabolism. At genes coregulated by CTCF and TFII-I, we find knockdown of TFII-I results in diminished CTCF binding, lack of cyclin-dependent kinase 8 (CDK8) recruitment, and an attenuation of RNA polymerase II phosphorylation at serine 5. Phenotypically, knockdown of TFII-I alters the cellular response to metabolic stress. Our data indicate that TFII-I directs CTCF binding to target genes, and in turn the two proteins cooperate to recruit CDK8 and enhance transcription initiation.

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Orphan nuclear receptor COUP-TFII enhances myofibroblasts glycolysis leading to kidney fibrosis

Project description:Recent studies demonstrated that metabolic disturbance, such as augmented glycolysis, contributes to fibrosis. The molecular regulation of this metabolic perturbation in fibrosis, however, has been elusive. COUP-TFII (also known as NR2F2) is an important regulator of glucose and lipid metabolism. Its contribution to organ fibrosis is undefined. Here, we found increased COUP-TFII expression in myofibroblasts in human fibrotic kidneys, lungs, kidney organoids, and mouse kidneys after injury. Genetic ablation of COUP-TFII in mice resulted in attenuation of injury-induced kidney fibrosis. A non-biased proteomic study revealed the suppression of fatty acid oxidation and the enhancement of glycolysis pathways in COUP-TFII overexpressing fibroblasts. Overexpression of COUP-TFII in fibroblasts induced augmented glycolysis and production of alpha smooth muscle actin (αSMA) and collagen1. Knockout of COUP-TFII decreased glycolysis and collagen1 levels in fibroblasts. Chip-qPCR revealed the binding of COUP-TFII on the promoter of PGC1α. Overexpression of COUP-TFII reduced the cellular level of PGC1α. Targeting COUP-TFII serves as a novel treatment approach for mitigating fibrosis in chronic kidney disease and potentially fibrosis in other organs.

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Genes regulated by COUP-TFII inhibitor

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Genome wide targeting of the epigenetic regulatory protein CTCF to gene promoters by the transcription factor TFII-I

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

2014-08-29 | E-GEOD-60918 | biostudies-arrayexpress

Genome wide targeting of the epigenetic regulatory protein CTCF to gene promoters by the transcription factor TFII-I

Project description:Genome wide targeting of the epigenetic regulatory protein CTCF to gene promoters by the transcription factor TFII-I

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Expression profile of COUP-TFII overexpressing mouse ventral midbrain

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Expression profile of COUP-TFII overexpressing hearts

Project description:Increased COUP-TFII levels are found in human dilated cardiomyopathy as well as in mouse models that develop cardiomyopathy. COUP-TFII overexpression in adult mouse hearts caused ventricular dilation and compromised cardiac functions. To gain insights on COUP-TFII’s effect in hearts, we identified the molecular profile of COUP-TFII overexpressing hearts through microarray analysis. The result may shred light on molecular mechanisms that mediate development of dilated cardiomyopathy.

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