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Designer epigenome modifiers enable robust and sustained gene silencing in clinically relevant human cells

ABSTRACT: Designer epigenome modifiers enable robust and sustained gene silencing in clinically relevant human cells

PROVIDER: PRJNA422251 | ENA |

REPOSITORIES: ENA

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Designer epigenome modifiers enable robust and sustained gene silencing in clinically relevant human cells [RNA-seq]

Project description:Designer epigenome modifiers enable robust and sustained gene silencing in clinically relevant human cells [RNA-seq]

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Designer epigenome modifiers enable robust and sustained gene silencing in clinically relevant human cells [ATAC-seq]

Project description:Designer epigenome modifiers enable robust and sustained gene silencing in clinically relevant human cells [ATAC-seq]

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Designer epigenome modifiers enable robust and sustained gene silencing in clinically relevant human cells [RNA-seq]

Project description:Targeted modulation of gene expression represents a valuable approach to understand the mechanisms governing gene regulation. In a therapeutic context, it can be exploited to selectively modify the aberrant expression of a disease-causing gene or to provide the target cells with a new function. Here, we have established a novel platform for achieving precision epigenome editing using designer epigenome modifiers (DEMs). DEMs combine in a single molecule a DNA binding domain based on highly specific transcription activator-like effectors (TALEs) and several effector domains capable of inducing DNA methylation and locally altering the chromatin structure to silence target gene expression. We designed DEMs to target two human genes, CCR5 and CXCR4, with the aim of epigenetically silencing their expression in primary human T lymphocytes. We observed robust and sustained target gene silencing associated with reduced chromatin accessibility, increased promoter methylation at the target sites and undetectable changes in global gene expression. Our results demonstrate that DEMs can be successfully used to silence target gene expression in primary human cells with remarkable high specificity, paving the way for the establishment of a potential new class of therapeutics.

2018-02-27 | GSE108029 | GEO

Designer epigenome modifiers enable robust and sustained gene silencing in clinically relevant human cells [ATAC-seq]

2018-02-27 | GSE108024 | GEO

Designer epigenome modifiers enable robust and sustained gene silencing in clinically relevant human cells.

Project description:Targeted modulation of gene expression represents a valuable approach to understand the mechanisms governing gene regulation. In a therapeutic context, it can be exploited to selectively modify the aberrant expression of a disease-causing gene or to provide the target cells with a new function. Here, we have established a novel platform for achieving precision epigenome editing using designer epigenome modifiers (DEMs). DEMs combine in a single molecule a DNA binding domain based on highly specific transcription activator-like effectors (TALEs) and several effector domains capable of inducing DNA methylation and locally altering the chromatin structure to silence target gene expression. We designed DEMs to target two human genes, CCR5 and CXCR4, with the aim of epigenetically silencing their expression in primary human T lymphocytes. We observed robust and sustained target gene silencing associated with reduced chromatin accessibility, increased promoter methylation at the target sites and undetectable changes in global gene expression. Our results demonstrate that DEMs can be successfully used to silence target gene expression in primary human cells with remarkably high specificity, paving the way for the establishment of a potential new class of therapeutics.

| S-EPMC5961145 | biostudies-literature

Designer epigenome modifiers enable robust and sustained gene silencing in clinically relevant human cells

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

2018-02-27 | GSE108030 | GEO

Expression data of sandwich cultured primary rat hepatocytes incubated to piperazine designer drugs

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miR expression microarray analysis on M2 macrophages treated with epigenetic modifiers

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A designer peptide against the EAG2-Kvβ2 potassium channel targets the interaction of cancer cells and neurons to treat glioblastoma

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Expression data of sandwich cultured primary rat hepatocytes incubated to piperazine designer drugs

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