Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

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

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR6372900.fastq.gz	Fastqsanger.gz
	SRR6372900_1.fastq.gz	Fastqsanger.gz
	SRR6372900_2.fastq.gz	Fastqsanger.gz
	SRR6372901.fastq.gz	Fastqsanger.gz
	SRR6372901_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 22

Similar Datasets

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]

| PRJNA422254 | ENA

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]

| PRJNA422250 | ENA

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

Bioorthogonal Chemical Epigenetic Modifiers Enable Dose-dependent CRISPR Targeted Gene Activation

Project description:Bioorthogonal Chemical Epigenetic Modifiers Enable Dose-dependent CRISPR Targeted Gene Activation

| PRJNA771351 | ENA

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

Project description:The piperazine derivatives most frequently consumed for recreational purposes are 1-benzylpiperazine (BZP), 1-(3,4-methylenedioxybenzyl)piperazine (MDBP), 1-(3-trifluoromethylphenyl)piperazine (TFMPP), and 1-(4-methoxyphenyl)piperazine (MeOPP). Currently it is unclear whether piperazine designer drugs induce mechanisms of hepatotoxicity and, if so, whether they act by a common mechanism. We performed a gene array study with rat hepatocytes incubated with the four designer drugs for 24 h in order to detail the global programme of gene expression Primary rat hepatocytes were cultured in collagen sandwich and incubated with the piperazine designer drugs. After 24 h, the RNA was extracted and the Affymetrix microarray analysis was performed.

2015-05-13 | E-GEOD-68785 | biostudies-arrayexpress

miR expression microarray analysis on M2 macrophages treated with epigenetic modifiers

Project description:Epigenetic regulation of gene expression involves DNA methylation, histone methylation or acetylation, and microRNA (miRNA)-mediated mRNA degradation. We studied, if epigenetic modifiers namely 5-aza-2'-deoxycytidine and trichostatin A could remodulate the miR expression in M2 macrophage and enable M2-M1 reprogramming.

2022-11-17 | GSE218160 | GEO

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

Project description:This dataset includes the raw single-cell RNAseq data from Xenograft GBM tumor (G411)-bearing NSG mice model treated with either control peptide K59-78TAT or designer peptide K90-114TAT and raw bulk RNAseq data from GBM cell (G411)-neuron coculture model treated with either control peptide K59-78TAT or designer peptide K90-114TAT. In this project, we focused on transcriptomic alteration caused by designer peptide in tumor cells.

2023-06-25 | GSE231577 | GEO

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