Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Homo sapiens

ABSTRACT: Epigenome Editing by a CRISPR/Cas9-Based Acetyltransferase Activates Genes from Promoters and Enhancers

PROVIDER: PRJNA277845 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR1909040.fastq.gz	Fastqsanger.gz
	SRR1909031.fastq.gz	Fastqsanger.gz
	SRR1909041.fastq.gz	Fastqsanger.gz
	SRR1909032.fastq.gz	Fastqsanger.gz
	SRR1909042.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 12

Similar Datasets

Epigenome Editing by a CRISPR/Cas9-Based Acetyltransferase Activates Genes from Promoters and Enhancers

Project description:Epigenetic modifications determine the structure and regulation of eukaryotic genomes and define key signatures of cell lineage specification. Technologies that facilitate the targeted manipulation of epigenetic marks could be used to precisely control cell phenotype or interrogate the relationship between the epigenome and transcriptional control. Here we have generated a programmable acetyltransferase based on the CRISPR/Cas9 gene regulation system, consisting of the nuclease-null dCas9 protein fused to the catalytic core of the human acetyltransferase p300. This fusion protein catalyzes acetylation of histone H3 lysine 27 (H3K27) at its target sites, leading to robust transcriptional activation of target genes from promoters, proximal enhancers, and distal enhancers. In contrast to conventional dCas9-based activators, the acetyltransferase fusion effectively activated genes from enhancer regions and with individual guide RNAs. The core p300 domain was also portable to other programmable DNA-binding proteins. This technology enables the targeted perturbation of native epigenetic architecture and will be useful for reprogramming the epigenome for applications in genomics, genetics, disease modeling, and manipulating cell fate.

2015-03-11 | GSE66742 | GEO

Project description:Can one predict the effect of CRISPR-Cas9-based epigenome editing?

| PRJNA892960 | ENA

Three-dimensional genome architectural CCCTC-binding factor makes choice in duplicated enhancers at Pcdhα locus. [ChIP-seq II]

Project description:By CRISPR/Cas9 DNA-fragment editing, in conjunction with chromosome conformation capture, ChIP-seq and RNA-seq technology, we studied CRISPR single cell clones of duplicated CBS-containing enhancers or promoters in the Pcdhα gene cluster. We found that CTCF plays an essential role in determining promoter choice and enhancer selection. In addition, the choices mediated by CTCF is based on the chromatin loops formed between forward-reverse convergent CBS pairs with the proximal one dominant.

2023-03-01 | GSE147279 | GEO

Three-dimensional genome architectural CCCTC-binding factor makes choice in duplicated enhancers at Pcdhα locus. [RNA-seq]

2023-03-01 | GSE147278 | GEO

Three-dimensional genome architectural CCCTC-binding factor makes choice in duplicated enhancers at Pcdhα locus. [4C-seq]

2023-03-01 | GSE147274 | GEO

Three-dimensional genome architectural CCCTC-binding factor makes choice in duplicated enhancers at Pcdhα locus. [ChIP-seq I]

2023-03-01 | GSE147193 | GEO

Increase genome editing efficiency by Cas9 transcriptional activator and histone acetyltransferase activator

Project description:The CRISPR/Cas9 system shows diverse levels of genome editing activities on eukaryotic genomic DNA targets, and experiments desire high-efficiency targets. Here we show that chromatin open status is a pivotal determinant of the Cas9 editing activity in mammalian cells, and increasing chromatin accessibility can efficiently improve Cas9 genome editing activity. However, the strategy that fusing the VP64 transcriptional activation domain at the C-terminus of Cas9 can only promote genome editing activity slightly at most tested CRISPR/Cas9 targets in Lenti-X 293T cells. Because histone acetylation increases eukaryotic chromatin accessibility, we further improve genome editing by elevating histone acetylation. We demonstrate that promoting histone acetylation using histone acetyltransferase (HAT) activator YF-2 can improve genome editing from Cas9 and more robustly from the Cas9 transcriptional activator. This provides a strategy to improve CRISPR/Cas9 genome editing activity and enables broader gRNA target choices in eukaryotes.

2022-04-21 | GSE200943 | GEO

miRNA-seq of HEK293 cell lines on Illumina iSeq100 instrument

Project description:A validation experiment performed on HEK293 cell lines after genome editing. The design contains three duplicate runs consisted of: HEK293 wild type cell line HEK293 with MIR484 gene knockdown using CRISPR-Cas9 HEK293 with MIR185 gene knockout using CRISPR-Cas9

2023-06-16 | E-MTAB-13009 | biostudies-arrayexpress

Defining super-enhancer landscape in triple-negative breast cancer by multiomic profiling

Project description:Here we apply integrated epigenomic and transcriptomic profiling to uncover super-enhancer heterogeneity between breast cancer subtypes, and provide clinically relevant biological insights towards TNBC. Using CRISPR/Cas9-mediated gene editing, we identify genes that are specifically regulated by TNBC-specific super-enhancers, including FOXC1 and MET, thereby unveiling a mechanism for specific overexpression of the key oncogenes in TNBC. We also identify ANLN as a novel TNBC-specific gene regulated by super-enhancer. Our studies reveal a TNBC-specific epigenomic landscape, contributing to the dysregulated oncogene expression in breast tumorigenesis.

2021-03-04 | PXD024505 |

CRISPR-Cas9 epigenome editing enables high-throughput screening for functional regulatory elements in the human genome [CERES]

Project description:Large genome mapping consortia and thousands of genome-wide association studies have identified non-protein coding elements in the genome as a having a central role in tissue development, cell-type specification, response to environmental or pharmacologic signals, and susceptibility to most common diseases. However, decoding the function of the millions of putative regulatory elements discovered in these studies remains a primary challenge. New CRISPR/Cas9-based epigenome editing technologies have enabled the precise perturbation of the activity of specific regulatory elements. Here we describe CRISPR/Cas9-based Epigenomic Regulatory Element Screening (CERES) for high-throughput screening of regulatory element activity within the native genomic context. We perform both loss- and gain-of-function screens with complementary epigenome editing tools to identify known and unknown regulatory elements of medically relevant genes in human cells. The high-throughput functional annotation of putative regulatory elements by CERES constitutes a new platform for screening biological mechanisms that cannot be perturbed by traditional methods.

2017-03-23 | GSE96875 | 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