Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Deciphering the role of RNA in regulating CTCF’s DNA binding affinity in leukemia cells [CTCF-ChIP]

ABSTRACT: Deciphering the role of RNA in regulating CTCF’s DNA binding affinity in leukemia cells [CTCF-ChIP]

PROVIDER: PRJNA1184930 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR31309114.fastq.gz	Fastqsanger.gz
	SRR31309115.fastq.gz	Fastqsanger.gz
	SRR31309116.fastq.gz	Fastqsanger.gz
	SRR31309117.fastq.gz	Fastqsanger.gz
	SRR31309123.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 7

Similar Datasets

Deciphering the role of RNA in regulating CTCF’s DNA binding affinity in leukemia cells [CTCF-ChIP]

Project description:CTCF, a highly studied transcription factor, is essential for chromatin interaction maintenance. Several independent studies have reported that CTCF interacts with RNAs in vitro and in cells. Yet continuous debates about the authenticity of the RNA-binding affinity of CTCF and its biological role remain in large part due to limited research techniques available, such as CLIP-seq. Here, we investigated the role RNA plays on CTCF’s transcription factor function through its chromatin occupancy. To systematically investigate whether RNAs affect CTCF’s ability to bind DNA, we perturbed CTCF-RNA interactions by three independent approaches and examined CTCF genome occupancy by ChIP-seq. Although RnaseA A and Triptolide treatment each affected a certain number of CTCF-binding peaks, few peaks overlapped between treatment groups indicating the effect of RNA in regulating CTCF’s DNA binding affinity was modest and variable between loci. In addition, limited transcriptional or chromatin accessibility changes were observed between cells expressing wild-type CTCF or CTCF lacking the RNA binding region. Our data provide a complementary approach and in silico evidence to reconsider the significance of RNA affecting CTCF’s DNA-binding affinity in a global manner.

2024-11-11 | GSE281633 | GEO

Deciphering the role of RNA in regulating CTCF’s DNA binding affinity in leukemia cells [CTCF-HA-ChIP]

Project description:Deciphering the role of RNA in regulating CTCF’s DNA binding affinity in leukemia cells [CTCF-HA-ChIP]

| PRJNA1085696 | ENA

Deciphering the role of RNA in regulating CTCF’s DNA binding affinity in leukemia cells

Project description:Deciphering the role of RNA in regulating CTCF’s DNA binding affinity in leukemia cells

| PRJNA1085765 | ENA

Deciphering the role of RNA in regulating CTCF’s DNA binding affinity in leukemia cells [CTCF-HA-ChIP]

Project description:CTCF is the most studied transcription factor, which is essential for chromatin interaction maintenance. Although several independent studies reported that CTCF protein could pull down RNAs in vitro and in cells, there are continuous debates about authenticity of the RNA-binding affinity of CTCF and its biological role, mainly due to the concerns of limited research techniques such as CLIP-seq. To systematically investigate the RNA-interaction with CTCF and the impact on gene regulation, we conducted in vivo CTCF ChIP-seq under three conditions, including RNase A treatment, Triptolide-mediated transcription inhibition and auxin-inducible degron mediated RNA-binding domain mutant swap. Our results consistently suggest that when RNA-interaction with CTCF protein was impaired in vivo, the DNA occupancy of CTCF remains the same at the genome-wide scale. Our data provide a complementary approach and in silico evidence to re-considerate the role of RNA-binding affinity of CTCF.

2024-03-08 | GSE261176 | GEO

X-chromosome dynamics revealed by the RNA interactome and chromosomal binding of CTCF

Project description:CTCF is a master regulator that plays a role in genome architecture and gene expression. A key aspect of CTCF’s mechanism involves bringing together distant genetic elements for intra- and inter-chromosomal interactions. Evidence from epigenetic processes, such as X-chromosome inactivation (XCI), suggests that CTCF may carry out its functions through interacting RNAs. Using genome-wide approaches to investigate the relationship between CTCF’s RNA interactome and its epigenomic landscape, here we report that CTCF interacts with thousands of transcripts in mouse embryonic stem cells (mESC), many in close proximity to CTCF’s genomic binding sites. Biochemical analysis demonstrates that CTCF is a high-affinity RNA binding protein that contacts RNA directly and specifically. In the XCI model, CTCF binds the active and inactive X-chromosomes allele-specifically. At the X-inactivation center, Tsix RNA binds CTCF and targets CTCF to a region associated with X-chromosome pairing. Our work implicates CTCF-RNA interactions in long-range chromosomal interactions in trans and adds a new layer of complexity to CTCF regulation. The genome-wide datasets reported here will provide a useful resource for further study of CTCF-mediated epigenomic regulation. CTCF RNA interactome was identified by UV-crosslinking and immunoprecipitation followed by high-throughput sequencing (CLIP-seq), and was compared to CTCF's epigenomic landscape as obtained by chromatin immunoprecipitation (ChIP-seq).

2015-01-09 | E-GEOD-58242 | biostudies-arrayexpress

X-chromosome dynamics revealed by the RNA interactome and chromosomal binding of CTCF

2015-01-09 | GSE58242 | GEO

Differences in CTCF binding site sequence are associated with unique regulatory and functional trends during embryonic stem cell differentiation [RNA-Seq]

Project description:CTCF (CCCTC-binding factor) is a highly conserved 11-zinc finger DNA binding protein with tens of thousands of binding sites genome-wide. CTCF acts as a multifunctional regulator of transcription, having been previously associated with activator, repressor, and insulator activity. These diverse regulatory functions are crucial for preimplantation development and are implicated in the regulation of numerous lineage-specific genes. Despite playing a critical role in developmental gene regulation, the mechanisms that underlie developmental changes in CTCF recruitment and function are poorly understood. Our previous work suggested that differences in CTCF’s binding site sequence may affect the regulation of CTCF recruitment, as well as CTCF’s regulatory function. To investigate these two possibilities directly during a developmental process, changes in genome-wide CTCF binding and gene expression were characterized during in vitro differentiation of mouse embryonic stem cells. CTCF binding sites were initially separated into three classes (named LowOc, MedOc, and HighOc) based on similarity to the consensus motif. The LowOc class, with lower-similarity to the consensus motif, is more likely to show changes in binding during differentiation. These more dynamically bound sites are enriched for motifs that confer a lower in vitro affinity for CTCF, suggesting a mechanism where sites with low-binding affinity are more amenable to developmental control. Additionally, by comparing changes in CTCF binding with changes in gene expression during differentiation, we show that LowOc and HighOc sites are associated with distinct regulatory functions. In sum, these results suggest that the regulatory control of CTCF’s binding and function is dependent in part upon specific motifs within its DNA binding site.

2013-10-11 | GSE39522 | GEO

Differences in CTCF binding site sequence are associated with unique regulatory and functional trends during embryonic stem cell differentiation [ChIP-Seq]

2013-10-11 | GSE39502 | GEO

Deciphering the role of RNA in regulating CTCF’s DNA binding affinity in leukemia cells

Project description:RNA-seq could be found under GSE205311(sample names with DeltaRBR). This SuperSeries is composed of the SubSeries listed below.

2024-03-09 | GSE261189 | GEO

Low affinity CTCF binding drives transcriptional regulation whereas high affinity binding encompasses architectural functions.

Project description:Low affinity CTCF binding drives transcriptional regulation whereas high affinity binding encompasses architectural functions.

| PRJNA856492 | ENA

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