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

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

PROVIDER: PRJNA1085696 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR21819064.fastq.gz	Fastqsanger.gz
	SRR21819065.fastq.gz	Fastqsanger.gz
	SRR21819066.fastq.gz	Fastqsanger.gz
	SRR21819067.fastq.gz	Fastqsanger.gz
	SRR21819068.fastq.gz	Fastqsanger.gz

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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 [RNA-Seq.New]

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 RNase 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.

2025-03-26 | GSE288854 | GEO

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

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

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

| PRJNA1184930 | 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

Project description:RNA-seq could be found under GSE205311(sample names with DeltaRBR). HA-tagged CTCF-ChIP-seq for dRBR could be found under GSE205408(sample names with Delta_RBR). This SuperSeries is composed of the SubSeries listed below.

2024-03-09 | GSE261189 | GEO

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

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

| PRJNA1085695 | ENA

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

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

| PRJNA1219631 | ENA

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

2025-03-26 | GSE261179 | 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

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