Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Binding domain mutations provide insight into CTCF's relationship with chromatin and its contribution to gene regulation

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Mus musculus

PROVIDER: GSE270669 | GEO | 2025/02/19

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Binding domain mutations provide insight into CTCF's relationship with chromatin and its contribution to gene regulation (Hi-C)

Project description:Here we used a series of CTCF mutations to explore CTCF’s relationship with chromatin and its contribution to gene regulation. CTCF’s impact depends on the genomic context of bound sites and the unique binding properties of WT and mutant CTCF proteins. Specifically, CTCF’s signal strength is linked to changes in accessibility, and the ability to block cohesin is linked to its binding stability. Multivariate modelling reveals that both CTCF and accessibility contribute independently to cohesin binding and insulation, however CTCF signal strength has a stronger effect. CTCF and chromatin have a bidirectional relationship such that at CTCF sites, accessibility is reduced in a cohesin-dependent, mutant specific fashion. In addition, each mutant alters TF binding and accessibility in an indirect manner, changes which impart the most influence on rewiring transcriptional networks and the cell’s ability to differentiate. Collectively, the mutant perturbations provide a rich resource for determining CTCF’s site-specific effects.

2025-02-20 | GSE270627 | GEO

Binding domain mutations provide insight into CTCF's relationship with chromatin and its contribution to gene regulation (Omni-ATAC)

2025-02-20 | GSE270626 | GEO

Binding domain mutations provide insight into CTCF's relationship with chromatin and its contribution to gene regulation (RNA-seq, exit from pluripotency)

2025-02-20 | GSE277846 | GEO

Binding domain mutations provide insight into CTCF's relationship with chromatin and its contribution to gene regulation

Project description:Binding domain mutations provide insight into CTCF's relationship with chromatin and its contribution to gene regulation

| PRJNA1127653 | ENA

Binding domain mutations provide insight into CTCF's relationship with chromatin and its contribution to gene regulation (Hi-C)

Project description:Binding domain mutations provide insight into CTCF's relationship with chromatin and its contribution to gene regulation (Hi-C)

| PRJNA1127593 | ENA

Binding domain mutations provide insight into CTCF's relationship with chromatin and its contribution to gene regulation (Omni-ATAC)

Project description:Binding domain mutations provide insight into CTCF's relationship with chromatin and its contribution to gene regulation (Omni-ATAC)

| PRJNA1127588 | ENA

Brain and cancer associated binding domain mutations provide insight into CTCF’s relationship with chromatin and its ability to act as a chromatin organizer (chip-seq)

Project description:Although only a fraction of CTCF motifs are bound in any cell type, and approximately half of the occupied sites overlap cohesin, the mechanisms underlying cell-type specific attachment and ability to function as a chromatin organizer remain unknown. To investigate the relationship between CTCF and chromatin we applied a combination of imaging, structural and molecular approaches, using a series of brain and cancer associated CTCF mutations that act as CTCF perturbations. We demonstrate that binding and the functional impact of WT and mutant CTCF depend not only on the unique properties of each protein, but also on the genomic context of bound sites. Our studies also highlight the reciprocal relationship between CTCF and chromatin, demonstrating that the unique binding properties of WT and mutant proteins have a distinct impact on accessibility, TF binding, cohesin overlap, chromatin interactivity and gene expression programs, providing insight into their cancer and brain related effects.

2025-02-20 | GSE270620 | GEO

Brain and cancer associated binding domain mutations provide insight into CTCF’s relationship with chromatin and its ability to act as a chromatin organizer (RNA-seq)

2025-02-20 | GSE270619 | GEO

Binding domain mutations provide insight into CTCF's relationship with chromatin and its contribution to gene regulation (RNA-seq, exit from pluripotency)

Project description:Binding domain mutations provide insight into CTCF's relationship with chromatin and its contribution to gene regulation (RNA-seq, exit from pluripotency)

| PRJNA1164318 | ENA

RASopathy mutations provide functional insight into the BRAF cysteine-rich domain and reveal the importance of autoinhibition in BRAF regulation.

Project description:BRAF is frequently mutated in human cancer and the RASopathy syndromes, with RASopathy mutations often observed in the cysteine-rich domain (CRD). Although the CRD participates in phosphatidylserine (PS) binding, the RAS-RAF interaction, and RAF autoinhibition, the impact of these activities on RAF function in normal and disease states is not well characterized. Here, we analyze a panel of CRD mutations and show that they increase BRAF activity by relieving autoinhibition and/or enhancing PS binding, with relief of autoinhibition being the major factor determining mutation severity. Further, we show that CRD-mediated autoinhibition prevents the constitutive plasma membrane localization of BRAF that causes increased RAS-dependent and RAS-independent function. Comparison of the BRAF- and CRAF-CRDs also indicates that the BRAF-CRD is a stronger mediator of autoinhibition and PS binding, and given the increased catalytic activity of BRAF, our studies reveal a more critical role for CRD-mediated autoinhibition in BRAF regulation.

| S-EPMC9677513 | biostudies-literature

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