Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Analysis of chromatin occupancy in erythroid cells by CUT&Tag following CRISPR editing of BCL11A enhancer

ABSTRACT: The mechanisms underlying the remarkable efficacy of CRISPR-mediated enhancer ablation remain poorly understood. Here, we employ CUT&Tag to investigate histone modifications following BCL11A enhancer editing or CTCF disruption.

ORGANISM(S): Homo sapiens

PROVIDER: GSE292695 | GEO | 2025/11/13

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Analysis of chromatin occupancy in erythroid cells by CUT&RUN following CRISPR editing of BCL11A enhancer

Project description:The mechanisms underlying the remarkable efficacy of CRISPR-mediated BCL11A enhancer ablation remain poorly understood. Here, we employ CUT&RUN to investigate active and repressive histone modifications, as well as cohesin and CTCF binding, to uncover epigenetic changes under various editing conditions.

2025-11-13 | GSE292753 | GEO

Analysis of chromatin accessbility in erythroid cells following CRISPR editing or ASO perturbation of BCL11A enhancer

Project description:CRISPR editing of an intronic enhancer within the BCL11A gene reactivates fetal hemoglobin (HbF) in adult erythroid cells, serving as a gene-based therapy for hemoglobinopathies. However, the mechanisms underlying the remarkable efficacy of CRISPR-mediated enhancer ablation remain poorly understood. We describe an evolutionarily conserved, enhancer-dependent chromatin architecture, the enhancer-CTCF rosette, essential for chromatin insulation and the developmental expression of BCL11A in hematopoiesis. CRISPR-mediated disruption of lineage-specific BCL11A enhancers impairs enhancer RNA transcription and NIPBL-cohesin loading, leading to destabilized chromatin configuration, impaired chromatin insulation, and epigenetic silencing of BCL11A. Antisense oligonucleotide-mediated depletion of enhancer RNA silences BCL11A by disrupting chromatin insulation in adult erythroid cells.

2025-11-13 | GSE292669 | GEO

Analysis of chromatin occupancy in erythroid cells by CUT&Tag following CRISPR editing of BCL11A enhancer

Project description:Analysis of chromatin occupancy in erythroid cells by CUT&Tag following CRISPR editing of BCL11A enhancer

| PRJNA1240843 | ENA

Analysis of nascent transcription by PRO-seq in HUDEP-2 cells following CRISPR editing of BCL11A enhancer

2025-11-13 | GSE292697 | GEO

Analysis of chromatin structure of the BCL11A locus in HUDEP-2 cells by Capture-Pore-C (CPC)

2025-11-13 | GSE292694 | GEO

Transcriptome of erythroid cells derived from human CD34+ cells edited at the BCL11A erythroid enahncer or at the HBG1 and HBG2 promoters using CRISPR-Cas9

Project description:BCL11A represses gamma globin expression by binding to the gamma globin gene (HBG1 and HBG2) promoters. Genome editing of the BCL11A erythroid enhancer in the intron 2 of BCL11A gene or the BCL11A binding site at the HBG1/2 promoters disrupts this pathway and leads to gamma globin induction. Transcriptomic profiling of erythroid cells derived from human CD34+ cells edited at either target site using CRISPR-Cas9 revealed broader transcriptome perturbation when edited at the BCL11A erythroid enhancer.

2024-12-10 | GSE264491 | GEO

Temporal resolution of gene derepression and proteome changes upon PROTAC-mediated degradation of BCL11A protein in erythroid cells

Project description:Reactivation of fetal hemoglobin expression by down-regulation of BCL11A is a promising treatment of -hemoglobinopathies. A detailed understanding of BCL11A-mediated repression of -globin gene (HBG1/2) transcription is lacking, as studies to date used perturbations by shRNA or CRISPR/Cas9 gene editing. We leveraged the dTAG PROTAC platform to acutely deplete BCL11A protein in erythroid cells and examined consequences by PRO-seq, proteomics, chromatin accessibility, and histone profiling. Among ≤ 31 genes repressed by BCL11A, HBG1/2 and HBZ show the most abundant and progressive changes in transcription and chromatin accessibility upon BCL11A loss. Transcriptional changes at HBG1/2 were detected in < 2h. Robust HBG1/2 reactivation upon acute BCL11A-depletion occurred without loss of promoter 5methylcytosine (5mC). Using targeted protein degradation, we establish a hierarchy of gene reactivation at BCL11A targets, in which nascent transcription is followed by increased chromatin accessibility, and both are uncoupled from promoter DNA methylation at the HBG1/2 loci.

2023-10-24 | PXD030307 | Pride

Temporal resolution of gene derepression and proteome changes upon PROTAC-mediated degradation of BCL11A protein in erythroid cells

2022-07-27 | PXD030301 | Pride

Human CD34-derived erythroid progenitors treated with BCL11A siRNAs

Project description:Differences in the amount of fetal hemoglobin (HbF) that persists into adulthood affect the severity of sickle cell disease and the beta-thalassemia syndromes. Genetic association studies have identified sequence variants in the gene BCL11A that influence HbF levels. Here we examine BCL11A as a potential regulator of HbF expression. The high HbF BCL11A genotype is associated with reduced BCL11A expression. Moreover, abundant expression of full-length forms of BCL11A is developmentally restricted to adult erythroid cells. Down-regulation of BCL11A expression in primary adult erythroid cells leads to robust HbF expression. Consistent with a direct role of BCL11A in globin gene regulation, we find that BCL11A occupies several discrete sites in the beta-globin gene cluster. BCL11A emerges as a therapeutic target for reactivation of HbF in beta-hemoglobin disorders. BCL11A siRNA label: B, NT siRNA label: N Keywords: cell type comparsion

2008-12-05 | GSE13284 | GEO

Expression data from BCL11A-null and wild-type bone marrow erythroid pregenitors

Project description:BCL11A is a critical mediator of hemoglobin switching and gamma-globin silencing. In this study, we showed the BCL11A is required in vivo for developmental silencing of gamma-globin genes in adult animals. We used microarray to determine the changes in gene expression profile after loss of BCL11A in adult erythroid cells CD71+Ter119+ erythroid progenitor cells were FACS-sorted from bone marrows of 6-week old control (Bcl11a +/+) and BCL11A knockout (Bcl11a fl/fl EpoR-Cre+) mice.

2012-03-22 | E-GEOD-28333 | biostudies-arrayexpress

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