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

ABSTRACT: We acutely depleted the BCL11A protein by using the dTAG PROTAC technology, and assessed its consequences on histone modification by ChIP-seq,and compared this to changes in nascent transcription, DNA methylation, Protein expression and chromatin accessibility.

ORGANISM(S): Homo sapiens

PROVIDER: GSE194342 | GEO | 2022/07/19

REPOSITORIES: GEO

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

Project description:We acutely depleted the BCL11A protein by using the dTAG PROTAC technology, and assessed its immediate consequences on DNA methylation at the HBG1/2 promoter region.

2022-07-19 | GSE194344 | GEO

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

Project description:We acutely depleted the BCL11A protein by using the dTAG PROTAC technology, and assessed its immediate consequences on DNA methylation, in the presence/absence of DNMT1 inhibitor AZAcytidine.

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Temporal resolution of gene derepression and proteome changes upon PROTAC-mediated degradation of BCL11A protein in erythroid cells [PRO-seq washout]

Project description:We acutely depleted the BCL11A protein by using the dTAG PROTAC technology, then performed a drug washout and and assessed its immediate consequences nascent transcription.

2022-07-19 | GSE194347 | GEO

Temporal resolution of gene derepression and proteome changes upon PROTAC-mediated degradation of BCL11A protein in erythroid cells [PRO-seq early]

Project description:We acutely depleted the BCL11A protein by using the dTAG PROTAC technology, and assessed its immediate consequences on nascent transcription, DNA methylation, Protein expression and HIstone modification and chromatin accessibility.

2022-07-19 | GSE194345 | GEO

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

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2022-07-19 | GSE194339 | 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

2022-07-27 | PXD030301 | Pride

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

2023-10-24 | PXD030307 | Pride

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

Project description:This SuperSeries is composed of the SubSeries listed below.

2022-07-19 | GSE194348 | GEO

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

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