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E-GEOD-13284

ABSTRACT: RNAi profiling by array of human CD34-derived erythroid progenitors treated with BCL11A siRNAs

OTHER RELATED OMICS DATASETS IN: GSE13285PRJNA109605PRJNA114015PRJNA114017

PROVIDER: E-GEOD-13284 | ExpressionAtlas | 2025-01-24

REPOSITORIES: ExpressionAtlas

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			Action	DRS
	E-GEOD-13284-analysis-methods.tsv	Tabular
	E-GEOD-13284-atlasExperimentSummary.Rdata	Rdata
	E-GEOD-13284-configuration.xml	Xml
	E-GEOD-13284-percentile-ranks.tsv	Tabular
	E-GEOD-13284.condensed-sdrf.tsv	Tabular

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Homo sapiens

Project description:Human CD34-derived erythroid progenitors treated with BCL11A siRNAs

| PRJNA114017 | ENA

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

E-GEOD-13762

Project description:Transcription profiling by array of human monocyte-derived dendritic cells treated with 1,25-dihydroxyvitamin D3

2025-01-24 | E-GEOD-13762 | ExpressionAtlas

RNAi profiling by array of 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 Experiment Overall Design: Microarray expression analysis from CD34-derived erythroid progenitors treated with either non-targeting (NT) control siRNAs or BCL11A targeting siRNAs. Six samples from the NT control and six samples from the BCL11A siRNA treatment are included. Cells were harvested on day 7 of erythroid differentiation after introduction of siRNAs on day 0 of the differentiation protocol. Experiment Overall Design: 6 BCL11A siRNA datasets, 6 control (NT) datasets

2009-01-13 | E-GEOD-13284 | biostudies-arrayexpress

E-GEOD-40245

Project description:Transcription profiling by array of Arabidopsis estradiol inducible RNAi-tor seedlings treated with glucose

2015-11-23 | E-GEOD-40245 | ExpressionAtlas

E-GEOD-11940

Project description:Transcription profiling by array of human hepatocytes treated with doxorubicin

2025-01-16 | E-GEOD-11940 | ExpressionAtlas

E-GEOD-5809

Project description:Transcription profiling by array of human endometrial stromal cells treated with human trophoblasts

2025-01-24 | E-GEOD-5809 | ExpressionAtlas

E-GEOD-11324

Project description:Transcription profiling by array of human MCF cells treated with estrogen

2025-01-16 | E-GEOD-11324 | ExpressionAtlas

E-GEOD-11941

Project description:Transcription profiling by array of human primary hepatocytes treated with trovafloxacin

2025-01-16 | E-GEOD-11941 | ExpressionAtlas

The glucocorticoid receptor elicited proliferative response in human erythropoiesis is BCL11A-dependent, microdeletion patients.

Project description:Prior evidence indicates that the erythroid cellular response to glucocorticoids (GC) has developmental specificity, namely, that developmentally more advanced cells that are undergoing or have undergone fetal to adult globin switching are more responsive to GC-induced expansion. To investigate the molecular underpinnings of this, we focused on the major developmental globin regulator BCL11A. We compared: a) levels of expression and nuclear content of BCL11A in adult erythroid cells upon GC stimulation; b) response to GC of CD34+ cells from patients with BCL11A microdeletions and reduced BCL11A expression, and; c) response to GC of two cellular models (HUDEP-2 and adult CD34+ cells) before and after reduction of BCL11A expression by shRNA. We observed that: a) GC-expanded erythroid cells from a large cohort of blood donors displayed amplified expression and nuclear accumulation of BCL11A; b) CD34+ cells from BCL11A microdeletion patients generated fewer erythroid cells when cultured with GC compared to their parents, while the erythroid expansion of the patients was similar to that of their parents in cultures without GC, and; c) adult CD34+ cells and HUDEP-2 cells with shRNA-depleted expression of BCL11A exhibit reduced expansion in response to GC. In addition, RNA-seq profiling of shRNA-BCL11A CD34+ cells cultured with and without GC was similar (very few differentially expressed genes), while GC-specific responses (differential expression of GILZ and of numerous additional genes) were observed only in controls cells with unperturbed BCL11A expression. These data indicate that BCL11A is an important participant of certain aspects of the stress pathway sustained by GC.

2024-09-01 | GSE275337 | GEO

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