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Links from GEO DataSets

Items: 20

1.

Human Fetal Hemoglobin Expression is Regulated by the Developmental Stage-Specific Repressor BCL11A

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.
Organism:
Homo sapiens; Mus musculus
Type:
Expression profiling by array
Platforms:
GPL1261 GPL570
22 Samples
Download data: CEL
Series
Accession:
GSE13285
ID:
200013285
2.

Human CD34-derived erythroid progenitors treated with BCL11A siRNAs

(Submitter supplied) 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. more...
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL570
12 Samples
Download data: CEL
Series
Accession:
GSE13284
ID:
200013284
3.

Mouse Erythroleukemia (MEL) Cells Expressing Tagged Versions of BCL11A

(Submitter supplied) 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. more...
Organism:
Mus musculus
Type:
Expression profiling by array
Platform:
GPL1261
10 Samples
Download data: CEL
Series
Accession:
GSE13283
ID:
200013283
4.

Direct Promoter Repression by BCL11A Controls the Fetal to Adult Hemoglobin Switch

(Submitter supplied) Fetal hemoglobin (HbF) level is genetically controlled and modifies severity of adult hemoglobin (HbA) disorders. Common genetic variation affects expression of BCL11A, a critical regulator of HbF silencing. Current models suggest that BCL11A acts at a distance from the gamma-globin genes via long-distance chromosomal interactions. Here we use a functional cellular assay and protein-binding microarray to establish a requirement for a zinc-finger cluster of BCL11A for globin repression, and identify a preferred DNA recognition sequence (TGACCA). more...
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL18573
36 Samples
Download data: BED, BROADPEAK, BW, GAPPEDPEAK, NARROWPEAK
Series
Accession:
GSE104676
ID:
200104676
5.

The LRF/ZBTB7A transcription factor is a BCL11A-independent repressor of fetal hemoglobin

(Submitter supplied) Hemoglobinopathies, including sickle cell disease and _-thalassemia, are global public health concerns. Induction of fetal-type hemoglobin (HbF) is a promising means to treat these disorders; however, precisely how HbF expression is silenced in adult erythroid cells is not fully understood. Here, we show that the LRF/ZBTB7A transcription factor is a potent repressor of HbF production. LRF inactivation derepresses embryonic/fetal _-globin expression in mouse and human adult erythroid cells. more...
Organism:
Mus musculus; Homo sapiens
Type:
Expression profiling by high throughput sequencing; Genome binding/occupancy profiling by high throughput sequencing
Platforms:
GPL17021 GPL16791
35 Samples
Download data: CSV, TDF
Series
Accession:
GSE74977
ID:
200074977
6.

Inactivation of BCL11A reactivates silenced human HbF in adult mice

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.
Organism:
Mus musculus
Type:
Expression profiling by array; Genome binding/occupancy profiling by high throughput sequencing
Platforms:
GPL14759 GPL1261
9 Samples
Download data: BED, CEL, WIG
Series
Accession:
GSE28355
ID:
200028355
7.

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

(Submitter supplied) 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
Organism:
Mus musculus
Type:
Expression profiling by array
Platform:
GPL1261
6 Samples
Download data: CEL
Series
Accession:
GSE28333
ID:
200028333
8.

HIC2 represses BCL11A transcription to regulate hemoglobin switching during development [CUT&RUN]

(Submitter supplied) The switch from fetal to adult hemoglobin production has been studied in great depth in part because of its relevance to the treatment of hemolobinopathies. Transcription factor BCL11A, which is essential for repression of the fetal beta-type globin (γ-globin) genes after birth, is largely controlled at the level of transcription but the mechanism of BCL11A developmental control is unknown. Here, using a CRISPR-Cas9 screen in human erythroblasts, we identify transcription factor HIC2 as a repressor of BCL11A transcription. more...
Organism:
Homo sapiens
Type:
Other
Platform:
GPL30173
8 Samples
Download data: BED, BIGWIG
Series
Accession:
GSE182530
ID:
200182530
9.

HIC2 represses BCL11A transcription to regulate hemoglobin switching during development

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.
Organism:
Homo sapiens; Mus musculus
Type:
Expression profiling by high throughput sequencing; Non-coding RNA profiling by array; Other
Platforms:
GPL30172 GPL30173
65 Samples
Download data: BED, BIGWIG, TSV
Series
Accession:
GSE173587
ID:
200173587
10.

HIC2 represses BCL11A transcription to regulate hemoglobin switching during development (RNA-Seq)

(Submitter supplied) The switch from fetal to adult hemoglobin production has been studied in great depth in part because of its relevance to the treatment of hemolobinopathies. Transcription factor BCL11A, which is essential for repression of the fetal beta-type globin (γ-globin) genes after birth, is largely controlled at the level of transcription but the mechanism of BCL11A developmental control is unknown. Here, using a CRISPR-Cas9 screen in human erythroblasts, we identify transcription factor HIC2 as a repressor of BCL11A transcription. more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL30173
10 Samples
Download data: TSV
11.

HIC2 represses BCL11A transcription to regulate hemoglobin switching during development (ChIP-Seq)

(Submitter supplied) The switch from fetal to adult hemoglobin production has been studied in great depth in part because of its relevance to the treatment of hemolobinopathies. Transcription factor BCL11A, which is essential for repression of the fetal beta-type globin (γ-globin) genes after birth, is largely controlled at the level of transcription but the mechanism of BCL11A developmental control is unknown. Here, using a CRISPR-Cas9 screen in human erythroblasts, we identify transcription factor HIC2 as a repressor of BCL11A transcription. more...
Organism:
Homo sapiens; Mus musculus
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platforms:
GPL30172 GPL30173
27 Samples
Download data: BED, BIGWIG
Series
Accession:
GSE173584
ID:
200173584
12.

HIC2 represses BCL11A transcription to regulate hemoglobin switching during development (Capture-C)

(Submitter supplied) The switch from fetal to adult hemoglobin production has been studied in great depth in part because of its relevance to the treatment of hemolobinopathies. Transcription factor BCL11A, which is essential for repression of the fetal beta-type globin (γ-globin) genes after birth, is largely controlled at the level of transcription but the mechanism of BCL11A developmental control is unknown. Here, using a CRISPR-Cas9 screen in human erythroblasts, we identify transcription factor HIC2 as a repressor of BCL11A transcription. more...
Organism:
Homo sapiens
Type:
Other
Platform:
GPL30173
8 Samples
Download data: BIGWIG
Series
Accession:
GSE173583
ID:
200173583
13.

HIC2 represses BCL11A transcription to regulate hemoglobin switching during development (ATAC-Seq)

(Submitter supplied) The switch from fetal to adult hemoglobin production has been studied in great depth in part because of its relevance to the treatment of hemolobinopathies. Transcription factor BCL11A, which is essential for repression of the fetal beta-type globin (γ-globin) genes after birth, is largely controlled at the level of transcription but the mechanism of BCL11A developmental control is unknown. Here, using a CRISPR-Cas9 screen in human erythroblasts, we identify transcription factor HIC2 as a repressor of BCL11A transcription. more...
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL30173
12 Samples
Download data: BIGWIG
Series
Accession:
GSE173582
ID:
200173582
14.

Gene expression data from E14.5 Pogz-WT and Pogz-KO fetal livers.

(Submitter supplied) Fetal and adult β-globin gene expression is tightly regulated during human development. Fetal globin genes are transcriptionally silenced during embryogenesis through the process of hemoglobin switching. Efforts to understand the transcriptional mechanism(s) behind fetal globin silencing have led to novel strategies to derepress fetal globin expression in the adult, which could alleviate symptoms in hereditary b-globin disorders including sickle cell disease (SCD) and β-thalassemia. more...
Organism:
Mus musculus
Type:
Expression profiling by array
Platform:
GPL1261
6 Samples
Download data: CEL, CHP
Series
Accession:
GSE113503
ID:
200113503
15.

Transcription factor competition at the γ-globin promoters controls hemoglobin switching [CRISPR Screen]

(Submitter supplied) BCL11A, the major regulator of HbF(α2γ2) level, represses γ-globin expression through direct promoter binding in adult erythroid cells in a switch to adult adult-type HbA (α2β2) production. Yet, the mechanism remains unclear. To uncover how BCL11A initiates repression, we used CRISPR/Cas9 and dCas9 screens to dissect the γ-globin promoters and identified an apparent activator element near the BCL11A binding region. more...
Organism:
Homo sapiens
Type:
Other
Platform:
GPL15520
24 Samples
Download data: BED, BEDGRAPH
Series
Accession:
GSE160456
ID:
200160456
16.

Transcription factor competition at the γ-globin promoters controls hemoglobin switching

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing; Expression profiling by high throughput sequencing
Platforms:
GPL24676 GPL18573 GPL15520
97 Samples
Download data: BEDGRAPH, BIGWIG, BW
Series
Accession:
GSE150530
ID:
200150530
17.

Transcription factor competition at the γ-globin promoters controls hemoglobin switching [CUT&RUN]

(Submitter supplied) BCL11A, the major regulator of HbF(α2γ2) level, represses γ-globin expression through direct promoter binding in adult erythroid cells in a switch to adult adult-type HbA (α2β2) production. Yet, the mechanism remains unclear. To uncover how BCL11A initiates repression, we used CRISPR/Cas9 and dCas9 screens to dissect the γ-globin promoters and identified an apparent activator element near the BCL11A binding region. more...
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platforms:
GPL18573 GPL24676
54 Samples
Download data: BIGWIG, BW
Series
Accession:
GSE150529
ID:
200150529
18.

Transcription factor competition at the γ-globin promoters controls hemoglobin switching [PRO-seq]

(Submitter supplied) BCL11A, the major regulator of HbF(α2γ2) level, represses γ-globin expression through direct promoter binding in adult erythroid cells in a switch to adult adult-type HbA (α2β2) production. Yet, the mechanism remains unclear. To uncover how BCL11A initiates repression, we used CRISPR/Cas9 and dCas9 screens to dissect the γ-globin promoters and identified an apparent activator element near the BCL11A binding region. more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL18573
8 Samples
Download data: BEDGRAPH, CSV
19.

Transcription factor competition at the γ-globin promoters controls hemoglobin switching [ChIP-seq]

(Submitter supplied) BCL11A, the major regulator of HbF(α2γ2) level, represses γ-globin expression through direct promoter binding in adult erythroid cells in a switch to adult adult-type HbA (α2β2) production. Yet, the mechanism remains unclear. To uncover how BCL11A initiates repression, we used CRISPR/Cas9 and dCas9 screens to dissect the γ-globin promoters and identified an apparent activator element near the BCL11A binding region. more...
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL18573
6 Samples
Download data: BW
Series
Accession:
GSE150490
ID:
200150490
20.

Transcription factor competition at the γ-globin promoters controls hemoglobin switching [ATACseq]

(Submitter supplied) BCL11A, the major regulator of HbF(α2γ2) level, represses γ-globin expression through direct promoter binding in adult erythroid cells in a switch to adult adult-type HbA (α2β2) production. Yet, the mechanism remains unclear. To uncover how BCL11A initiates repression, we used CRISPR/Cas9 and dCas9 screens to dissect the γ-globin promoters and identified an apparent activator element near the BCL11A binding region. more...
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL18573
5 Samples
Download data: BIGWIG, BW
Series
Accession:
GSE150488
ID:
200150488
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