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Links from GEO DataSets

Items: 20

1.

Enhancer profiling of chronic lymphocytic leukemia cells

(Submitter supplied) Enhancer profiling has emerged as a powerful approach for discovering the cis-regulatory elements that define transcriptional core regulatory circuits. Characteristic biochemical and biophysical attributes of chromatin mark active enhancer elements, which can be leveraged with genome-wide assay technologies for discovery. This includes chromatin immunoprecipitation followed by sequencing (ChIP-seq) for histone H3 acetylated lysine 27 (H3K27ac). more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing; Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL18573
36 Samples
Download data: BEDGRAPH, XLSX
2.

NF-kB coordinates rapid, BRD4-dependent remodeling of proinflammatory super-enhancers [Chem-Seq]

(Submitter supplied) Proinflammatory stimuli rapidly and globally remodel chromatin landscape, thereby enabling transcriptional responses. Yet, the mechanisms coupling chromatin regulators to the master regulatory inflammatory transcription factor NF-kB remain poorly understood.  We report in human endothelial cells (ECs) that activated NF-kB binds to enhancers, provoking a rapid, global redistribution of BRD4 preferentially at super-enhancers, large enhancer domains highly bound by chromatin regulators. more...
Organism:
Homo sapiens
Type:
Other
Platform:
GPL11154
3 Samples
Download data: WIG
Series
Accession:
GSE60051
ID:
200060051
3.

NF-kB coordinates rapid, BRD4-dependent remodeling of proinflammatory super-enhancers

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.
Organism:
Homo sapiens
Type:
Expression profiling by array; Genome binding/occupancy profiling by high throughput sequencing; Other
Platforms:
GPL11154 GPL16043
36 Samples
Download data: CEL, WIG
Series
Accession:
GSE54000
ID:
200054000
4.

NF-kB coordinates rapid, BRD4-dependent remodeling of proinflammatory super-enhancers [Affymetrix]

(Submitter supplied) Proinflammatory stimuli rapidly and globally remodel chromatin landscape, thereby enabling transcriptional responses. Yet, the mechanisms coupling chromatin regulators to the master regulatory inflammatory transcription factor NF-kB remain poorly understood.  We report in human endothelial cells (ECs) that activated NF-kB binds to enhancers, provoking a rapid, global redistribution of BRD4 preferentially at super-enhancers, large enhancer domains highly bound by chromatin regulators. more...
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL16043
12 Samples
Download data: CEL
Series
Accession:
GSE53999
ID:
200053999
5.

NF-kB coordinates rapid, BRD4-dependent remodeling of proinflammatory super-enhancers [ChIP-Seq]

(Submitter supplied) Proinflammatory stimuli rapidly and globally remodel chromatin landscape, thereby enabling transcriptional responses. Yet, the mechanisms coupling chromatin regulators to the master regulatory inflammatory transcription factor NF-kB remain poorly understood.  We report in human endothelial cells (ECs) that activated NF-kB binds to enhancers, provoking a rapid, global redistribution of BRD4 preferentially at super-enhancers, large enhancer domains highly bound by chromatin regulators. more...
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL11154
21 Samples
Download data: WIG
Series
Accession:
GSE53998
ID:
200053998
6.

Linking aberrant chromatin features in chronic lymphocytic leukemia to deregulated transcription factor networks

(Submitter supplied) In chronic lymphocytic leukemia (CLL) a diverse set of genetic mutations is embedded in a deregulated epigenetic landscape that drives cancerogenesis. To elucidate the role of aberrant chromatin features, we mapped DNA methylation, 7 histone modifications, nucleosome positions, chromatin accessibility, binding of EBF1 and CTCF as well as the transcriptome of B cells from CLL patients and healthy donors. more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing; Genome binding/occupancy profiling by high throughput sequencing; Methylation profiling by high throughput sequencing
Platforms:
GPL20301 GPL11154
519 Samples
Download data: BIGBED, BW
Series
Accession:
GSE113336
ID:
200113336
7.

BRD4 profiling identifies critical Chronic Lymphocytic Leukemia oncogenic circuits and reveals sensitivity to PLX51107, a novel structurally distinct BET inhibitor

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.
Organism:
Homo sapiens
Type:
Expression profiling by array; Genome binding/occupancy profiling by high throughput sequencing
Platforms:
GPL18573 GPL17586 GPL20301
58 Samples
Download data: BED, CEL, CHP
Series
Accession:
GSE109593
ID:
200109593
8.

BRD4 profiling identifies critical Chronic Lymphocytic Leukemia oncogenic circuits and reveals sensitivity to PLX51107, a novel structurally distinct BET inhibitor [expression profiling]

(Submitter supplied) Bromodomain and extra-terminal (BET) family proteins are key regulators of gene expression in cancer. Herein, we utilize BRD4 profiling to identify critical pathways involved in pathogenesis of chronic lymphocytic leukemia (CLL). BRD4 is over-expressed in CLL and is enriched proximal to genes up-regulated or de novo expressed in CLL with known function in disease pathogenesis and progression. These genes, including key members of the BCR signaling pathway, provide rationale for this therapeutic approach to identify new targets in alternative types of cancer. more...
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL17586
9 Samples
Download data: CEL, CHP
Series
Accession:
GSE109587
ID:
200109587
9.

BRD4 profiling identifies critical Chronic Lymphocytic Leukemia oncogenic circuits and reveals sensitivity to PLX51107, a novel structurally distinct BET inhibitor [ChIP-seq]

(Submitter supplied) Bromodomain and extra-terminal (BET) family proteins are key regulators of gene expression in cancer. Herein, we utilize BRD4 profiling to identify critical pathways involved in pathogenesis of chronic lymphocytic leukemia (CLL). BRD4 is over-expressed in CLL and is enriched proximal to genes up-regulated or de novo expressed in CLL with known function in disease pathogenesis and progression. These genes, including key members of the BCR signaling pathway, provide rationale for this therapeutic approach to identify new targets in alternative types of cancer. more...
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platforms:
GPL20301 GPL18573
49 Samples
Download data: BED, XLSX
Series
Accession:
GSE109411
ID:
200109411
10.

HDAC1 regulates the chromatin landscape to control transcriptional dependencies in chronic lymphocytic leukemia

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing; Genome binding/occupancy profiling by high throughput sequencing; Non-coding RNA profiling by high throughput sequencing
Platforms:
GPL18573 GPL20301
71 Samples
Download data: BROADPEAK, NARROWPEAK
Series
Accession:
GSE216290
ID:
200216290
11.

HDAC1 regulates the chromatin landscape to control transcriptional dependencies in chronic lymphocytic leukemia [miRNA-seq]

(Submitter supplied) Chronic lymphocytic leukemia (CLL) is a quiescent B-cell malignancy that depends on transcriptional dysregulation for survival. The histone deacetylases are transcriptional regulators whose role within the regulatory chromatin and consequence on the CLL transcriptome is poorly characterized. Here, we profiled and integrated the genome wide occupancy of HDAC1, BRD4, H3K27Ac and H3K9Ac signals with chromatin accessibility, Pol2 occupancy and target expression signatures in CLL cells. more...
Organism:
Homo sapiens
Type:
Non-coding RNA profiling by high throughput sequencing
Platform:
GPL20301
20 Samples
Download data: TXT
Series
Accession:
GSE216289
ID:
200216289
12.

HDAC1 regulates the chromatin landscape to control transcriptional dependencies in chronic lymphocytic leukemia [RNA-seq]

(Submitter supplied) Chronic lymphocytic leukemia (CLL) is a quiescent B-cell malignancy that depends on transcriptional dysregulation for survival. The histone deacetylases are transcriptional regulators whose role within the regulatory chromatin and consequence on the CLL transcriptome is poorly characterized. Here, we profiled and integrated the genome wide occupancy of HDAC1, BRD4, H3K27Ac and H3K9Ac signals with chromatin accessibility, Pol2 occupancy and target expression signatures in CLL cells. more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL20301
20 Samples
Download data: TXT
Series
Accession:
GSE216288
ID:
200216288
13.

HDAC1 regulates the chromatin landscape to control transcriptional dependencies in chronic lymphocytic leukemia [ChIP-seq]

(Submitter supplied) Chronic lymphocytic leukemia (CLL) is a quiescent B-cell malignancy that depends on transcriptional dysregulation for survival. The histone deacetylases are transcriptional regulators whose role within the regulatory chromatin and consequence on the CLL transcriptome is poorly characterized. Here, we profiled and integrated the genome wide occupancy of HDAC1, BRD4, H3K27Ac and H3K9Ac signals with chromatin accessibility, Pol2 occupancy and target expression signatures in CLL cells. more...
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL18573
31 Samples
Download data: BROADPEAK, NARROWPEAK
Series
Accession:
GSE216287
ID:
200216287
14.

ChIPSeq data from melanoma cancer cell line CHL-1 after Bromodomain and extra terminal (Bet) domain inhibitor treatment

(Submitter supplied) Bromodomain and extra terminal domain (BET) inhibition reduces occupancy of BET-family proteins at promoter and enhancer sites finally leading to genome wide changes in gene transcription. We used ChIPSeq profiling to investigate genome wide changes in promoter and enhancer occupancy induced by BET inhibitors BAY 1238097 and OTX-015, respectively.
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL16791
18 Samples
Download data: BW
Series
Accession:
GSE95585
ID:
200095585
15.

BET Bromodomain Inhibition Suppresses the Function of Hematopoietic Transcription Factors in Acute Myeloid Leukemia

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing; Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL13112
37 Samples
Download data: BIGWIG, TXT
Series
Accession:
GSE66123
ID:
200066123
16.

BET Bromodomain Inhibition Suppresses the Function of Hematopoietic Transcription Factors in Acute Myeloid Leukemia [ChIP-Seq]

(Submitter supplied) The bromodomain and extraterminal (BET) protein Brd4 is a validated drug target in leukemia, yet its regulatory function in this disease is not well understood. Here, we show that Brd4 chromatin occupancy in acute myeloid leukemia closely correlates with the hematopoietic transcription factors (TFs) Pu.1, Fli1, Erg, C/EBPα, C/EBPβ, and Myb at nucleosome-depleted enhancer and promoter regions. We provide evidence that these TFs, in conjunction with the lysine acetyltransferase activity of p300/CBP, facilitate Brd4 recruitment to their occupied sites to promote transcriptional activation. more...
Organism:
Mus musculus
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL13112
29 Samples
Download data: BIGWIG
Series
Accession:
GSE66122
ID:
200066122
17.

BET Bromodomain Inhibition Suppresses the Function of Hematopoietic Transcription Factors in Acute Myeloid Leukemia [RNA-Seq]

(Submitter supplied) The bromodomain and extraterminal (BET) protein Brd4 is a validated drug target in leukemia, yet its regulatory function in this disease is not well understood. Here, we show that Brd4 chromatin occupancy in acute myeloid leukemia closely correlates with the hematopoietic transcription factors (TFs) Pu.1, Fli1, Erg, C/EBPα, C/EBPβ, and Myb at nucleosome-depleted enhancer and promoter regions. We provide evidence that these TFs, in conjunction with the lysine acetyltransferase activity of p300/CBP, facilitate Brd4 recruitment to their occupied sites to promote transcriptional activation. more...
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL13112
8 Samples
Download data: TXT
Series
Accession:
GSE66068
ID:
200066068
18.

Enhancer Domains in Gastrointestinal Stromal Tumor Regulate KIT Expression and are Targetable by BET Bromodomain Inhibition

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing; Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL18573
36 Samples
Download data: WIG
Series
Accession:
GSE113217
ID:
200113217
19.

Enhancer Domains in Gastrointestinal Stromal Tumor Regulate KIT Expression and are Targetable by BET Bromodomain Inhibition [RNA-seq]

(Submitter supplied) Gastrointestinal stromal tumor (GIST) is a mesenchymal neoplasm characterized by activating mutations in the related receptor tyrosine kinases KIT or PDGFRA. GIST relies on expression of these unamplified receptor tyrosine kinase (RTK) genes through a large enhancer domain, producing high expression levels of the oncogene required for tumor growth. Though kinase inhibition is an effective therapy for many GIST patients, disease progression from kinase resistance mutations is common, and no other efficacious classes of systemic therapy exist. more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL18573
18 Samples
Download data: TXT
20.

Enhancer Domains in Gastrointestinal Stromal Tumor Regulate KIT Expression and are Targetable by BET Bromodomain Inhibition [ChIP-seq]

(Submitter supplied) Gastrointestinal stromal tumor (GIST) is a mesenchymal neoplasm characterized by activating mutations in the related receptor tyrosine kinases KIT or PDGFRA. GIST relies on expression of these unamplified receptor tyrosine kinase (RTK) genes through a large enhancer domain, producing high expression levels of the oncogene required for tumor growth. Though kinase inhibition is an effective therapy for many GIST patients, disease progression from kinase resistance mutations is common, and no other efficacious classes of systemic therapy exist. more...
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL18573
18 Samples
Download data: WIG
Series
Accession:
GSE113207
ID:
200113207
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