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Links from GEO DataSets

Items: 20

1.

Distal regulation of c-myb expression in human myeloid leukemia cells

(Submitter supplied) The transcription factor c-Myb a key regulator in proliferation and differentiation of hematopoietic progenitor cells, is precisely regulated during essential cellular processes. Overexpression and rearrangement of c-myb has been reported in human tumors including myeloid leukemia, but exact regulatory mechanisms have remained elusive. Here, we identified, using 4C assay with the c-myb promoter as an anchor, the interaction site at -34k region upstream of c-myb gene that are involved in c-myb expression. more...
Organism:
Homo sapiens
Type:
Other
Platform:
GPL20795
10 Samples
Download data: BEDGRAPH
Series
Accession:
GSE140321
ID:
200140321
2.

Distal regulation of c-myb expression during IL-6 induced differentiation in murine myeloid progenitor M1 cells

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.
Organism:
Mus musculus
Type:
Genome binding/occupancy profiling by high throughput sequencing; Other
Platforms:
GPL9185 GPL9250
3 Samples
Download data: XLSX
Series
Accession:
GSE81031
ID:
200081031
3.

Distal regulation of c-myb expression during IL-6 inudced differentiation in murine myeloid progenitor M1 cells [DHS-seq]

(Submitter supplied) We report DNAase1 hypersensitive sites located upstream of the c-myb gene,associated with gene expression
Organism:
Mus musculus
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL9250
2 Samples
Download data: TXT
Series
Accession:
GSE81030
ID:
200081030
4.

Distal regulation of c-myb expression during IL-6 induced differentiation in murine myeloid progenitor M1 cells [4C-seq]

(Submitter supplied) We report genome-wide long-range interactions of the c-myb promoter in M1 cells.
Organism:
Mus musculus
Type:
Other
Platform:
GPL9185
1 Sample
Download data: XLSX
Series
Accession:
GSE81029
ID:
200081029
5.

ChIP-on-chip from murine myeloid cell line M1 and virus-induced myeloid leukemia cell lines for H3K4me3, H3K9/14ac, H3K4me1, H3K27me3, H3K9me3 and CTCF

(Submitter supplied) Histone modifcations and CTCF binding at the c-myb locus were compared in cell lines with c-myb expressing, which are myeloblatic M1 cells and leukemia cells with virus integration, VS. M1 cells without c-myb expression induced by IL-6. Distribution of active histone marks at the c-myb gene and the upstream regions are associated with active c-myb transcription. The enrichment of all of these active histone marks decreased with differentiation-induced down-regulation of c-myb, but increased and spread in tumor cells.
Organism:
Mus musculus
Type:
Genome binding/occupancy profiling by array
4 related Platforms
28 Samples
Download data: TXT
Series
Accession:
GSE34770
ID:
200034770
6.

Expression profiling by high throughput sequencing of THP-1 cells treated with AT or HA

(Submitter supplied) Deregulation of transcription factor MYB contributes to the development of leukemia and other human cancers, making MYB an attractive target for drug development. We demonstrate that the natural sesquiterpene lactone (STL) 4,15-iso-atriplicolide tiglate (AT) is a novel potent inhibitor of MYB-dependent transcription. Further analysis revealed that C/EBPb, a transcription factor cooperating with MYB in myeloid cells, rather than MYB itself is inhibited by AT and related STLs. more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL18573
9 Samples
Download data: CNT, TXT
7.

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
8.

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
9.

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
10.

An Oncogenic Super-Enhancer Formed through Somatic Mutation of a Noncoding Intergenic Element

(Submitter supplied) In many cancers, critical oncogenes are driven from large regulatory elements, called super-enhancers, which recruit much of the cell’s transcriptional apparatus and are defined by extensive H3K27 acetylation. We found that in T-cell acute lymphoblastic leukemia (T-ALL), somatic heterozygous mutations introduce MYB binding motifs in a precise noncoding site, which nucleate a super-enhancer upstream of the TAL1 oncogene. more...
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platforms:
GPL16791 GPL11154 GPL9115
20 Samples
Download data: WIG
Series
Accession:
GSE59657
ID:
200059657
11.

Promoter-distal RNA polymerase II binding discriminates active from inactive CCAAT/enhancer-binding protein beta binding sites

(Submitter supplied) Transcription factors (TFs) bind to thousands of DNA sequences in mammalian genomes, but most of these binding events appear to have no direct effect on gene expression. It is unclear why only a subset of transcription factor bound sites are actively involved in transcriptional regulation, nor are the key genomic features known that discriminate between active and inactive TF binding events. Recent studies have identified promoter-distal RNA polymerase II (RNAP2) binding at enhancer elements, suggesting that these interactions may serve as a potential marker for active regulatory sequences. more...
Organism:
Homo sapiens
Type:
Other
Platform:
GPL11154
8 Samples
Download data: TXT
Series
Accession:
GSE73183
ID:
200073183
12.

MYB ChIP-Seq of K562 cells

(Submitter supplied) We analyzed genome-wide chromatin binding of the transcription factor c-Myb using ChIP-Seq. K-562 cell lines stably expressing N-termianl 3xTY tagged Myb (pEFneo-3xTY-Myb) and control cell lines expressing the tag (pEFneo-3xTY) were used.
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL18573
12 Samples
Download data: BW
Series
Accession:
GSE124541
ID:
200124541
13.

RNA-seq analysis in ARIEL knockdown Jurkat samples

(Submitter supplied) RNA-seq of control, shARIEL Jurkat cells
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL20301
4 Samples
Download data: TXT
14.

ATF4 regulates MYB to increase g-globin in response to loss of β-globin

(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
Platforms:
GPL20301 GPL18573
31 Samples
Download data: BIGWIG
Series
Accession:
GSE153768
ID:
200153768
15.

ATF4 regulates MYB to increase g-globin in response to loss of β-globin [ChIP-seq]

(Submitter supplied) Boontanrart et al model the cellular stress that occurs upon reduction in β-globin in human erythroid cells. Decrease in β-globin attenuates the eIF2aP-ATF4 pathway and results in upregulating fetal -globin. Down-regulation of ATF4 leads to decreased levels of the -globin repressor MYB through direct binding at the HBS1L-MYB intergenic region.
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL18573
13 Samples
Download data: BIGWIG
Series
Accession:
GSE153767
ID:
200153767
16.

ATF4 regulates MYB to increase g-globin in response to loss of β-globin [RNA-seq]

(Submitter supplied) Boontanrart et al model the cellular stress that occurs upon reduction in β-globin in human erythroid cells. Decrease in β-globin attenuates the eIF2aP-ATF4 pathway and results in upregulating fetal g-globin. Down-regulation of ATF4 leads to decreased levels of the g-globin repressor MYB through direct binding at the HBS1L-MYB intergenic region.
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL20301
18 Samples
Download data: TXT
Series
Accession:
GSE153764
ID:
200153764
17.

Interaction of c-Myb with p300 is required for the induction of acute myeloid leukemia (AML) by human AML oncogenes

(Submitter supplied) The MYB oncogene is widely expressed in acute leukemias and is important for the continued proliferation of leukemia cells, raising the possibility that MYB may be a therapeutic target. However realization of this potential requires (i) a significant therapeutic window for MYB inhibition, given its essential role in normal hematopoiesis; and (ii) an approach for developing an effective therapeutic. more...
Organism:
Mus musculus
Type:
Expression profiling by array
Platform:
GPL6885
16 Samples
Download data: TXT
Series
Accession:
GSE34224
ID:
200034224
18.

The AAA+ ATPAse RUVBL2 is essential for the oncogenic function of c-MYB in acute myeloid leukemia

(Submitter supplied) Subtype-specific leukemia oncogenes drive aberrant gene expression profiles that converge on common essential mediators to ensure leukemia self-renewal and inhibition of differentiation. The transcription factor c-MYB functions as one such mediator in a diverse range of leukemias. Here we show that transcriptional repression of myeloid differentiation associated c-MYB target genes in AML is enforced by the AAA+ ATPAse RUVBL2. more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL18573
4 Samples
Download data: BW
Series
Accession:
GSE117224
ID:
200117224
19.

Gene expression changes in THP1 cells at day 2 and 4 following shRNA knock-down of RUVBL2

(Submitter supplied) We used an inducible shRNA system and RNA-Seq to examine gene expression changes in acute myeloid leukemia THP1 cells following silencing of RUVBL2. RUVBL2 is a AAA+ ATPase that functions in a number of cellular processes, including chromatin remodeling and transcriptional control, and is critical for survival of acute myeloid leukemia cells and in vivo disease progression.
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL18573
12 Samples
Download data: CSV
20.

APOBEC Signature Mutation Forms an Oncogenic Enhancer Upstream of LMO1 in T-ALL

(Submitter supplied) Oncogenic driver mutations are those that provide a proliferative or survival advantage to neoplastic cells resulting in clonal selection. Although most cancer causing mutations have been detected in the protein-­coding regions of the cancer genome, driver mutations have recently also been discovered within noncoding genomic sequences. Thus, a current challenge is to gain precise understanding of how these unique genomic elements function in cancer pathogenesis, while clarifying mechanisms of gene regulation and identifying new targets for therapeutic intervention. more...
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL16791
1 Sample
Download data: WIG
Series
Accession:
GSE94391
ID:
200094391
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