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Links from GEO DataSets

Items: 20

1.

Notch1-driven transcriptional changes in a mouse model of T-ALL

(Submitter supplied) T-cell acute lymphoblastic leukemia (T-ALL) is an immature hematopoietic malignancy driven mainly by oncogenic activation of NOTCH1 signaling. In this study we used a mouse model of T-ALL through the overexpression of the intarcellular transcriptionally active part of Notch1 (N1-IC). This model faithfully recapitulates the major characteristics of the human disease. Comparison of the leukemic cells from peripheral tumors(thymoma) of this mouse model to normal thymic cells Double Positive (DP) for the markers CD4 and CD8 that express very low levels of Notch1 showed major expression changes in pathways controlling the transition from physiology to disease. more...
Organism:
Mus musculus
Type:
Expression profiling by array
Dataset:
GDS4303
Platform:
GPL1261
4 Samples
Download data: CEL
Series
Accession:
GSE34554
ID:
200034554
2.

Notch1-driven epigenetic changes in a mouse model of T cell Acute Lymphoblastic Leukemia (T-ALL)

(Submitter supplied) T-cell acute lymphoblastic leukemia (T-ALL) is an immature hematopoietic malignancy driven mainly by oncogenic activation of NOTCH1 signaling. In this study we used a mouse model of T-ALL through the overexpression of the intarcellular transcriptionally active part of Notch1 (N1-IC). This model faithfully recapitulates the major characteristics of the human disease. Comparison of the leukemic cells from peripheral tumors(thymoma) of this mouse model to normal thymic cells Double Positive (DP) for the markers CD4 and CD8 that express very low levels of Notch1 showed major expression changes (please see GSE34554) in pathways controlling the transition from physiology to disease. more...
Organism:
Mus musculus
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL9250
18 Samples
Download data: BED
Series
Accession:
GSE34954
ID:
200034954
3.
Full record GDS4303

Notch1 overexpression model of T-cell acute lymphoblastic leukemia: double positive CD4+/8+ cells

Analysis of DP (CD4+/8+) cells from an intracellular Notch1 (Notch1-IC)-induced T-ALL model that recapitulates most features of human T-ALL. T-ALL malignancy is driven by oncogenic activation of NOTCH1 signaling. Results provide insight into the molecular basis of Notch1-driven leukemogenesis.
Organism:
Mus musculus
Type:
Expression profiling by array, count, 2 tissue sets
Platform:
GPL1261
Series:
GSE34554
4 Samples
Download data: CEL
4.

Leucegene: ALL sequencing

(Submitter supplied) RNA sequencing of human leukemia
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL11154
12 Samples
Download data: TXT
5.

The Polycomb Repressive Complex 2 Is Required For MLL-AF9 Leukemia

(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:
GPL13112 GPL1261
23 Samples
Download data: CEL, WIG
Series
Accession:
GSE34963
ID:
200034963
6.

Epigenetic profiling of WT and Ezh2-null MLL-AF9 murine leukemic cells

(Submitter supplied) Chromatin immunoprecipitation (ChIP) for H3K27me3 followed by Solexa sequencing in WT and Ezh2-null leukemic cells from primary and secondary recipients.
Organism:
Mus musculus
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL13112
4 Samples
Download data: WIG
Series
Accession:
GSE34962
ID:
200034962
7.

Expression profiling of secondary wild type (WT) and Ezh2-null murine MLL-AF9 AML

(Submitter supplied) We evaluated gene expression changes in secondary recipient murine leukemia caused by retroviral overexpression of MLL-AF9. We compared wild-type (WT) leukemia cells with mutant leukemia cells after cre-mediated inactivation of a homozygous conditional allele for Ezh2, a component of the Polycomb Repressive Complex2.
Organism:
Mus musculus
Type:
Expression profiling by array
Platform:
GPL1261
9 Samples
Download data: CEL, TXT
Series
Accession:
GSE34961
ID:
200034961
8.

Expression profiling of primary wild type (WT), Ezh2-null and Eed-null murine MLL-AF9 AML

(Submitter supplied) We evaluated gene expression changes in murine leukemia caused by retroviral overexpression of MLL-AF9. We compared wild-type (WT) leukemia cells with mutant leukemia cells after cre-mediated inactivation of homozygous conditional alleles for Ezh2 or Eed, both of which are components of the Polycomb Repressive Complex2.
Organism:
Mus musculus
Type:
Expression profiling by array
Platform:
GPL1261
10 Samples
Download data: CEL, TXT
Series
Accession:
GSE34959
ID:
200034959
9.

DMSO control and DZNep treated MOLM-14 cells

(Submitter supplied) We demonstrated that 3-Deazaneplanocin A (DZNep), a histone methyltransferase inhibitor, induce robust apoptosis in AML cells through increased ROS production and ER stress. We identified a core gene signature including TXNIP, a major redox control molecule which is crucial in DZNep-induced apoptosis.
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL6244
4 Samples
Download data: CEL
Series
Accession:
GSE30315
ID:
200030315
10.

Expression data from CD4-CD8-(DN) thymic cells isolated from WT, Ezh2Δ/Δ, p53Δ/Δ, and Ezh2Δ/Δp53Δ/Δ mice

(Submitter supplied) Loss-of-function mutations in EZH2 are associated with poor outcomes in patients with early T cell precursor ALL (ETP-ALL). To understand how EZH2 insufficiency is involved in the pathogenesis of ETP-ALL, we generated mice compound for both Ezh2 and Trp53 conditional deletions.
Organism:
Mus musculus
Type:
Expression profiling by array
Platform:
GPL10787
14 Samples
Download data: TXT
Series
Accession:
GSE95655
ID:
200095655
11.

Ezh2 and H3K27me3 in cardiomyocytes

(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
5 Samples
Download data: GFF, TXT
Series
Accession:
GSE29997
ID:
200029997
12.

ChIP-seq of Ezh2 and H3K27me3 in E12.5 heart apex

(Submitter supplied) Ezh2 and H3K27me3 binding sites in E12.5 heart apex
Organism:
Mus musculus
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL13112
3 Samples
Download data: GFF, TXT
Series
Accession:
GSE29994
ID:
200029994
13.

Genome-wide profiling of E12.5 cardiomyocytes RNA expression in both heterozygous control and mutant

(Submitter supplied) Congenital heart disease is among the most frequent major birth defects. Epigenetic marks are crucial for organogenesis, but their role in heart development is poorly understood. Polycomb Repressive Complex 2 (PRC2) trimethylates histone H3 at lysine 27, establishing H3K27me3 repressive epigenetic marks that promote tissue-specific differentiation by silencing ectopic gene programs. We studied the function of the catalytic subunit of PRC2, EZH2, in murine heart development. more...
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL13112
2 Samples
Download data: TXT
Series
Accession:
GSE29992
ID:
200029992
14.

Genome-wide mapping of Polycomb target genes unravels their roles in cell fate transitions

(Submitter supplied) The Polycomb group (PcG) proteins form chromatin-modifying complexes that are essential for embryonic development and stem cell renewal and are commonly deregulated in cancer. Here, we identify their target genes using genome-wide location analysis in human embryonic fibroblasts. We find that Polycomb-Repressive Complex 1 (PRC1), PRC2, and tri-methylated histone H3K27 co-occupy >1000 silenced genes with a strong functional bias for embryonic development and cell fate decisions. more...
Organism:
Homo sapiens
Type:
Expression profiling by array
Dataset:
GDS2445
Platform:
GPL96
15 Samples
Download data: CEL
Series
Accession:
GSE6015
ID:
200006015
15.
Full record GDS2445

Polycomb group protein depletion effect on embryonic fibroblasts

Analysis of embryonic fibroblasts depleted of the polycomb group (PcG) proteins EZH2, EED, SUZ12, or BMI-1. PcG proteins form complexes that regulate the expression of homeotic genes during development. Results provide insight into the mechanisms employed by PcGs to control development.
Organism:
Homo sapiens
Type:
Expression profiling by array, count, 5 protocol sets
Platform:
GPL96
Series:
GSE6015
15 Samples
Download data: CEL
16.

Expression data from Ezh2-null erythrocyte/megakaryocyte progenitor (MEP)

(Submitter supplied) The polycomb group (PcG) proteins function in gene silencing through histone modifications. They form chromatin-associated multiprotein complexes, termed polycomb repressive complex (PRC) 1 and PRC2. These two complexes work in a coordinated manner in the maintenance of cellular memories through transcriptional repression of target genes. EZH2 is a catalytic component of PRC2 and trimethylates histone H3 at lysine 27 to transcriptionally repress the target genes. more...
Organism:
Mus musculus
Type:
Expression profiling by array
Platform:
GPL10333
4 Samples
Download data: TXT
Series
Accession:
GSE32929
ID:
200032929
17.

Comparison Ezh1 and Ezh2 binding by ChIP on chip in F9 mouse cells

(Submitter supplied) Comparison of Ezh2 and Ezh1 promoter binding in F9 mouse teratoma cell line.
Organism:
Mus musculus
Type:
Genome binding/occupancy profiling by genome tiling array
Platforms:
GPL4129 GPL4128
8 Samples
Download data: TXT
Series
Accession:
GSE13467
ID:
200013467
18.

Epigenetic antagonism between Snf5 and Ezh2 during oncogenic transformation and elevated levels of H3K27me3 in Snf5-deficient cells

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.
Organism:
Mus musculus
Type:
Expression profiling by array; Genome binding/occupancy profiling by genome tiling array
Platforms:
GPL8321 GPL5811
28 Samples
Download data: BAR, BED, CEL
Series
Accession:
GSE23659
ID:
200023659
19.

Elevated levels of H3K27me3 in Snf5-deficient cells

(Submitter supplied) Epigenetic alterations have been increasingly implicated in oncogenesis. Analysis of Drosophila mutants suggests that Polycomb and SWI/SNF complexes can serve antagonistic developmental roles. However, the relevance of this relationship to human disease is unclear. Here we have investigated functional relationships between these epigenetic regulators in oncogenic transformation. Mechanistically, we show that loss of the SNF5 tumor suppressor leads to elevated expression of the Polycomb gene EZH2 and that Polycomb targets are broadly H3K27-trimethylated and repressed in SNF5-deficient fibroblasts and cancers. more...
Organism:
Mus musculus
Type:
Genome binding/occupancy profiling by genome tiling array
Platform:
GPL5811
5 Samples
Download data: BAR, BED, CEL
Series
Accession:
GSE23658
ID:
200023658
20.

Epigenetic antagonism between Snf5 and Ezh2 during oncogenic transformation

(Submitter supplied) Epigenetic alterations have been increasingly implicated in oncogenesis. Analysis of Drosophila mutants suggests that Polycomb and SWI/SNF complexes can serve antagonistic developmental roles. However, the relevance of this relationship to human disease is unclear. Here we have investigated functional relationships between these epigenetic regulators in oncogenic transformation. Mechanistically, we show that loss of the SNF5 tumor suppressor leads to elevated expression of the Polycomb gene EZH2 and that Polycomb targets are broadly H3K27-trimethylated and repressed in SNF5-deficient fibroblasts and cancers. more...
Organism:
Mus musculus
Type:
Expression profiling by array
Platform:
GPL8321
23 Samples
Download data: CEL
Series
Accession:
GSE23656
ID:
200023656
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