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Links from GEO DataSets

Items: 20

1.

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
2.

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
3.

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
4.

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
5.

Eed inactivation in Cdkn2a-null MLL-AF9 transformed cells

(Submitter supplied) We sequenced mRNA from MLL-AF9 transformed Cdkn2ako murine LSK-cells with and without a functional Eed locus
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL13112
2 Samples
Download data: TXT
Series
Accession:
GSE70904
ID:
200070904
6.

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
7.

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
8.

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
9.

PRC2 is required for acute myeloid leukemias initiated by MLL-AF9

(Submitter supplied) The transcriptional activating and repressive functions performed by Trithorax and Polycomb group complexes, respectively, are critical for to maintain cellular fates in ontogeny and in cancer. Here we report that leukemias initiated by a Trithorax-related oncogene, MLL-AF9, depend upon the Polycomb Repressive Complex 2 (PRC2) to sustain a transformed cellular state. RNAi mediated suppression of PRC2 subunits is sufficient to inhibit proliferation of MLL-AF9 leukemias, with little impact on growth of non-transformed cells. more...
Organism:
Mus musculus
Type:
Expression profiling by array
Platform:
GPL6246
9 Samples
Download data: CEL
Series
Accession:
GSE34183
ID:
200034183
10.

An Ezh2 and Ezh1 dual inhibitor, UNC1999, re-shapes the landscape of H3K27me3 versus H3K27ac in MLL-AF9-transformed murine leukemia

(Submitter supplied) Ezh2 and EZH1 are histone H3 lysine 27 (H3K27)-specific methyltransferases. Their hyperactive mutations and overexpression were found in cancer including various hematological malignancies. UNC1999 is a highly selective inhibitor for both enzymes. It suppresses H3K27 tri- and di-methylation globally and inhibits growth of MLL-rearranged acute leukemia. Here we performed ChIP-Seq to profile how UNC1999 affects distribution of H3K27me3 and its antagonizing H3K27ac in MLL-AF9-immortalized leukemia cells. more...
Organism:
Mus musculus
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL13112
11 Samples
Download data: WIG
Series
Accession:
GSE62437
ID:
200062437
11.

Expression data of MLL-AF9-transformed murine leukemia progenitor cells, following treatment with UNC1999, a dual Ezh1 and Ezh2 inhibitor, or knockdown of EED

(Submitter supplied) Ezh2 and EZH1 are histone H3 lysine 27 specific methyltransferase. Their hyperactive mutations and overexpression were found in cancer including various hematological malignancies. UNC1999 is a highly selective inhibitor for both enzymes. It suppresses H3K27 tri- and di-methylation globally and inhibits growth of MLL-rearranged acute leukemia cell lines. UNC2400, a di-methylated derivative of UNC1999, is employed an inactive analog compound for assessment of off-target effects. more...
Organism:
Mus musculus
Type:
Expression profiling by array
Platform:
GPL17400
22 Samples
Download data: CEL
Series
Accession:
GSE62198
ID:
200062198
12.

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
13.

Bap1 loss results in EZH2 dependent transformation

(Submitter supplied) Analysis of sorted granulocyte macrophage progenitors (GMPs) in control and Bap1-deficient bone marrow cells. Loss of Bap1 in the hematopoietic compartments results in an MDS-like disease. These data allow for the examination of the genetic underpinnings of Bap1 loss in disease.
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL18635
6 Samples
Download data: TXT
Series
Accession:
GSE61577
ID:
200061577
14.

Bap1 loss results in EZH2 dependent transformation

(Submitter supplied) BAP1 and ASXL1 interact to form a polycomb deubiquitinase complex that removes monoubiquitin from histone H2A lysine 119 (H2AK119Ub). However, BAP1 and ASXL1 are mutated in distinct cancer types, consistent with independent roles in regulating epigenetic state and malignant transformation. Here we demonstrate that Bap1 loss results in increased trimethylated histone H3 lysine 27 (H3K27me3), elevated Ezh2 expression, and enhanced repression of Polycomb Repressive Complex 2 (PRC2) targets. more...
Organism:
Mus musculus
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL13112
11 Samples
Download data: BW
Series
Accession:
GSE61360
ID:
200061360
15.

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
16.

ChIP-on-chip from acute myeloid leukemia cell lines and clinical samples for H3K4me3, H3K27me3, and EZH2

(Submitter supplied) Histone modifcations at the p15INK4b gene were compared in sample with p15INK4b DNA methylation vs. samples with no DNA methylation AML clinical samples without DNA methylation exhibit bivalent histone modifications at p15INK4b, while clinical samples with DNA methylation display lower H3K4me3 and retain H3K27me3
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by genome tiling array
Platform:
GPL8754
40 Samples
Download data: TXT
Series
Accession:
GSE16730
ID:
200016730
17.

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
18.

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
19.
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
20.

H3K9me3 ChIP-seq in MLL-rearranged leukemic stem cells and hematopoietic stem cells

(Submitter supplied) Acute myeloid leukemia (AML) with rearrangement of the mixed-lineage leukemia (MLL) gene are the most aggressive hematopoietic malignancies. Previous studies demonstrated the distribution of several epigenetic modifications including H3K9me3, H3K79me2, H3K36me3, H3K4me3 and H3K27me3, in MLL-AF9 transformed murine cells. Here, we examined the H3K9me3 distribution in c-Kit+ cells (enriched with stem/progenitor cells) from both MLL-AF9 transformed murine cells in parallel with control wild-type cells, and found an overall lower distribution of H3K9me3 in leukemia stem cells than normal hematopoietic stem/progenitor cells.
Organism:
Mus musculus
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL17021
8 Samples
Download data: WIG
Series
Accession:
GSE132175
ID:
200132175
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