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Links from GEO DataSets

Items: 20

1.

Gene expression analysis of leukemia-initiating cells of preleukemic compound URE-/+::Msh2-/- mice

(Submitter supplied) Expression profiling of FACS purified Lin-cKit+ cells from preleukemic compound URE-/+::Msh2-/- mice and control animals (two separate pools of 3 mice each)
Organism:
Mus musculus
Type:
Expression profiling by array
Platform:
GPL6246
4 Samples
Download data: CEL
Series
Accession:
GSE65669
ID:
200065669
2.

Gene expression analysis of leukemia-initiating cells of URE-/+::Msh2-/- mice

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.
Organism:
Mus musculus
Type:
Expression profiling by array
Platform:
GPL6246
9 Samples
Download data: CEL
Series
Accession:
GSE65671
ID:
200065671
3.

Gene expression analysis of leukemia-initiating cells of compound URE-/+::Msh2-/- mice

(Submitter supplied) Expression profiling of FACS purified Lin-cKit+ cells from compound URE-/+::Msh2-/- mice with AML and control animals
Organism:
Mus musculus
Type:
Expression profiling by array
Platform:
GPL6246
7 Samples
Download data: CEL
Series
Accession:
GSE65668
ID:
200065668
4.

Essential role of Jun family transcription factors in PU.1-induced leukemic stem cells

(Submitter supplied) Knockdown of the transcription factor PU.1 (Spi1) leads to acute myeloid leukemia (AML) in mice. We examined the transcriptome of PU.1 knockdown hematopoietic stem cells (HSC) in the preleukemic phase by linear amplification and genome-wide array analysis to identify transcriptional changes preceding malignant transformation. Hierarchical cluster analysis and principal component analysis clearly distinguished PU.1 knockdown from wildtype HSC. more...
Organism:
Mus musculus
Type:
Expression profiling by array
Dataset:
GDS2411
Platform:
GPL1261
6 Samples
Download data
Series
Accession:
GSE5654
ID:
200005654
5.
Full record GDS2411

Transcription factor PU.1 knockdown effect on hematopoietic stem cells

Analysis of preleukemic hematopoietic stem cells from animals knocked down for the transcription factor PU.1. PU.1 knockdown leads to acute myeloid leukemia in the animal. Results provide insight into the molecular changes preceding malignant transformation.
Organism:
Mus musculus
Type:
Expression profiling by array, count, 2 protocol sets
Platform:
GPL1261
Series:
GSE5654
6 Samples
Download data
DataSet
Accession:
GDS2411
ID:
2411
6.

Identification of CITED2 and PU.1 target genes in human CB

(Submitter supplied) CB CD34+ cells were isolated by Miltenyi miniMACS column. Cells were prestimulated in HPGM with 100 ng/ml KITL, FLT3L and TPO for 12 hrs. Cells were transduced with control, CITED2 overexpression lentivectors, shRNA PU.1 lentivectors or both, in two rounds over 48 hrs. Transduced cells were sorted after which RNA was isolated for Illumina beadchip arrays HT12 v4
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL10558
8 Samples
Download data: TXT
Series
Accession:
GSE118036
ID:
200118036
7.

Expression data from PU.1low URE-/- AML cell line after treatment with small molecule acting as PU.1 inhibitor

(Submitter supplied) Downregulation of the hematopoietic transcription factor PU.1 in PU.1 low acute myeloid leukemia cells (AML) by novel heterocyclic diamidines or PU.1 inhibitors leads to decrease cell proliferation and apoptosis, representing a new therapeutic strategy for AML treatment. These inhibitors induces decreased PU.1 binding on its target sites, as well as deregulation in PU.1 canonical target genes We used microarray to identify the pathways deregulated after drug treatment.
Organism:
Mus musculus
Type:
Expression profiling by array
Platform:
GPL16570
6 Samples
Download data: CEL, CHP
Series
Accession:
GSE77651
ID:
200077651
8.

LSD1 inhibition by tranylcypromine derivatives interferes with GFI1-mediated repression of PU.1 target genes and induces differentiation in AML

(Submitter supplied) Lsd1KO and ATRA treatment in Hoxa9/Meis1- and MN1-transformed myeloid progenitor cells LSD1 has emerged as a promising epigenetic target in the treatment of acute myeloid leukemia (AML). Inhibition of LSD1 has been shown to induce differentiation and facilitate the responsiveness of AML cells to all-trans retinoic acid. We used two murine AML models based on retroviral overexpression of Hoxa9/Meis1 (H9M) or MN1 to study the effect of Lsd1 knockout in AML. more...
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing; Genome binding/occupancy profiling by high throughput sequencing
Platforms:
GPL21103 GPL17021
26 Samples
Download data: BED, TXT, XLSX
Series
Accession:
GSE110178
ID:
200110178
9.

PU.1-dependent enhancer inhibition separates clonal hematopoiesis from malignant transformation (oxBS-Seq)

(Submitter supplied) Hematopoietic stem cells sustain life-long blood production. While they are the known cellular origin of aging-associated myeloid malignancies, such as acute myeloid leukemia (AML), mechanisms driving their malignant transformation have remained elusive. Epigenetic dysregulation following acquired loss-of-function mutations of DNA methyl-cytosine dioxygenase Ten-Eleven Translocation-2 (TET2) occurs frequently in the elderly leading to cytosine hypermethylation in and around DNA binding sites of master transcription factors, including PU.1. more...
Organism:
Mus musculus
Type:
Methylation profiling by high throughput sequencing
Platform:
GPL21103
16 Samples
Download data: BEDGRAPH
Series
Accession:
GSE194170
ID:
200194170
10.

PU.1-dependent enhancer inhibition separates Tet2 deficient clonal hematopoiesis from malignant transformation

(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
Platforms:
GPL17021 GPL21103
41 Samples
Download data: BEDGRAPH
Series
Accession:
GSE191053
ID:
200191053
11.

PU.1-dependent enhancer inhibition separates clonal hematopoiesis from malignant transformation (ATAC-Seq)

(Submitter supplied) Hematopoietic stem cells sustain life-long blood production. While they are the known cellular origin of aging-associated myeloid malignancies, such as acute myeloid leukemia (AML), mechanisms driving their malignant transformation have remained elusive. Epigenetic dysregulation following acquired loss-of-function mutations of DNA methyl-cytosine dioxygenase Ten-Eleven Translocation-2 (TET2) occurs frequently in the elderly leading to cytosine hypermethylation in and around DNA binding sites of master transcription factors, including PU.1. more...
Organism:
Mus musculus
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL21103
8 Samples
Download data: NARROWPEAK
Series
Accession:
GSE191052
ID:
200191052
12.

PU.1-dependent enhancer inhibition separates clonal hematopoiesis from malignant transformation (RNA-Seq)

(Submitter supplied) Hematopoietic stem cells sustain life-long blood production. While they are the known cellular origin of aging-associated myeloid malignancies, such as acute myeloid leukemia (AML), mechanisms driving their malignant transformation have remained elusive. Epigenetic dysregulation following acquired loss-of-function mutations of DNA methyl-cytosine dioxygenase Ten-Eleven Translocation-2 (TET2) occurs frequently in the elderly leading to cytosine hypermethylation in and around DNA binding sites of master transcription factors, including PU.1. more...
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL17021
17 Samples
Download data: TXT
Series
Accession:
GSE186146
ID:
200186146
13.

Identification of CITED2 target genes in human CB

(Submitter supplied) CB CD34+ cells were were transduced with control (tNGFR) or CITED2 overexpression lentivectors, or control (shSCR) or shRNA CITED2 lentivectors and mRNA was isolated in order to investigate global gene expression changes upon perturbation of CITED2.
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL10558
6 Samples
Download data: TXT
Series
Accession:
GSE47218
ID:
200047218
14.

PU.1 promotes cell cycle exit in the murine myeloid lineage associated with down-regulation of E2F1

(Submitter supplied) A doxycycline-inducible system was used to induce PU.1 expression in cultured myeloid cell lines. The parent cell line used was BN (Kamath et al., Leukemia 22:1214-1225, 2008).
Organism:
Mus musculus
Type:
Expression profiling by array
Platform:
GPL16570
6 Samples
Download data: CEL
Series
Accession:
GSE52577
ID:
200052577
15.

Single cell expression profiling of murine p53-/- shPU.1 AML cells following PU.1 restoration

(Submitter supplied) We have utilized advanced RNAi technology to dynamically restore endogenous PU.1 expression in p53-deficient AML cells.
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL19057
1 Sample
Download data: CSV, TXT
Series
Accession:
GSE109100
ID:
200109100
16.

Transcriptome time course of mouse acute myeloid leukemia cells upon PU.1 restoration and knockdown

(Submitter supplied) We have utilized advanced RNAi technology to dynamically restore and subsequently knock down endogenous PU.1 expression in p53-deficient AML cells, which respectively causes differentiation and de-differentiation
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL19057
16 Samples
Download data: TXT
Series
Accession:
GSE108946
ID:
200108946
17.

PU.1 ChIP-seq time course in mouse acute myeloid leukemia cells upon PU.1 restoration and knockdown

(Submitter supplied) We have utilized advanced RNAi technology to dynamically restore and subsequently knock down endogenous PU.1 expression in p53-deficient AML cells, which respectively causes differentiation and de-differentiation
Organism:
Mus musculus
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL19057
8 Samples
Download data: BED, BEDGRAPH
Series
Accession:
GSE108945
ID:
200108945
18.

ATAC-seq time course in mouse acute myeloid leukemia cells upon PU.1 restoration and knockdown

(Submitter supplied) We have utilized advanced RNAi technology to dynamically restore and subsequently knock down endogenous PU.1 expression in p53-deficient AML cells, which respectively causes differentiation and de-differentiation
Organism:
Mus musculus
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL19057
8 Samples
Download data: BED, BEDGRAPH
Series
Accession:
GSE108944
ID:
200108944
19.

Reversible transitions between transformed and differentiated states in AML

(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
Platforms:
GPL13112 GPL19057
53 Samples
Download data: BED, BEDGRAPH, TXT
Series
Accession:
GSE76934
ID:
200076934
20.

PU.1 ChIP-seq in p53-/- shPU.1 AML cells following acute PU.1 restoration

(Submitter supplied) We have utilized advanced RNAi technology to dynamically restore endogenous PU.1 expression and perform PU.1 ChIP-seq in p53-deficient shPU.1 AML cells in vivo. This causes rapid cell cycle shutdown and myeloid differentiation. PU.1 restoration results in regression and clearance and prolongs survival.
Organism:
Mus musculus
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL13112
5 Samples
Download data: BED, BEDGRAPH
Series
Accession:
GSE76933
ID:
200076933
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