U.S. flag

An official website of the United States government

Format
Items per page
Sort by

Send to:

Choose Destination

Links from GEO DataSets

Items: 20

1.

Transcriptional and epigenetic reprogramming mediated by chronic IL1β exposure drives self-renewal ability and myeloid priming in TET2 deficient stem and progenitor cells [10x_scRNAseq]

(Submitter supplied) Clonal hematopoiesis (CH) increases risk for the development of hematological malignancy and cardiovascular disease. IL1β is elevated in patients with CH and its inhibition mitigates cardiovascular risk in murine models with Tet2 loss-of-function. How IL1β alters population dynamics of hematopoietic cells upon Tet2 deletion (Tet2-KO) is not well understood. We demonstrated IL1β expands Tet2-KO neutrophils, monocytes/macrophages, and long-term hematopoietic stem cells with reduced lymphopoiesis. more...
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL24247
16 Samples
Download data: MTX, TSV, TXT
Series
Accession:
GSE209994
ID:
200209994
2.

Transcriptional and epigenetic reprogramming mediated by chronic IL1β exposure drives self-renewal ability and myeloid priming in TET2 deficient stem and progenitor cells

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing; Methylation profiling by high throughput sequencing
Platform:
GPL24247
64 Samples
Download data: COV
Series
Accession:
GSE210026
ID:
200210026
3.

Transcriptional and epigenetic reprogramming mediated by chronic IL1β exposure drives self-renewal ability and myeloid priming in TET2 deficient stem and progenitor cells [Bisulfite-Seq]

(Submitter supplied) Clonal hematopoiesis (CH) increases risk for the development of hematological malignancy and cardiovascular disease. IL1β is elevated in patients with CH and its inhibition mitigates cardiovascular risk in murine models with Tet2 loss-of-function. How IL1β alters population dynamics of hematopoietic cells upon Tet2 deletion (Tet2-KO) is not well understood. We demonstrated IL1β expands Tet2-KO neutrophils, monocytes/macrophages, and long-term hematopoietic stem cells with reduced lymphopoiesis. more...
Organism:
Mus musculus
Type:
Methylation profiling by high throughput sequencing
Platform:
GPL24247
48 Samples
Download data: COV
Series
Accession:
GSE210025
ID:
200210025
4.

RNA-Seq of TET2 uniallelic mutated and wild type CFU colonies from rhesus macaque HSPCs

(Submitter supplied) Gene expression profile of individual CFU-GM colonies identified as uniallelic TET2 mutant versus TET2 wild type was analyzed via RNA-Seq to verify the impact of TET2 editing on gene expression in the rhesus macaque clonal hematopoiesis model.
Organism:
Macaca mulatta
Type:
Expression profiling by high throughput sequencing
Platform:
GPL23804
6 Samples
Download data: TXT
Series
Accession:
GSE148132
ID:
200148132
5.

Tet2-mediated clonal hematopoiesis in nonconditioned mice accelerates age-associated cardiac dysfunction

(Submitter supplied) Clonal hematopoiesis of indeterminate potential is prevalent in elderly individuals and associated with increased risks of all-cause mortality and cardiovascular disease. However, mouse models to study the dynamics of clonal hematopoiesis and its consequences on the cardiovascular system under homeostatic conditions are lacking. We used a model of clonal hematopoiesis using adoptive transfer of unfractionated ten-eleven translocation 2-mutant (Tet2-mutant) bone marrow cells into nonirradiated mice. more...
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL21103
6 Samples
Download data: TSV
Series
Accession:
GSE146812
ID:
200146812
6.

Identify the key signaling pathway involved in the Tet2 deficiency-induced clonal hematopoiesis

(Submitter supplied) To investigate the signaling pathway required for the Tet2 mutant associated clonal hematopoiesis, we identified the activated signaling pathway in Tet2-deficient hematopoietic stem/progenitor cells compared to WT cells and using transgentic mouse model to validate our findings. In short, the cGAS-STING pathway is activated in Tet2-deficient HSPCs and promotes the development of CH associated with Tet2 deficiency.
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL24247
55 Samples
Download data: CSV, TXT
Series
Accession:
GSE232384
ID:
200232384
7.

Genome-wide maping of chromatin state and gene exoression in hematopoietic stem and progenitor cells.

(Submitter supplied) We report the application of H3K27me3 ChI-seq assays in hematopoietic stem and progenitors cells (HSPCs) from p53+/+ and p53R248W/+ mutant mice. We also performed RNA-seq assays to examine the impact of p53 on gene expression in hematopoietic stem and progenitor cells.
Organism:
Mus musculus
Type:
Genome binding/occupancy profiling by high throughput sequencing; Expression profiling by high throughput sequencing
Platforms:
GPL19057 GPL21103
11 Samples
Download data: BW, TXT
Series
Accession:
GSE137126
ID:
200137126
8.

Restoration of genome-wide 5-hydroxymethylation by azacitidine and ascorbate in TET2-deficient human pre-leukemic HSPCs

(Submitter supplied) The conversion of 5-methylcytosine (5mC) to 5-hydroxymethylcytosine (5hmC) is a key step in DNA demethylation that is mediated by ten-eleven-translocation (TET) enzymes, which require ascorbate/vitamin C. Here, we report the 5hmC landscape of normal hematopoiesis and identify cell type-specific 5hmC profiles associated with active transcription and chromatin accessibility of key hematopoietic regulators. more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing; Other
Platforms:
GPL21697 GPL24676
326 Samples
Download data: TSV
Series
Accession:
GSE198908
ID:
200198908
9.

p300 suppresses the transition of myelodysplastic syndrome to acute myeloid leukemia [ChIP-seq II]

(Submitter supplied) The p300 lysine acetyltransferase (KAT) can function as an oncogene or a tumor suppressor in hematologic malignancies. We have identified a tumor suppressor role for p300 in myelodysplastic syndrome (MDS) driven by Tet2 deficiency. Compared to Tet2-null hematopoietic stem and progenitor cells (HSPCs), HSPCs lacking both p300 and Tet2 (double knock out, DKO) displayed enhanced proliferation and impaired differentiation. more...
Organism:
Mus musculus
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL19057
2 Samples
Download data: BIGWIG, NARROWPEAK
Series
Accession:
GSE154493
ID:
200154493
10.

p300 suppresses the transition of myelodysplastic syndrome to 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; Methylation profiling by high throughput sequencing
4 related Platforms
74 Samples
Download data: BIGWIG, BW, NARROWPEAK
Series
Accession:
GSE145878
ID:
200145878
11.

p300 suppresses the transition of myelodysplastic syndrome to acute myeloid leukemia [DIP-seq]

(Submitter supplied) The p300 lysine acetyltransferase (KAT) can function as an oncogene or a tumor suppressor in hematologic malignancies. We have identified a tumor suppressor role for p300 in myelodysplastic syndrome (MDS) driven by Tet2 deficiency. Compared to Tet2-null hematopoietic stem and progenitor cells (HSPCs), HSPCs lacking both p300 and Tet2 (double knock out, DKO) displayed enhanced proliferation and impaired differentiation. more...
Organism:
Mus musculus
Type:
Methylation profiling by high throughput sequencing
Platform:
GPL13112
24 Samples
Download data: BW
Series
Accession:
GSE145877
ID:
200145877
12.

p300 suppresses the transition of myelodysplastic syndrome to acute myeloid leukemia [ChIP-seq]

(Submitter supplied) The p300 lysine acetyltransferase (KAT) can function as an oncogene or a tumor suppressor in hematologic malignancies. We have identified a tumor suppressor role for p300 in myelodysplastic syndrome (MDS) driven by Tet2 deficiency. Compared to Tet2-null hematopoietic stem and progenitor cells (HSPCs), HSPCs lacking both p300 and Tet2 (double knock out, DKO) displayed enhanced proliferation and impaired differentiation. more...
Organism:
Mus musculus
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL19057
20 Samples
Download data: BW, NARROWPEAK
Series
Accession:
GSE145876
ID:
200145876
13.

p300 suppresses the transition of myelodysplastic syndrome to acute myeloid leukemia [ATAC-Seq]

(Submitter supplied) The p300 lysine acetyltransferase (KAT) can function as an oncogene or a tumor suppressor in hematologic malignancies. We have identified a tumor suppressor role for p300 in myelodysplastic syndrome (MDS) driven by Tet2 deficiency. Compared to Tet2-null hematopoietic stem and progenitor cells (HSPCs), HSPCs lacking both p300 and Tet2 (double knock out, DKO) displayed enhanced proliferation and impaired differentiation. more...
Organism:
Mus musculus
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL24247
16 Samples
Download data: NARROWPEAK
Series
Accession:
GSE145875
ID:
200145875
14.

p300 suppresses the transition of myelodysplastic syndrome to acute myeloid leukemia [RNA-Seq]

(Submitter supplied) The p300 lysine acetyltransferase (KAT) can function as an oncogene or a tumor suppressor in hematologic malignancies. We have identified a tumor suppressor role for p300 in myelodysplastic syndrome (MDS) driven by Tet2 deficiency. Compared to Tet2-null hematopoietic stem and progenitor cells (HSPCs), HSPCs lacking both p300 and Tet2 (double knock out, DKO) displayed enhanced proliferation and impaired differentiation. more...
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL17021
12 Samples
Download data: XLSX
Series
Accession:
GSE145819
ID:
200145819
15.

Gene expression profiling in pre-leukemic hematopoietic stem cells carrying both NrasG12D/+ and Tet2+/- mutations

(Submitter supplied) By using a genetically accurate mouse model, we demonstrate that endogenous expression of oncogenic N-RasG12D and Tet2 haploinsufficiency collaborate to accelerate CMML development in mice. Gene expression was compared across all genotypes (WT, Tet2+/-, NrasG12D/+ and double mutants) in bone marrow-derived hematopoietic stem cells (CD150+CD48-Lin-Sca1+cKit+) using RNA-seq. N-RasG12D and Tet2 haploinsufficiency cooperate to induce both unique and overlapping effects on HSC gene expression programs.
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL17021
12 Samples
Download data: TXT
Series
Accession:
GSE97640
ID:
200097640
16.

TET2 binding to enhancers facilitates transcription factor recruitment in hematopoietic cells

(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:
GPL21626
66 Samples
Download data: BIGWIG, NARROWPEAK
Series
Accession:
GSE115972
ID:
200115972
17.

TET2 binding to enhancers facilitates transcription factor recruitment in hematopoietic cells [RNA-Seq]

(Submitter supplied) The epigenetic regulator TET2 is frequently mutated in hematological diseases. Mutations have been shown to arise in hematopoietic stem cells early in disease development, lead to altered DNA methylation landscapes and to an increased risk of hematopoietic malignancy. Here, we show by genome-wide mapping of TET2 binding sites in different cell types that TET2 localizes to regions of open chromatin and cell-type specific enhancers. more...
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL21626
16 Samples
Download data: TXT
Series
Accession:
GSE115967
ID:
200115967
18.

TET2 binding to enhancers facilitates transcription factor recruitment in hematopoietic cells [TET2 ChIP-seq hematopoietic cells]

(Submitter supplied) The epigenetic regulator TET2 is frequently mutated in hematological diseases. Mutations have been shown to arise in hematopoietic stem cells early in disease development, lead to altered DNA methylation landscapes and to an increased risk of hematopoietic malignancy. Here, we show by genome-wide mapping of TET2 binding sites in different cell types that TET2 localizes to regions of open chromatin and cell-type specific enhancers. more...
Organism:
Mus musculus
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL21626
12 Samples
Download data: TXT
Series
Accession:
GSE115965
ID:
200115965
19.

TET2 binding to enhancers facilitates transcription factor recruitment in hematopoietic cells [TET2 ChIP-seq ES cells]

(Submitter supplied) The epigenetic regulator TET2 is frequently mutated in hematological diseases. Mutations have been shown to arise in hematopoietic stem cells early in disease development, lead to altered DNA methylation landscapes and to an increased risk of hematopoietic malignancy. Here, we show by genome-wide mapping of TET2 binding sites in different cell types that TET2 localizes to regions of open chromatin and cell-type specific enhancers. more...
Organism:
Mus musculus
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL21626
10 Samples
Download data: BIGWIG, NARROWPEAK
Series
Accession:
GSE115964
ID:
200115964
20.

TET2 binding to enhancers facilitates transcription factor recruitment in hematopoietic cells [ATAC-Seq]

(Submitter supplied) The epigenetic regulator TET2 is frequently mutated in hematological diseases. Mutations have been shown to arise in hematopoietic stem cells early in disease development, lead to altered DNA methylation landscapes and to an increased risk of hematopoietic malignancy. Here, we show by genome-wide mapping of TET2 binding sites in different cell types that TET2 localizes to regions of open chromatin and cell-type specific enhancers. more...
Organism:
Mus musculus
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL21626
28 Samples
Download data: BIGWIG
Series
Accession:
GSE115962
ID:
200115962
Format
Items per page
Sort by

Send to:

Choose Destination

Supplemental Content

db=gds|term=|query=1|qty=4|blobid=MCID_674ebc758c9ed417fb218e53|ismultiple=true|min_list=5|max_list=20|def_tree=20|def_list=|def_view=|url=/Taxonomy/backend/subset.cgi?|trace_url=/stat?
   Taxonomic Groups  [List]
Tree placeholder
    Top Organisms  [Tree]

Find related data

Recent activity

Your browsing activity is empty.

Activity recording is turned off.

Turn recording back on

See more...
Support Center