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Links from GEO DataSets

Items: 20

1.

Non-catalytic functions of Tet2 are essential to regulate hematopoietic stem and progenitor cell homeostasis

(Submitter supplied) To identify genes that are influenced by the catalytic and non-catalytic functions of Tet2 in hematopoietic stem and progenitor cells (HSPCs), we analyzed the gene expression profiles of Tet2 catalytic mutant (Tet2 Mut), Tet2 knockout (Tet2 KO) and wild-type HSPCs (or LSK, Lin–Sca-1+c-Kit+) and multi-potent progenitor (or MPP, Lin–) cells by RNA-seq.
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL19057
12 Samples
Download data: TXT
Series
Accession:
GSE132090
ID:
200132090
2.

Comparative analysis of Tet2 catalytic deficient and knockout bone marrow over time

(Submitter supplied) In this study, we investigated the role of Tet2 in regulation of hematopoietic genes by performing transcriptomic analysis of Tet2 WT, Mut, and KO LSK and Lin– cells at 3, 6, 9, and 12 months by RNA-seq, and mapping the DNA methylation landscape of 3-month-old Tet2 WT, Mut, and KO LSK and Lin– cells. (1) We find that loss of Tet2 (Tet2 KO) vs. a loss of Tet2 catalytic function (Tet2 Mut) at different time points and cell types causes distinct gene expression changes when compared to WT samples as assessed by RNA-seq. more...
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing; Methylation profiling by high throughput sequencing
Platforms:
GPL21103 GPL24247
30 Samples
Download data: BW, CSV
Series
Accession:
GSE227977
ID:
200227977
3.

SIRT1 Activation Disrupts Maintenance of Myelodysplastic Syndrome Stem and Progenitor Cells by Restoring TET2 Function

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.
Organism:
Homo sapiens
Type:
Methylation profiling by high throughput sequencing; Expression profiling by array
Platforms:
GPL16791 GPL22448
16 Samples
Download data: BEDGRAPH, NARROWPEAK, TXT
Series
Accession:
GSE117383
ID:
200117383
4.

SIRT1 Activation Disrupts Maintenance of Myelodysplastic Syndrome Stem and Progenitor Cells by Restoring TET2 Function [hMeDIP-Seq]

(Submitter supplied) Improved understanding of mechanisms regulating myelodysplastic syndrome (MDS) hematopoietic stem/progenitor cell (HSPC) growth and self-renewal is critical for developing MDS therapy. We revealed a novel regulatory axis that SIRT1-deficiency induced TET2 hyperacetylation promotes MDS HSPC functions, and provide an approach to target MDS HSPCs by activating SIRT1 deacetylase.
Organism:
Homo sapiens
Type:
Methylation profiling by high throughput sequencing
Platform:
GPL16791
6 Samples
Download data: BEDGRAPH, NARROWPEAK
Series
Accession:
GSE117363
ID:
200117363
5.

SIRT1 Activation Disrupts Maintenance of Myelodysplastic Syndrome Stem and Progenitor Cells by Restoring TET2 Function [microarray expression profiling]

(Submitter supplied) Improved understanding of mechanisms regulating myelodysplastic syndrome (MDS) hematopoietic stem/progenitor cell (HSPC) growth and self-renewal is critical for developing MDS therapy. We revealed a novel regulatory axis that SIRT1-deficiency induced TET2 hyperacetylation promotes MDS HSPC functions, and provide an approach to target MDS HSPCs by activating SIRT1 deacetylase. Four Groups: Group1: MDS-L cells transduced with lentiviral vector targeting non-silence squence (control shRNA for SIRT1); Group2: MDS-L cells transduced with lentiviral vector containing interference squence targeting SIRT1 (SIRT shRNA); Group 3: MDS-L cells transduced with lentiviral vector targeting non-silence squence (control shRNA for TET2); Group 4: MDS-L cells transduced with lentiviral vector containing interference squence targeting TET2 (TET2 shRNA).
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL22448
10 Samples
Download data: TXT
Series
Accession:
GSE117272
ID:
200117272
6.

Tet2 loss dysregulates the behavior of bone marrow derived mesenchymal stromal cells

(Submitter supplied) TET2 plays an important role in regulating the behavior of bone marrow derived MSCs in addition to its intrinsic role in HSPCs to participate in aberrant hematopoiesis. Moreover, MSCs are the most important niche cell components in Tet2-/- mice that contribute to the progression of Tet2 deletion-driven myeloid malignancies. 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:
GPL17021
8 Samples
Download data: BW
Series
Accession:
GSE100073
ID:
200100073
7.

Tet2 loss dysregulates the behavior of bone marrow derived mesenchymal stromal cells [hME-Seal]

(Submitter supplied) Identification the genome-wide distribution of 5-hmC in WT-MSCs and Tet2-/--MSCs by Genome-wide 5hmc Profiling.
Organism:
Mus musculus
Type:
Methylation profiling by high throughput sequencing
Platform:
GPL17021
4 Samples
Download data: BW
Series
Accession:
GSE100072
ID:
200100072
8.

Tet2 loss dysregulates the behavior of bone marrow derived mesenchymal stromal cells [RNA-seq]

(Submitter supplied) Bone marrow–derived mesenchymal stem/progenitor cell mRNA profiles of WT and Tet2−/− mice were generated by deep sequencing.
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL17021
4 Samples
Download data: XLS
Series
Accession:
GSE100071
ID:
200100071
9.

TET2 protects the genome from mutagenicity through interacting with MSH6

(Submitter supplied) Ten eleven translocation 2 (TET2) is a member of dioxygenases that catalyze the multi-step 5-methylcytosine oxidation. Loss-of-function TET2 mutations frequently occur in various types of hematological malignancies; however, the underlying mechanism remains poorly understood. Here, we show that Tet2-/- mice develop spontaneous myeloid, T- and B-cell malignancies. Exome sequencing of Tet2-/- tumors reveals acquisition of numerous mutations. more...
Organism:
Mus musculus
Type:
Methylation profiling by high throughput sequencing
Platform:
GPL9185
6 Samples
Download data: BED, TXT
Series
Accession:
GSE74390
ID:
200074390
10.

Epigenome analysis of patients with various myeloid malignancies including differential levels of 5-hydroxymethylcytosine

(Submitter supplied) TET2 is a close relative of TET1, an enzyme that converts 5-methylcytosine (5mC) to 5-hydroxymethylcytosine (5hmC) in DNA. The gene encoding TET2 resides at chromosome 4q24, in a region showing recurrent microdeletions and copy-neutral loss of heterozygosity (CN-LOH) in patients with diverse myeloid malignancies. Somatic TET2 mutations are frequently observed in myelodysplastic syndromes (MDS), myeloproliferative neoplasms (MPN), MDS/MPN overlap syndromes including chronic myelomonocytic leukaemia (CMML), acute myeloid leukaemias (AML) and secondary AML (sAML). more...
Organism:
Homo sapiens
Type:
Methylation profiling by array
Platform:
GPL8490
81 Samples
Download data: TXT
Series
Accession:
GSE25706
ID:
200025706
11.

miRNA Expression Profiles in Human AML Samples And in Human and Mouse Blood Cell Lines

(Submitter supplied) miRNA expression profiles of a human cohort of 67 cytogenetically normal AML samples, including both TET2 wildtype and TET2 mutants, and human and mouse cell lines comaring control with TET2 overexpression or TET2 knockdown
Organism:
Mus musculus; Homo sapiens; human gammaherpesvirus 4
Type:
Non-coding RNA profiling by array
Platform:
GPL16690
85 Samples
Download data: TXT
Series
Accession:
GSE50092
ID:
200050092
12.

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
13.

Reduced representation bisulfite-sequencing of human leukemia cells and mouse hematopoietic progenitors

(Submitter supplied) Human leukemia cells treated with vitamin C for 12 and 72hrs and mouse hematopoietic progenitor cells with knockdown and Tet2 restoration
Organism:
Mus musculus; Homo sapiens
Type:
Methylation profiling by high throughput sequencing
Platforms:
GPL17021 GPL16791
34 Samples
Download data: TXT
Series
Accession:
GSE100041
ID:
200100041
14.

hMeDIP sequencing of human leukemia cells

(Submitter supplied) Human leukemia cells treated with vitamin C for 72hrs.
Organism:
Homo sapiens
Type:
Methylation profiling by high throughput sequencing
Platform:
GPL16791
12 Samples
Download data: BED
Series
Accession:
GSE99953
ID:
200099953
15.

Genetic and pharmacological restoration of TET2 function blocks stem cell self-renewal and progression of leukemia

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.
Organism:
Mus musculus; Homo sapiens
Type:
Expression profiling by high throughput sequencing; Methylation profiling by high throughput sequencing
Platforms:
GPL16791 GPL17021
80 Samples
Download data: BED, TXT
Series
Accession:
GSE97442
ID:
200097442
16.

RNA-sequencing of human leukemia cells and mouse hematopoietic progenitors

(Submitter supplied) human leukemia cells treated with vitamin C for 12 and 72hrs and mouse hematopoietic progenitor cells with knockdown and Tet2 restoration
Organism:
Mus musculus; Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platforms:
GPL16791 GPL17021
34 Samples
Download data: CSV
Series
Accession:
GSE97440
ID:
200097440
17.

Tet2 loss leads to increased hematopoietic stem cell self-renewal and myeloid transformation

(Submitter supplied) Recurrent somatic mutations in TET2 and in other genes that regulate the epigenetic state have been identified in patients with myeloid malignancies and in other cancers. However, the in vivo effects of Tet2 loss have not been delineated. We report here that Tet2 loss leads to increased stem-cell self-renewal and to progressive stem cell expansion. Consistent with human mutational data, Tet2 loss leads to myeloproliferation in vivo, notable for splenomegaly and monocytic proliferation. more...
Organism:
Mus musculus
Type:
Expression profiling by array
Dataset:
GDS4287
Platform:
GPL1261
14 Samples
Download data: CEL
Series
Accession:
GSE27816
ID:
200027816
18.
Full record GDS4287

Effect of Tet2 loss in bone marrow progenitors

Analysis of sorted bone marrow progenitor populations (LSK, CMP, GMP) deficient in ten-eleven translocation 2 (TET2). Tet2 loss causes increased hematopoietic stem cell self-renewal and myeloid transformation. Results provide insight into the molecular mechanisms underlying myeloid malignancies.
Organism:
Mus musculus
Type:
Expression profiling by array, count, 4 cell type, 2 genotype/variation sets
Platform:
GPL1261
Series:
GSE27816
14 Samples
Download data: CEL
19.

DNMT3A and TET2 Mutations Increase Hematopoietic Stem Cell Fitness Through Distinct Mechanisms

(Submitter supplied) Epigenetic modifying enzymes DNMT3A and TET2 are recurrently mutated in hematological disorders despite possessing opposing biochemical functions in the DNA methylation processes. Using conditional ablation, we show these contrasting genotypes result in different functional effects in hematopoietic stem cells (HSCs). Loss of Dnmt3a bestows enhanced self-renewal on HSCs in serial, competitive repopulation assays while Tet2 loss functionally depletes HSCs after a tertiary transplant despite an initial competitive advantage. more...
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing; Genome binding/occupancy profiling by high throughput sequencing
Platforms:
GPL19057 GPL24247
36 Samples
Download data: BW, TSV
Series
Accession:
GSE139911
ID:
200139911
20.

Expression data from Tet2-hypomorph (knockdown) and/or Ezh2-null Lineage-Sca-1+c-Kit+ (LSK) cells and granulocyte-macrophage progenitors (GMPs)

(Submitter supplied) PcG proteins form the polycomb repressive complexes (PRC) 1 and 2, functioning as transcriptional repressors through histone modifications. They have been implicated in the maintenance of self-renewing somatic and cancer stem cells. PcG genes have been characterized as tumor suppressor genes as exemplified by somatic inactivating mutations of EZH2, a gene encoding histone methyltransferase in PRC2, in myeloid malignancy. more...
Organism:
Mus musculus
Type:
Expression profiling by array
Platform:
GPL13912
12 Samples
Download data: TXT
Series
Accession:
GSE42666
ID:
200042666
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