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Links from GEO DataSets

Items: 20

1.

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
2.

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
3.

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
4.

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
5.

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
6.
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
7.

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
8.

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
9.

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
10.

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
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:
Homo sapiens; Mus musculus; human gammaherpesvirus 4
Type:
Non-coding RNA profiling by array
Platform:
GPL16690
85 Samples
Download data: TXT
Series
Accession:
GSE50092
ID:
200050092
12.

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
13.

RNA-seq of Wnt7b overexpressing bone

(Submitter supplied) We report the application of RNA sequencing technology for high-throughput profiling of gene expression in Wnt7b overexpressing bone and wide-type bones.To increase Wnt7b in bone we crossed 9.6kb DMP1-Cre mice and R26-Wnt7b mice. 9.6kb DMP1-Cre; R26-Wnt7b mice were set as OE mice meanwhile their littermates of R26-Wnt7b were controls (Ctrl). Owing to heterozygotes and homozygotes of OE mice didn’t show any different phenotypes all OE mice used in this study were homozygotes. more...
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL17021
6 Samples
Download data: TXT
Series
Accession:
GSE116628
ID:
200116628
14.

Tet1 and Tet2 Maintain Mesenchymal Stem Cell Homeostasis via demethylation of P2rX7 promoter

(Submitter supplied) Ten-eleven translocation (Tet) family-mediated DNA oxidation represents a novel epigenetic modification capable of converting 5-methylcytosine (5-mC) to 5-hydroxymethylcytosine (5-hmC) to regulate various biological processes. However, it is unknown whether the Tet family affects mesenchymal stem cells (MSCs) or the skeletal system. Here we show that depletion of Tet1 and Tet2 resulted in impaired self-renewal and differentiation of bone marrow MSCs (BMMSCs) and a significant osteopenia phenotype. more...
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL17021
6 Samples
Download data: TXT
Series
Accession:
GSE108872
ID:
200108872
15.

Combined loss of Tet1 and Tet2 promotes B-cell, but not myeloid malignancies in mice

(Submitter supplied) TET1/2/3 are methylcytosine dioxygenases regulating cytosine hydroxymethylation in the genome. Tet1 and Tet2 are abundantly expressed in HSC/HPCs and implicated in the pathogenesis of hematological malignancies. Tet2-deletion in mice causes myeloid malignancies, while Tet1-null mice develop B-cell lymphoma after an extended period of latency. Interestingly, TET1 and TET2 were often concomitantly down-regulated in acute B-lymphocytic leukemia. more...
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing; Methylation profiling by high throughput sequencing
Platform:
GPL9185
28 Samples
Download data: BED, FPKM_TRACKING
Series
Accession:
GSE73611
ID:
200073611
16.

Tet2 facilitates the de-repression of myeloid target genes during C/EBPa induced transdifferentiation of pre-B cells

(Submitter supplied) Tet2 is an enzyme that hydroxylates methylated cytosines and has been implicated in hematopoietic differentiation and the formation of myeloid malignancies when mutated. An ideal system to study the role of Tet2 in myelopoeisis is C/EBPa induced transdifferentiation of pre-B cells into macrophages, where many myeloid genes become rapidly upregulated. Here we found that C/EBPa binds to upstream regions of Tet2 and that the gene becomes activated. more...
Organism:
Mus musculus
Type:
Expression profiling by array
Platform:
GPL10333
8 Samples
Download data: TXT
Series
Accession:
GSE39666
ID:
200039666
17.

Loss of Asxl1 Alters Mesenchymal Stem Cell Fate through H3K4me3

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.
Organism:
Mus musculus
Type:
Genome binding/occupancy profiling by high throughput sequencing; Expression profiling by high throughput sequencing
Platforms:
GPL19057 GPL17021
12 Samples
Download data: FPKM_TRACKING, TXT
Series
Accession:
GSE75788
ID:
200075788
18.

Loss of Asxl1 Alters Self-Renewal and Cell Fate of Bone Marrow Stromal Cell

(Submitter supplied) De novo ASXL1 mutations are found in patients with Bohring-Opitz syndrome, a disease with severe developmental defects and early childhood fatality. The underlying pathologic mechanisms remain largely unknown. Using Asxl1-targeted murine models,we found that Asxl1 global loss or conditional deletion in osteoblasts and their progenitors in mice leads to significant bone loss and markedly decreased numbers of marrow mesenchymal stem/progenitor cells (MSPCs) compared with wild-type (WT) littermates. more...
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL17021
4 Samples
Download data: FPKM_TRACKING, TXT
Series
Accession:
GSE75787
ID:
200075787
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.

Bmi1 suppresses adipogenesis in the hematopoietic stem cell niche

(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
24 Samples
Download data: BEDGRAPH
Series
Accession:
GSE121290
ID:
200121290
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