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Links from GEO DataSets

Items: 12

1.

Effect of TET deletion on the global DNA methylation status of osteoclasts (MeDIP-Seq)

(Submitter supplied) Epigenetic regulation is a fundamental mechanism mediating various cellular processes. However, epigenetic mechanisms in osteoclastogenesis remain incompletely understood. We performed MeDIP-seq analysis to investigate DNA methylation in osteoclasts derived from wild-type and Tet2Rank–/–; Tet3aRank+/– mice.
Organism:
Mus musculus
Type:
Methylation profiling by high throughput sequencing
Platform:
GPL21493
4 Samples
Download data: BW
Series
Accession:
GSE156128
ID:
200156128
2.

Effect of TET deletion on the global DNA methylation status of osteoclasts

(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
Platforms:
GPL21493 GPL17021
10 Samples
Download data: BW
Series
Accession:
GSE156130
ID:
200156130
3.

Effect of TET deletion on the global DNA methylation status of osteoclasts (RNA-Seq)

(Submitter supplied) Epigenetic regulation is a fundamental mechanism mediating various cellular processes. However, epigenetic mechanisms in osteoclastogenesis remain incompletely understood. We performed RNA-seq analysis to investigate gene expression in osteoclasts derived from wild-type and Tet2Rank–/–; Tet3aRank+/– mice.
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL17021
6 Samples
Download data: TXT
Series
Accession:
GSE156129
ID:
200156129
4.

Expression data from cultured macrophages and osteoclasts

(Submitter supplied) Osteoclastogenesis is induced by the stimulation of RANKL. In the early stage of osteoclast differentiation, the osteoclast progenitor cells are primed by M-CSF, following a tightly controlled genetic program where specific sets of genes are up-regulated by RANKL. Some of them, for instance, control differentiation, cell-cell fusion and bone resorption. We used microarrays to detail the global program of gene expression underlying osteoclastogenesis and identified various up-regulated genes during this process.
Organism:
Mus musculus
Type:
Expression profiling by array
Platform:
GPL1261
2 Samples
Download data: CEL, CHP
Series
Accession:
GSE20850
ID:
200020850
5.

Genome Wide Chromatin Mapping of H3K27me3 and H3K4me3 histone modifications in wild type and ASXL1-/- Osteoclast

(Submitter supplied) We report a novel role of ASXL1 protein in altering epigentic profile of osteoclast. ASXL1 is an ETP protein that bind to polycomb repressive complex. We asked if ASXL1 regulates osteoclast differentiation by maintaining balance between positive and negative epigenetic regulators. To address this question, we performed ChIP-seq using H3K27me3 and H3K4me3 antbody in day2 osteoclast. Our data reveals that there was a global loss of H3K27me3 in ASXl1-/- osteoclast which includes loss of this repressive methylation of NFATc1 promoter, which is a master regulator of osteoclastogenesis.
Organism:
Mus musculus
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL17021
5 Samples
Download data: BW
Series
Accession:
GSE111852
ID:
200111852
6.

Tumor hypoxia causes DNA hypermethylation by reducing TET activity

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.
Organism:
Mus musculus; Homo sapiens
Type:
Methylation profiling by array; Methylation profiling by high throughput sequencing; Other; Expression profiling by high throughput sequencing
Platforms:
GPL16304 GPL11154 GPL17021
99 Samples
Download data: IDAT
Series
Accession:
GSE71403
ID:
200071403
7.

Tumor hypoxia causes DNA hypermethylation by reducing TET activity (TAB-Seq)

(Submitter supplied) Hypermethylation of tumor suppressor gene (TSG) promoters confers growth advantages to cancer cells, but how these changes arise is poorly understood. Here, we report that tumor hypoxia reduces the activity of oxygen-dependent TET enzymes, which catalyze DNA de-methylation through 5-methylcytosine oxidation. This occurs independently of hypoxia-associated alterations in TET gene expression, basal metabolism, HIF activity or nuclear reactive oxygen species, but directly depends on oxygen shortage. more...
Organism:
Mus musculus
Type:
Methylation profiling by high throughput sequencing
Platform:
GPL17021
13 Samples
Download data: TXT
Series
Accession:
GSE71402
ID:
200071402
8.

Tumor hypoxia causes DNA hypermethylation by reducing TET activity (RNA-Seq)

(Submitter supplied) Hypermethylation of tumor suppressor gene (TSG) promoters confers growth advantages to cancer cells, but how these changes arise is poorly understood. Here, we report that tumor hypoxia reduces the activity of oxygen-dependent TET enzymes, which catalyze DNA de-methylation through 5-methylcytosine oxidation. This occurs independently of hypoxia-associated alterations in TET gene expression, basal metabolism, HIF activity or nuclear reactive oxygen species, but directly depends on oxygen shortage. more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL11154
6 Samples
Download data: TXT
9.

Tumor hypoxia causes DNA hypermethylation by reducing TET activity (DIP-Seq)

(Submitter supplied) Hypermethylation of tumor suppressor gene (TSG) promoters confers growth advantages to cancer cells, but how these changes arise is poorly understood. Here, we report that tumor hypoxia reduces the activity of oxygen-dependent TET enzymes, which catalyze DNA de-methylation through 5-methylcytosine oxidation. This occurs independently of hypoxia-associated alterations in TET gene expression, basal metabolism, HIF activity or nuclear reactive oxygen species, but directly depends on oxygen shortage. more...
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL11154
28 Samples
Download data: TXT
Series
Accession:
GSE71400
ID:
200071400
10.

Tumor hypoxia causes DNA hypermethylation by reducing TET activity (Bisulfite-Seq)

(Submitter supplied) Hypermethylation of tumor suppressor gene (TSG) promoters confers growth advantages to cancer cells, but how these changes arise is poorly understood. Here, we report that tumor hypoxia reduces the activity of oxygen-dependent TET enzymes, which catalyze DNA de-methylation through 5-methylcytosine oxidation. This occurs independently of hypoxia-associated alterations in TET gene expression, basal metabolism, HIF activity or nuclear reactive oxygen species, but directly depends on oxygen shortage. more...
Organism:
Homo sapiens
Type:
Methylation profiling by high throughput sequencing
Platform:
GPL11154
4 Samples
Download data: TXT
Series
Accession:
GSE71399
ID:
200071399
11.

Tumor hypoxia causes DNA hypermethylation by reducing TET activity (BeadChip)

(Submitter supplied) Genome wide DNA methylation profiling of normoxic and hypoxic non-small-cell lung cancer samples for 5mC and 5hmC. The Illumina Infinium 450k Human DNA methylation Beadchip v1.2 was used to obtain DNA methylation and hydroxymethylation profiles across 485,512 CpGs from DNA extracted from fresh-frozen tumor samples. Samples included 12 hypoxic and 12 normoxic tumor samples, with hypoxia determined according to the hypoxia metagene score (Buffa et al, Br J Cancer 2010). more...
Organism:
Homo sapiens
Type:
Methylation profiling by array
Platform:
GPL16304
48 Samples
Download data: IDAT, TXT
Series
Accession:
GSE71398
ID:
200071398
12.

Microarray analysis of Macrophages and Osteoclasts

(Submitter supplied) Comparaison of genes expression between bone marrow derived macrophages and osteoclasts in C57BL/6J mice
Organism:
Mus musculus
Type:
Expression profiling by array
Platform:
GPL6887
2 Samples
Download data: TXT
Series
Accession:
GSE86998
ID:
200086998
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