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Links from GEO DataSets

Items: 20

1.

After demyelination in the adult CNS, oligodendrocyte precursor cells revert to an immature mRNA profile and express immune cues favoring their migration

(Submitter supplied) In multiple sclerosis (MS) and experimental models of demyelination, myelin repair is mostly achieved by oligodendrocyte precursor cells (OPCs). To gain insight into the biological specificity of these adult precursors, in the perspective to better understand why remyelination often fails in MS, we performed a micro-array analysis on purified populations of murine OPCs and oligodendrocytes. We demonstrated that, in a control environment, “quiescent” adult OPCs are more mature than neonatal OPCs, with a mRNA profile closer to oligodendrocytes. more...
Organism:
Mus musculus
Type:
Expression profiling by array
Platform:
GPL11202
18 Samples
Download data: TXT
Series
Accession:
GSE48872
ID:
200048872
2.

TET1-mediated DNA hydroxy-methylation regulates adult remyelination

(Submitter supplied) Adult myelination is essential for brain function and response to injury, but the molecular mechanisms remain elusive. Here we identify DNA hydroxy-methylation, an epigenetic mark catalyzed by Ten-Eleven translocation (TET) enzymes, as necessary for adult myelin repair. While DNA hydroxy-methylation and high levels of TET1 were detected in young adult mice during myelin regeneration after demyelination, this process was defective in old mice. more...
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL21103
12 Samples
Download data: TXT
Series
Accession:
GSE137611
ID:
200137611
3.

Age-dependent decline of TET1-mediated DNA hydroxy-methylation impairs myelin regeneration after injury

(Submitter supplied) Adult myelination is recognized as essential for brain function and response to injury and yet, its molecular understanding is mostly inferred from developmental studies. In this study, we identify DNA hydroxy-methylation, an epigenetic mark catalyzed by Ten-Eleven translocation (TET) enzymes, as necessary for adult, but not for developmental, myelin formation. While hydroxy-methylation and high levels of TET1 were detected in young adult mice during myelin regeneration after lysolecithin-induced demyelination, this process was defective in older mice. more...
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing; Methylation profiling by high throughput sequencing
Platforms:
GPL17021 GPL13112
12 Samples
Download data: TXT
Series
Accession:
GSE122446
ID:
200122446
4.

Tet1-mediated Epigenetic Programming Regulates Calcium Homeostasis and Stage-specific CNS Myelination and Regeneration

(Submitter supplied) DNA hydroxymethylation by epigenetic modifiers TET dioxygenases is critical for gene transcription in various biological processes, however, its role in oligodendrocyte maturation and functions remain elusive. Here, we found that mice lacking Tet1 in the oligodendrocyte lineage exhibited hypomyelination in the CNS in the juvenile stage, leading to defects in action potential propagation, motor coordination, anxiety-like behavior and spatial memory capacities. more...
Organism:
Mus musculus; Rattus norvegicus
Type:
Expression profiling by high throughput sequencing; Methylation profiling by high throughput sequencing; Genome binding/occupancy profiling by high throughput sequencing
Platforms:
GPL25947 GPL17021 GPL21103
13 Samples
Download data: BED, TXT
Series
Accession:
GSE122838
ID:
200122838
5.

MYC deregulates TET1 and TET2 expression to control global DNA (hydroxy)methylation and gene expression to maintain a neoplastic phenotype in T-ALL

(Submitter supplied) We performed methylation, hydroxymethylation, and gene expression profiling using MeDIP-seq, hMeDIP-seq, and RNA-seq, respectively, to investigate the role of TET1 and TET2 in MYC-driven tumor maintenance. We compared T-ALL tumor cells before and upon MYC inactivation and revealed genome-wide changes in the DNA methylation and hydroxymethylation patterns. Furthermore, TET1 knock-down or ectopic TET2 expression in T-ALL revealed genome-wide changes in DNA methylation and hydroxymethylation patterns corresponding to changes in gene expression.
Organism:
Homo sapiens; Mus musculus
Type:
Methylation profiling by high throughput sequencing; Expression profiling by high throughput sequencing
Platforms:
GPL21103 GPL20301
18 Samples
Download data: TXT, WIG
Series
Accession:
GSE126029
ID:
200126029
6.

Drug-based modulation of endogenous stem cells promotes functional remyelination in vivo

(Submitter supplied) Multiple sclerosis involves an aberrant autoimmune response and progressive failure of remyelination in the central nervous system. Prevention of neural degeneration and subsequent disability requires remyelination through the generation of new oligodendrocytes, but current treatments exclusively target the immune system. Oligodendrocyte progenitor cells are stem cells in the central nervous system and the principal source of myelinating oligodendrocytes. more...
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL17021
22 Samples
Download data: TSV
Series
Accession:
GSE63804
ID:
200063804
7.

Transcriptome analysis of freshly isolated young and aged rat oligodendrocyte progenitor cells (OPCs)

(Submitter supplied) The age-related failure to regenerate lost oligodendrocytes from oligodendrocyte progenitor cells (OPCs) is associated with irreversible neurodegeneration in multiple sclerosis. Consequently, regenerative therapies for chronic demyelinating diseases remain a long sought after but elusive goal. Here we show that adult OPCs lose their inherent differentiation potential with increasing age. Moreover, aged OPCs do not remain responsive to pro-differentiation signals, posing significant constraints on the effectiveness of remyelination therapies based on the enhancement of OPC differentiation. more...
Organism:
Rattus norvegicus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL22396
6 Samples
Download data: TXT
Series
Accession:
GSE134765
ID:
200134765
8.

BMP receptor blockade overcomes extrinsic inhibition of remyelination and restores neurovascular homeostasis

(Submitter supplied) Extrinsic inhibitors at sites of blood-brain barrier (BBB) disruption and neurovascular damage contribute to remyelination failure in neurological diseases. However, therapies to overcome extrinsic inhibition of remyelination are not widely available and the dynamics of glial progenitor niche remodeling at site of neurovascular dysfunction are largely unknown. By integrating in vivo two-photon (2P) imaging co-registered with electron microscopy and transcriptomics in chronic neuroinflammatory lesions, we found repressed anticoagulation pathways in oligodendrocyte precursor cells (OPCs) that clustered perivascularly at sites of limited remyelination with deposition of fibrinogen, a blood coagulation factor abundantly deposited in multiple sclerosis lesions. more...
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL19057
6 Samples
Download data: XLSX
Series
Accession:
GSE166675
ID:
200166675
9.

Inhibition of phosphodiesterase-4 promotes oligodendrocyte precursor cell differentiation and enhances CNS remyelination

(Submitter supplied) We used transcription-profiling to identify mitogen-activated protein kinase (Mapk) signaling as an important regulator involved in the differentiation of oligodendrocyte progenitor cells (OPCs) into oligodendrocytes. We show in tissue culture that activation of Mapk signaling by elevation of intracellular levels of cAMP using administration of either dibutyryl-cAMP or inhibitors of the cAMP-hydrolyzing enzyme phosphodiesterase-4 (Pde4) enhances OPC differentiation. more...
Organism:
Rattus norvegicus
Type:
Expression profiling by array; Third-party reanalysis
Platform:
GPL6247
15 Samples
Download data: CEL, TXT
Series
Accession:
GSE50042
ID:
200050042
10.

Retinoid X receptor gamma signaling accelerates CNS remyelination

(Submitter supplied) The molecular basis of CNS myelin regeneration (remyelination) is poorly understood. Here we generate a comprehensive transcriptional profile of the separate stages of spontaneous remyelination following focal demyelination in the rat CNS. White matter tracts in the rat caudal cerebellar peduncles were focally demyelinated using 0.1% ethidium bromide, the lesions were isolated using laser capture microdissection at 5, 14 and 28 days postlesion, followed by RNA extraction and Illumina beadarray analysis of differentially expressed transcripts. more...
Organism:
Rattus norvegicus
Type:
Expression profiling by array
Platform:
GPL6101
9 Samples
Download data: TXT
Series
Accession:
GSE24821
ID:
200024821
11.

TET1 is a tumour suppressor that inhibits colon cancer growth by derepressing inhibitors of the WNT pathway

(Submitter supplied) Ten eleven translocation (TET) enzymes catalyse the oxidative reactions of 5-methylcytosine (5mC) to promote the demethylation process. The reaction intermediate 5-hydroxymethylcytosine (5hmC) has been shown to be abundant in embryonic stem cells and tissues, but strongly depleted in human cancers. Genetic mutations of TET2 gene were associated with lleukemia, whereas TET1 downregulation has been shown to promote malignancy in breast cancer. more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL15456
2 Samples
Download data: BEDGRAPH
Series
Accession:
GSE53172
ID:
200053172
12.

Tet1 and Tet2 mediate epigenetic regulation of developmental genes by protecting DNA methylation canyons against hypermethylation

(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:
GPL13112
8 Samples
Download data: BW
Series
Accession:
GSE58611
ID:
200058611
13.

Tet1 and Tet2 mediate epigenetic regulation of developmental genes by protecting DNA methylation canyons against hypermethylation [Bisulfite-Seq]

(Submitter supplied) This study uses whole methylome sequencing to characterize the methylomes of mouse embryonic fibroblasts (MEF's). Two conditions were analyzed, MEF cells with intact TET1/TET2 enzymes (WT) and MEF cells with TET1/TET2 knocked out (DKO). Our results identify sets of differentially methylated genes which are correlated with TET1/TET2 induced expression changes of the corresponding genes.
Organism:
Mus musculus
Type:
Methylation profiling by high throughput sequencing
Platform:
GPL13112
6 Samples
Download data: BW
Series
Accession:
GSE58610
ID:
200058610
14.

Tet1 and Tet2 mediate epigenetic regulation of developmental genes by protecting DNA methylation canyons against hypermethylation [RNA-Seq]

(Submitter supplied) This study uses whole-transcriptome sequencing to characterize the transcriptomes of mouse embryonic fibroblasts (MEF's). Two conditions were analyzed, MEF cells with intact TET1/TET2 enzymes (WT) and MEF cells with TET1/TET2 knocked out (DKO). Our results identify sets of differentially expressed genes which are correlated with TET1/TET2 induced methylation changes of the corresponding genes.
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL13112
2 Samples
Download data: TXT
Series
Accession:
GSE58609
ID:
200058609
15.

Role of TET1-mediated epigenetic modulation in Alzheimer's disease

(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:
GPL24247 GPL21273
25 Samples
Download data: TXT
Series
Accession:
GSE226056
ID:
200226056
16.

Role of TET1-mediated epigenetic modulation in Alzheimer’s disease [RNA-Seq]

(Submitter supplied) To investigate the influence the partial loss of Tet1 has on AD pathogenesis in 5xFAD mice, we crossed a Tet1 KO mouse line with the 5xFAD mouse line to generate WT, 5xFAD, Tet1(+/-), and FAD/Tet1(+/-) mice. We then performed gene expression profiling analysis using data obtained from RNA-seq from biological replicates of mice comprised of 4 different genotypes.
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL24247
12 Samples
Download data: TXT
Series
Accession:
GSE226053
ID:
200226053
17.

Role of TET1-mediated epigenetic modulation in Alzheimer’s disease [5hmC-Capture]

(Submitter supplied) To investigate the influence the partial loss of Tet1 has on AD pathogenesis in 5xFAD mice, we crossed a Tet1 KO mouse line with the 5xFAD mouse line to generate WT, 5xFAD, Tet1(+/-), and FAD/Tet1(+/-) mice.
Organism:
Mus musculus
Type:
Methylation profiling by high throughput sequencing
Platform:
GPL21273
13 Samples
Download data: NARROWPEAK
Series
Accession:
GSE226043
ID:
200226043
18.

Distinct roles of Tet1 and Tet2 in mouse embryonic stem cells [MeDIP-Seq]

(Submitter supplied) The TET proteins TET1, TET2 and TET3 constitute a new family of dioxygenases that utilize molecular oxygen and the cofactors Fe(II) and 2-oxoglutarate to convert 5-methylcytosine (5mC) to 5-hydroxy-methylcytosine (5hmC) and further oxidation products in DNA1-5. Here we show that Tet1 and Tet2 have distinct roles in regulating 5hmC deposition and gene expression in mouse embryonic stem cells (mESC). Tet1 depletion in mESC primarily diminishes 5hmC levels at transcription start sites (TSS), whereas Tet2 depletion is mostly associated with decreased 5hmC in gene bodies relative to TSS. 5hmC is enriched at exon start and end sites, especially in exons that are highly expressed, and is significantly decreased upon Tet2 knockdown at the boundaries of high-expressed exons that are selectively regulated by Tet2. In differentiating murine B cells, Tet2 deficiency is associated with selective exon exclusion in the gene encoding the transmembrane phosphatase CD45. Tet2 depletion is associated with increased 5hmC and decreased 5mC at promoters/ TSS regions, possibly because of the redundant activity of Tet1. Together, these data indicate a complex interplay between Tet1 and Tet2 in mESC, and show that loss-of-function of a single TET protein does not necessarily lead to loss of 5hmC and a corresponding gain of 5mC, as generally assumed. The relation between Tet2 loss-of-function and selective changes in exon expression could potentially explain the frequent occurrence of both TET2 loss-of-function mutations and mutations in proteins involved in pre-mRNA splicing in myeloid malignancies in humans.
Organism:
Mus musculus
Type:
Methylation profiling by high throughput sequencing
Platform:
GPL13112
6 Samples
Download data: BED, TXT
Series
Accession:
GSE63771
ID:
200063771
19.

Distinct roles of Tet1 and Tet2 in mouse embryonic stem cells

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing; Other; Methylation profiling by high throughput sequencing
5 related Platforms
34 Samples
Download data: BED
Series
Accession:
GSE50201
ID:
200050201
20.

Distinct roles of Tet1 and Tet2 in mouse embryonic stem cells (CMS-Seq)

(Submitter supplied) The TET proteins TET1, TET2 and TET3 constitute a new family of dioxygenases that utilize molecular oxygen and the cofactors Fe(II) and 2-oxoglutarate to convert 5-methylcytosine (5mC) to 5-hydroxy-methylcytosine (5hmC) and further oxidation products in DNA1-5. Here we show that Tet1 and Tet2 have distinct roles in regulating 5hmC deposition and gene expression in mouse embryonic stem cells (mESC). Tet1 depletion in mESC primarily diminishes 5hmC levels at transcription start sites (TSS), whereas Tet2 depletion is mostly associated with decreased 5hmC in gene bodies relative to TSS. 5hmC is enriched at exon start and end sites, especially in exons that are highly expressed, and is significantly decreased upon Tet2 knockdown at the boundaries of high-expressed exons that are selectively regulated by Tet2. In differentiating murine B cells, Tet2 deficiency is associated with selective exon exclusion in the gene encoding the transmembrane phosphatase CD45. Tet2 depletion is associated with increased 5hmC and decreased 5mC at promoters/ TSS regions, possibly because of the redundant activity of Tet1. Together, these data indicate a complex interplay between Tet1 and Tet2 in mESC, and show that loss-of-function of a single TET protein does not necessarily lead to loss of 5hmC and a corresponding gain of 5mC, as generally assumed. The relation between Tet2 loss-of-function and selective changes in exon expression could potentially explain the frequent occurrence of both TET2 loss-of-function mutations and mutations in proteins involved in pre-mRNA splicing in myeloid malignancies in humans.
Organism:
Mus musculus
Type:
Other
Platforms:
GPL15103 GPL9250
16 Samples
Download data: TXT
Series
Accession:
GSE50200
ID:
200050200
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