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Links from GEO DataSets

Items: 20

1.

Epigenomic analysis of Atrx deficiency in murine glioma cells of orgin

(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:
GPL17021
50 Samples
Download data: BED, TXT, WIG
Series
Accession:
GSE100465
ID:
200100465
2.

Epigenomic analysis of Atrx deficiency in murine glioma cells of orgin [RNA-seq]

(Submitter supplied) The chromatin regulator ATRX is inactivated in large subsets of adult and pediatric glioma. Whether and how ATRX deficiency promotes oncogenesis by epigenomic dysregulation remains unclear. We found that Atrx loss, especially when coupled with Tp53 inactivation, promoted cell motility and modulated differentiation state in primary murine neuroepithelial progenitors, recapitulating characteristic disease phenotypes and molecular features. more...
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL17021
12 Samples
Download data: TXT
Series
Accession:
GSE100464
ID:
200100464
3.

Epigenomic analysis of Atrx deficiency in murine glioma cells of orgin [H3.3 ChIP]

(Submitter supplied) The chromatin regulator ATRX is inactivated in large subsets of adult and pediatric glioma. Whether and how ATRX deficiency promotes oncogenesis by epigenomic dysregulation remains unclear. We found that Atrx loss, especially when coupled with Tp53 inactivation, promoted cell motility and modulated differentiation state in primary murine neuroepithelial progenitors, recapitulating characteristic disease phenotypes and molecular features. more...
Organism:
Mus musculus
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL17021
18 Samples
Download data: BROADPEAK
Series
Accession:
GSE100463
ID:
200100463
4.

Epigenomic analysis of Atrx deficiency in murine glioma cells of orgin [Atrx ChIP]

(Submitter supplied) The chromatin regulator ATRX is inactivated in large subsets of adult and pediatric glioma. Whether and how ATRX deficiency promotes oncogenesis by epigenomic dysregulation remains unclear. We found that Atrx loss, especially when coupled with Tp53 inactivation, promoted cell motility and modulated differentiation state in primary murine neuroepithelial progenitors, recapitulating characteristic disease phenotypes and molecular features. more...
Organism:
Mus musculus
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL17021
14 Samples
Download data: BED
Series
Accession:
GSE100462
ID:
200100462
5.

Epigenomic analysis of Atrx deficiency in murine glioma cells of orgin [ATAC-seq]

(Submitter supplied) The chromatin regulator ATRX is inactivated in large subsets of adult and pediatric glioma. Whether and how ATRX deficiency promotes oncogenesis by epigenomic dysregulation remains unclear. We found that Atrx loss, especially when coupled with Tp53 inactivation, promoted cell motility and modulated differentiation state in primary murine neuroepithelial progenitors, recapitulating characteristic disease phenotypes and molecular features. more...
Organism:
Mus musculus
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL17021
6 Samples
Download data: BED, WIG
Series
Accession:
GSE100461
ID:
200100461
6.

A single-cell epigenetic atlas of human IDH-mutant glioma

(Submitter supplied) Recent single-cell transcriptomic studies report that IDH-mutant gliomas share a common hierarchy of cellular phenotypes, independent of genetic subtype. However, the genetic differences between IDH-mutant glioma subtypes are prognostic, predictive of response to chemotherapy, and correlate with distinct tumor microenvironments. To reconcile these findings, we profiled 22 human IDH-mutant gliomas via single-cell assay for transposase-accessible chromatin (scATAC-seq). more...
Organism:
Mus musculus; Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing; Expression profiling by high throughput sequencing
Platforms:
GPL24676 GPL24247
23 Samples
Download data: BED, MTX, TSV, TXT
Series
Accession:
GSE155430
ID:
200155430
7.

Zebrafish Samples for Loss of ATRX cooperates with p53-Deficiency to promote the Development of Sarcomas and other Malignancies

(Submitter supplied) The SWI/SNF-family chromatin remodeling protein ATRX is a tumor suppressor in sarcomas, gliomas and other malignancies. Its loss of function facilitates the alternative lengthening of telomeres (ALT) pathway in tumor cells, while it also affects Polycomb repressive complex 2 (PRC2) silencing of its target genes. To further define the role of inactivating ATRX mutations in carcinogenesis, we knocked out atrx in our previously published p53/nf1-deficient zebrafish line that develops malignant peripheral nerve sheath tumors and gliomas. more...
Organism:
Danio rerio
Type:
Expression profiling by high throughput sequencing
Platform:
GPL20828
10 Samples
Download data: FPKM_TRACKING, TXT
Series
Accession:
GSE125040
ID:
200125040
8.

ATRX loss in glioma results in epigenetic dysregulation of cell cycle phase transition

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.
Organism:
Homo sapiens; Mus musculus
Type:
Expression profiling by high throughput sequencing
Platforms:
GPL24676 GPL19057
8 Samples
Download data: MTX, TSV
Series
Accession:
GSE178116
ID:
200178116
9.

ATRX loss in glioma results in epigenetic dysregulation of cell cycle phase transition [scRNA-seq]

(Submitter supplied) ATRX, a chromatin remodeler protein, is recurrently mutated in H3F3A-mutant pediatric glioblastoma (GBM) and IDH-mutant grade 2/3 adult glioma. Previous work has shown that ATRX-deficient GBM cells show enhanced sensitivity to irradiation, but the etiology remains unclear. We found that ATRX binds regulatory elements of cell cycle phase transition genes in GBM cells, and there is a marked reduction in Checkpoint Kinase 1 (CHEK1) expression with ATRX loss, leading to early release of G2/M entry after irradiation. more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL24676
2 Samples
Download data: MTX, TSV
Series
Accession:
GSE178114
ID:
200178114
10.

ATRX loss in glioma results in epigenetic dysregulation of cell cycle phase transition [RNA-seq]

(Submitter supplied) ATRX, a chromatin remodeler protein, is recurrently mutated in H3F3A-mutant pediatric glioblastoma (GBM) and IDH-mutant grade 2/3 adult glioma. Previous work has shown that ATRX-deficient GBM cells show enhanced sensitivity to irradiation, but the etiology remains unclear. We found that ATRX binds regulatory elements of cell cycle phase transition genes in GBM cells, and there is a marked reduction in Checkpoint Kinase 1 (CHEK1) expression with ATRX loss, leading to early release of G2/M entry after irradiation. more...
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL19057
6 Samples
Download data: CSV
Series
Accession:
GSE178113
ID:
200178113
11.

mRNA array of CRISPR-Cas9 medicated ATRX gene editing in glioma cells

(Submitter supplied) Glioma is the most common primary malignant brain tumor in adults. Chemo resistance of temozolomide (TMZ), the first-line chemotherapeutic agent, is a major issue in the management of patients with glioma. Alterations of ATRX constitute one of the most prevalent genetic abnormalities in gliomas. Therefore, it is urgent to further elucidate the role of ATRX contributing to TMZ resistance in glioma. We used microarrays to detail the global programme of gene expression underlying cellularisation and identified distinct classes of up-regulated and down-regulated genes after ATRX knockout.
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL23126
6 Samples
Download data: CEL
Series
Accession:
GSE131781
ID:
200131781
12.

Functional loss of ATRX and telomerase activates Alternative Lengthening of Telomeres (ALT)

(Submitter supplied) The presence of ALT is strongly associated with recurrent cancer-specific somatic inactivating mutations in the ATRX-DAXX chromatin remodeling complex. Here, we generate an ALT-positive adenocarcinoma cell line following functional inactivation of ATRX and telomerase in a telomerase-positive carcinoma cell line.
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL13497
8 Samples
Download data: TXT
Series
Accession:
GSE129448
ID:
200129448
13.

H9-hESC derived human neural stem cells with combinations of mutant IDH1-R132H overexpression, P53 shRNA knockdown and/or ATRX shRNA knockdown

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing; Methylation profiling by genome tiling array; Other
Platforms:
GPL13534 GPL16791
20 Samples
Download data: BEDGRAPH, IDAT
Series
Accession:
GSE94962
ID:
200094962
14.

SOX2 promoter 4C-seq of H9-hESC derived human neural stem cells with mutant IDH1-R132H overexpression, P53 shRNA knockdown and ATRX shRNA knockdown

(Submitter supplied) 4C-seq was performed to assess genomic contacts with the SOX2 protmoter, human neural stem cells with no oncogenic alterations were compared to those with concurrent IDH1-R132H overexpression, P53 shRNA knockdown and ATRX shRNA knockdown.
Organism:
Homo sapiens
Type:
Other
Platform:
GPL16791
4 Samples
Download data: BEDGRAPH
Series
Accession:
GSE94961
ID:
200094961
15.

450k methylation array of H9-hESC derived human neural stem cells with combinations of mutant IDH1-R132H overexpression, P53 shRNA knockdown and/or ATRX shRNA knockdown

(Submitter supplied) Methylation profiling was performed to assess methylation alterations by the addition of serial oncogenic hits (mutant-IDH1, P53 knockdown and ATRX knockdown) in human neural stem cells.
Organism:
Homo sapiens
Type:
Methylation profiling by genome tiling array
Platform:
GPL13534
8 Samples
Download data: IDAT
Series
Accession:
GSE94956
ID:
200094956
16.

RNA-seq of H9-hESC derived human neural stem cells with combinations of mutant IDH1-R132H overexpression, P53 shRNA knockdown and/or ATRX shRNA knockdown

(Submitter supplied) RNA-seq was performed to assess gene expression alterations by the addition of serial oncogenic hits (mutant-IDH1, P53 knockdown and ATRX knockdown) in human neural stem cells.
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL16791
8 Samples
Download data: TXT
17.

Gene expression differences between wildtype and Atrx conditional knockout mouse retina tissues

(Submitter supplied) Loss of the Atrx chromatin remodeling protein causes dysfunction and death of post-mitotic retinal interneurons in mice. Embryonic conditional deletion of Atrx from multipotent retinal progenitor cells results in the selective loss of the retinal inhibitory interneurons, namely amacrine and horizontal cells. The cell death occurs postnatally after the development of these cell types, peaking at postntal day 17 in the mouse retina. more...
Organism:
Mus musculus
Type:
Expression profiling by array
Platform:
GPL16570
6 Samples
Download data: CEL, CHP
Series
Accession:
GSE78877
ID:
200078877
18.

The chromatin remodelling factor ATRX suppresses R-loops in transcribed telomeric repeats

(Submitter supplied) ATRX is a chromatin remodelling factor found at a wide range of tandemly repeated sequences including telomeres (TTAGGG)n. Acquired mutations in ATRX are found in nearly all tumours which maintain their telomeres via the alternative lengthening of telomere (ALT) pathway and ATRX is known to suppress this pathway. Here we show that recruitment of ATRX to telomeric repeats is dependent on their number, their orientation and, critically, on their transcription. more...
Organism:
Mus musculus
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL13112
6 Samples
Download data: BED
Series
Accession:
GSE96768
ID:
200096768
19.

Examining the role of ATRX-RNA interactions in ATRX and PRC2 localization and gene expression.

(Submitter supplied) We disrupted the RNA binding region in endogenous ATRX and tested localization of ATRX, EZH2 and H3K27me3 by CUT&RUN. We show that ATRX-RNA binding is important to regulate ATRX and PRC2 localization to specific genes.
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing; Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL19057
26 Samples
Download data: BROADPEAK, BW, TXT
Series
Accession:
GSE130452
ID:
200130452
20.

ATRX is necessary for cellular senescence and represses HRAS to drive cells from quiescence into senescence

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing; Expression profiling by high throughput sequencing
Platform:
GPL16791
29 Samples
Download data: BW, NARROWPEAK
Series
Accession:
GSE74621
ID:
200074621
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Supplemental Content

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