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Links from GEO DataSets

Items: 9

1.

CSB ablation induced apoptosis is mediated by Increased Endoplasmic Reticulum Stress Response: a gene expression study

(Submitter supplied) The DNA repair protein, Cockayne syndrome group B (CSB), has been recently identified as a promising anticancer target. Suppression, by antisense technology, of this protein causes devastating effects on tumor cells viability, through a massive induction of apoptosis, while being non-toxic to non-transformed cells. To gain insights into the mechanisms underlying the pro-apoptotic effects observed after CSB ablation, global gene expression patterns were determined, to identify genes that were significantly differentially regulated as a function of CSB expression. more...
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL17077
16 Samples
Download data: TXT
Series
Accession:
GSE83367
ID:
200083367
2.

Cockayne syndrome A and B proteins regulate the transcription arrest upon genotoxic stress through a ubiquitin/proteasome degradation process

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing; Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL20301
25 Samples
Download data
Series
Accession:
GSE87564
ID:
200087564
3.

Cockayne syndrome A and B proteins regulate the transcription arrest upon genotoxic stress through a ubiquitin/proteasome degradation process (ChIP-seq)

(Submitter supplied) The rare genetic disease Cockayne syndrome (CS) results in mutations in CSA and CSB. Upon UV irradiation, RNA synthesis was arrested: RNA-seq showed 70% of down-regulated genes in common between CSA and CSB deficient cells. ATF3, the product of an immediate early gene was overexpressed and bound to its CRE/ATF site to inhibit its responsive genes. ChIP experiments showed that CSA/CUL4A/DDB1 together with CSB and MDM2, target ATF3. more...
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL20301
17 Samples
Download data: XLSX
Series
Accession:
GSE87562
ID:
200087562
4.

Cockayne syndrome A and B proteins regulate the transcription arrest upon genotoxic stress through a ubiquitin/proteasome degradation process (RNA-seq)

(Submitter supplied) The rare genetic disease Cockayne syndrome (CS) results in mutations in CSA and CSB. Upon UV irradiation, RNA synthesis was arrested: RNA-seq showed 70% of down-regulated genes in common between CSA and CSB deficient cells. ATF3, the product of an immediate early gene was overexpressed and bound to its CRE/ATF site to inhibit its responsive genes. ChIP experiments showed that CSA/CUL4A/DDB1 together with CSB and MDM2, target ATF3. more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL20301
8 Samples
Download data: XLSX
Series
Accession:
GSE87540
ID:
200087540
5.

Cockayne syndrome (CSB) fibroblasts

(Submitter supplied) Cockayne syndrome (CS) is an inherited neurodevelopmental disorder with progeroid features. Although the genes responsible for CS have been implicated in a variety of DNA repair- and transcription-related pathways, the nature of the molecular defect in CS remains mysterious. We sought to define this defect by expression analysis of cells lacking functional CSB, a SWI/SNF-like ATPase that is responsible for most CS cases. more...
Organism:
Homo sapiens
Type:
Expression profiling by array
Datasets:
GDS2175 GDS2176
Platforms:
GPL96 GPL97
16 Samples
Download data: CEL
Series
Accession:
GSE3407
ID:
200003407
6.
Full record GDS2176

Cockayne syndrome group B protein-null fibroblast rescue (HG-U133B)

Analysis of Cockayne syndrome group B (CSB) protein-null fibroblasts rescued by expression of CSB cDNA. CS, a neurodegenerative disorder, arises mostly from CSB defects. Results provide insight into how CSB defects cause CS.
Organism:
Homo sapiens
Type:
Expression profiling by array, count, 3 protocol sets
Platform:
GPL97
Series:
GSE3407
8 Samples
Download data: CEL
7.
Full record GDS2175

Cockayne syndrome group B protein-null fibroblast rescue (HG-U133A)

Analysis of Cockayne syndrome group B (CSB) protein-null fibroblasts rescued by expression of CSB cDNA. CS, a neurodegenerative disorder, arises mostly from CSB defects. Results provide insight into how CSB defects cause CS.
Organism:
Homo sapiens
Type:
Expression profiling by array, count, 3 protocol sets
Platform:
GPL96
Series:
GSE3407
8 Samples
Download data: CEL
8.

Genomic localization of Cockayne syndrom B protein upon genotoxic stresses

(Submitter supplied) Cockayne syndrome is an inherited premature aging syndrome associated with developmental and neurological disorders. Mutations in the genomic locus encoding CSB are associated with 80% Cockayne syndrome cases. CSB is invovled in relieving UV-induced and oxidative stree. To gain more insights into the fucntion of CSB under these stress, we use ChIP-seq to determine the genomic localization of CSB 1 hour after UV irradiation and menadione treatment.
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL11154
2 Samples
Download data: BED
Series
Accession:
GSE50925
ID:
200050925
9.

c-Jun Targets Cockayne Syndrome protein B to Specific Genomic Region for Transcription Regulation

(Submitter supplied) Cockayne syndrome is an inherited premature aging syndrome associated with developmental and neurological disorders. Mutations in the genomic locus encoding CSB are associated with 80% Cockayne syndrome cases. Transcription profiling assays reveal the association of mis-regulation of gene expression with Cockayne syndrome, highlighting the importance of CSB in transcription regulation. However, many questions remain unanswered as how CSB regulates transcription. more...
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL11154
4 Samples
Download data: BED
Series
Accession:
GSE50171
ID:
200050171
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