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Links from GEO DataSets

Items: 17

1.

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
2.

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
3.

Cockayne syndrome group B deficiency reduces H3K9me3 chromatin remodeler SETDB1 and exacerbates cellular aging

(Submitter supplied) Cockayne syndrome (CS) is an accelerated aging disorder, caused by mutations in the CSA or CSB genes. In CSB-deficient cells, poly (ADP ribose) polymerase (PARP) is persistently activated by unrepaired DNA damage and PARP consumes and depletes cellular nicotinamide adenine dinucleotide (NAD), which leads to mitochondrial dysfunction. Here, the distribution of poly (ADP ribose) (PAR) was determined in CSB-deficient cells using ADPr-ChAP (ADP ribose-chromatin affinity purification), and the results show striking enrichment of PAR at transcription start sites (TSS), depletion of heterochromatin, and downregulation of H3K9me3-specific methyltransferases SUV39H1 and SETDB1. more...
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL11154
22 Samples
Download data: BED, BIGWIG, BW, TXT
Series
Accession:
GSE133176
ID:
200133176
4.

Regulatory interplay of Cockayne syndrome B ATPase and stress-response gene ATF3 following genotoxic stress

(Submitter supplied) Gene expression profile in CS1AN deficient and CSBwt restored cell lines after 24 hours of UV or alphe-amanitin treatment (only for restored). The comaprison of expression profile between 0 and 24 hours revealed continouse suppresion of transcription upon UV treatment in CS1AN cell line and alpha-amanitin treated CS1AN CSBwt restored cells.
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL6244
10 Samples
Download data: CEL
Series
Accession:
GSE57923
ID:
200057923
5.

Genome binding profile of the conserved CSB-PGBD3 fusion protein in CSB-null UVSS1KO cells

(Submitter supplied) The CSB-PGBD3 fusion protein arose over 43 million years ago when a 2.5 kb piggyBac 3 (PGBD3) transposon inserted into intron 5 of the Cockayne syndrome Group B (CSB) gene in the common ancestor of all higher primates. The CSB-PGBD3 fusion protein binds internally-deleted PGBD3 elements called MER85s in vitro, and induces a strong interferon-like innate antiviral immune response when expressed in CSB-null UVSS1KO cells. more...
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL9115
2 Samples
Download data: BED, WIG
Series
Accession:
GSE37919
ID:
200037919
6.

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
7.
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
8.
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
9.

DNA architectural protein CTCF facilitates subset-specific chromatin interactions to limit the formation of memory CD8+ T cells

(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
4 related Platforms
56 Samples
Download data
Series
Accession:
GSE205083
ID:
200205083
10.

CTCF facilitates subset-specific chromatin interactions to limit the formation of memory CD8+ T cells [HiC]

(Submitter supplied) CD8+ T cells provide protection from infection and tumor growth, and many current immunotherapies target molecules that enhance CD8+ T cell function and differentiation. The transcriptional programs orchestrating CD8+ T cell differentiation in response to infection has been described, but the changes in spatial chromatin organization accompanying effector and memory CD8+ T cell differentiation is unknown, despite research showing the importance of long-range chromatin interactions for transcriptional regulation in various cell types. more...
Organism:
Mus musculus
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL30215
6 Samples
Download data: COOL
Series
Accession:
GSE205081
ID:
200205081
11.

CTCF facilitates subset-specific chromatin interactions to limit the formation of memory CD8+ T cells [RNA-Seq]

(Submitter supplied) CD8+ T cells provide protection from infection and tumor growth, and many current immunotherapies target molecules that enhance CD8+ T cell function and differentiation. The transcriptional programs orchestrating CD8+ T cell differentiation in response to infection has been described, but the changes in spatial chromatin organization accompanying effector and memory CD8+ T cell differentiation is unknown, despite research showing the importance of long-range chromatin interactions for transcriptional regulation in various cell types. more...
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL19057
8 Samples
Download data: TXT
Series
Accession:
GSE205079
ID:
200205079
12.

CTCF facilitates subset-specific chromatin interactions to limit the formation of memory CD8+ T cells [ChIP-Seq]

(Submitter supplied) CD8+ T cells provide protection from infection and tumor growth, and many current immunotherapies target molecules that enhance CD8+ T cell function and differentiation. The transcriptional programs orchestrating CD8+ T cell differentiation in response to infection has been described, but the changes in spatial chromatin organization accompanying effector and memory CD8+ T cell differentiation is unknown, despite research showing the importance of long-range chromatin interactions for transcriptional regulation in various cell types. more...
Organism:
Mus musculus
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platforms:
GPL21103 GPL24247
34 Samples
Download data: BED, BW, TXT
Series
Accession:
GSE205077
ID:
200205077
13.

CTCF facilitates subset-specific chromatin interactions to limit the formation of memory CD8+ T cells [ATAC-Seq]

(Submitter supplied) CD8+ T cells provide protection from infection and tumor growth, and many current immunotherapies target molecules that enhance CD8+ T cell function and differentiation. The transcriptional programs orchestrating CD8+ T cell differentiation in response to infection has been described, but the changes in spatial chromatin organization accompanying effector and memory CD8+ T cell differentiation is unknown, despite research showing the importance of long-range chromatin interactions for transcriptional regulation in various cell types. more...
Organism:
Mus musculus
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platforms:
GPL24247 GPL21103
8 Samples
Download data: BED, BW, TXT
Series
Accession:
GSE205076
ID:
200205076
14.

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
15.

Expression data in induced pluripotent stem cells (iPSCs) derived from a DNA repair deficient fibroblast

(Submitter supplied) Cockayne syndrome (CS) is an autossomal human disorder characterized by premature aging along with other symptoms. At the molecular level, CS is characterized by a deficiency in the Transcription-couple DNA repair pathway caused by a mutation mainly in ERCC6 gene and the absence of its functional protein. It has been shown that the presence of DNA damage and the lack of some functional proteins related to DNA repair constitute a barrier for somatic cell reprogramming. more...
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL6244
24 Samples
Download data: CEL
Series
Accession:
GSE36648
ID:
200036648
16.

CGGBP1 regulates chromatin barrier activity and CTCF occupancy at repeats

(Submitter supplied) To study the role of CGGBP1 in regulation of CTCF occupancy, we performed CTCF ChIP-seq in HEK293T cells with three different levels of CGGBP1: (i) endogenous levels of CGGBP1 (ii) CGGBP1 knockdown, and (iii) CGGBP1 overexpression. Here, we show that CTCF binds to repeats as well as canonical CTCF-motifs and CGGBP1 determines the CTCF occupancy preference for repeats over canonical CTCF-motif. By combining CTCF ChIP-seq with histone modifications ChIP-seq (for H3K4me3, H3K9me3 and H3K27me3) under conditions of normal or CGGBP1 knockdown, we demonstrate that CTCF binding sites regulated by CGGBP1 correspond to chromatin barrier elements with profound effects on H3K9me3 distribution. more...
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL23934
10 Samples
Download data: BED
Series
Accession:
GSE129548
ID:
200129548
17.

Metabolic regulation of CTCF expression and chromatin association dictates starvation response in mice and flies

(Submitter supplied) Temporal and coordinated control of gene expression is vital to mount appropriate physiological responses, especially in the context of dynamic metabolic transitions. Despite this, the interplay between chromatin architectural proteins and metabolism in regulating transcription is largely unknown. Here, we demonstrate that CTCF, the transcriptional regulator and boundary insulating protein, is itself regulated by metabolic inputs and its expression is associated with fed/fasted states. more...
Organism:
Mus musculus
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL21103
12 Samples
Download data: BED, BIGWIG
Series
Accession:
GSE207692
ID:
200207692
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