Format
Items per page
Sort by

Send to:

Choose Destination

Links from GEO DataSets

Items: 16

1.
Full record GDS5426

Hutchinson Gilford Progeria Syndrome cell line response to oncogenic challenge

Analysis of skin fibroblasts from Hutchinson Gilford Progeria Syndrome (HGPS) patients challenged by retroviral introduction of telomerase reverse transcriptase (TERT), V12-HRAS and SV40 large and small T antigens. Results provide insight into molecular basis of transformation resistance in HGPS.
Organism:
Homo sapiens
Type:
Expression profiling by array, count, 2 disease state, 4 individual, 2 protocol sets
Platform:
GPL570
Series:
GSE60518
8 Samples
Download data: CEL
2.

BRD4 binding sites in transformed fibroblasts

(Submitter supplied) Analysis of BRD4 ChIP-seq data of two types of human transformed fibroblasts (WT and HGPS) to identify specific and common binding sites for BRD4. Transformed cell lines were obtained by retroviral introduction of TERT (T), V12-HRAS (R) and SV40 large and small T antigens (S) of primary skin fibroblasts for HGPS patients (TRS-HGPS) and age-matched control wild-type individuals (TRS-WT) Abstract: Advanced age and DNA damage accumulation are strong risk factors for cancer. more...
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL11154
8 Samples
Download data: BED
Series
Accession:
GSE61325
ID:
200061325
3.

Expression data from transformed WT and HGPS cell lines, including HGPS cells after knock-down of BRD4

(Submitter supplied) Primary skin fibroblasts from a HGPS patient and an age-matched control wild-type individual were challenged in a standard transformation assay by retroviral introduction of TERT (T), V12-HRAS (R) and SV40 large and small T antigens (S). Knock-down of BRD4 in this TRS-HGPS cell line (TRS-HGPS-shBRD4) was achieved by retroviral introduction of independent shRNAs (shBRD4-1 to -3) Abstract: Advanced age and DNA damage accumulation are strong risk factors for cancer. more...
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL15207
7 Samples
Download data: CEL, CHP
Series
Accession:
GSE60519
ID:
200060519
4.

Expression data from immortalized and transformed WT and HGPS cell lines

(Submitter supplied) Primary skin fibroblasts from HGPS patients and an age-matched control wild-type individuals were challenged in a standard transformation assay by retroviral introduction of TERT (T), V12-HRAS (R) and SV40 large and small T antigens (S). TERT-Immortalized cell lines from the same sources were also generated. Abstract: Advanced age and DNA damage accumulation are strong risk factors for cancer. The premature-aging disorder Hutchinson Gilford Progeria Syndrome (HGPS) provides a unique opportunity to study the interplay between DNA damage and aging-associated tumor mechanisms, since HGPS patients do not develop tumors despite elevated levels of DNA damage. more...
Organism:
Homo sapiens
Type:
Expression profiling by array
Dataset:
GDS5426
Platform:
GPL570
8 Samples
Download data: CEL
Series
Accession:
GSE60518
ID:
200060518
5.

Expression data from young and old healthy humans, as well as HGPS patients

(Submitter supplied) HGPS is a rare premature ageing disease, caused by a mutation in the LMNA gene, which activates a cryptic splice site, resulting in the production of a mutant lamin A isoform, called progerin. Sporadic usage of the same cryptic splice site has been observed with normal physiological aging. As it is unknown how HGPS causes premature ageing defects, we set out to determine the gene signature of both young healthy individuals, old healthy individuals, as well as HGPS patients.
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL570
12 Samples
Download data: CEL
Series
Accession:
GSE69391
ID:
200069391
6.

Recapitulation of human premature aging by using iPSCs from Hutchinson-Gilford progeria syndrome

(Submitter supplied) Hutchinson-Gilford progeria syndrome (HGPS) is a rare and fatal human premature aging disease1-5, characterized by premature atherosclerosis and degeneration of vascular smooth muscle cells (SMCs)6-8. HGPS is caused by a single-point mutation in the LMNA gene, resulting in the generation of progerin, a truncated mutant of lamin A. Accumulation of progerin leads to various aging-associated nuclear defects including disorganization of nuclear lamina and loss of heterochromatin9-12. more...
Organism:
Homo sapiens
Type:
Expression profiling by array
Dataset:
GDS3892
Platform:
GPL570
10 Samples
Download data: CEL
Series
Accession:
GSE24487
ID:
200024487
7.
Full record GDS3892

Induced pluripotent stem cell-based accelerated aging model

Analysis of iPSCs generated from fibroblasts from patients with Hutchinson-Gilford progeria syndrome (HGPS), a rare and fatal premature aging disease. Premature aging was recapitulated by differentiation of the HGPS-iPSCs. Results provide insight into molecular mechanisms underlying premature aging.
Organism:
Homo sapiens
Type:
Expression profiling by array, transformed count, 3 cell line, 2 genotype/variation sets
Platform:
GPL570
Series:
GSE24487
10 Samples
Download data: CEL
8.

Correlated alterations in genome organization, histone methylation, and DNA-lamina interactions in Hutchinson-Gilford progeria syndrome

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.
Organism:
Homo sapiens
Type:
Expression profiling by array; Genome binding/occupancy profiling by high throughput sequencing
Platforms:
GPL9115 GPL9052 GPL570
28 Samples
Download data: BED, CEL, TXT
Series
Accession:
GSE41764
ID:
200041764
9.

Correlated alterations in genome organization, histone methylation, and DNA-lamina interactions in Hutchinson-Gilford progeria syndrome (Hi-C)

(Submitter supplied) Hutchinson-Gilford progeria syndrome (HGPS) is a premature aging disease that is frequently caused by a de novo point mutation at position 1824 in LMNA. This mutation activates a cryptic splice donor site in exon 11, and leads to an in-frame deletion within the prelamin A mRNA and the production of a dominant negative lamin A protein, known as progerin. Here we show that HGPS cells experience genome-wide alterations in patterns of H3K27me3 deposition, changes in the associations of genomic loci with nuclear lamin A/C, and, at late passages, genome-wide loss of spatial compartmentalization of active and inactive chromatin domains that characterizes chromosome folding in normal cells. more...
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL9115
4 Samples
Download data: TXT
Series
Accession:
GSE41763
ID:
200041763
10.

Correlated alterations in genome organization, histone methylation, and DNA-lamina interactions in Hutchinson-Gilford progeria syndrome (ChIP-seq)

(Submitter supplied) Hutchinson-Gilford progeria syndrome (HGPS) is a premature aging disease that is frequently caused by a de novo point mutation at position 1824 in LMNA. This mutation activates a cryptic splice donor site in exon 11, and leads to an in-frame deletion within the prelamin A mRNA and the production of a dominant negative lamin A protein, known as progerin. Here we show that HGPS cells experience genome-wide alterations in patterns of H3K27me3 deposition, changes in the associations of genomic loci with nuclear lamin A/C, and, at late passages, genome-wide loss of spatial compartmentalization of active and inactive chromatin domains that characterizes chromosome folding in normal cells. more...
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL9052
18 Samples
Download data: BED
Series
Accession:
GSE41757
ID:
200041757
11.

Correlated alterations in genome organization, histone methylation, and DNA-lamina interactions in Hutchinson-Gilford progeria syndrome (expression)

(Submitter supplied) Hutchinson-Gilford progeria syndrome (HGPS) is a premature aging disease that is frequently caused by a de novo point mutation at position 1824 in LMNA. This mutation activates a cryptic splice donor site in exon 11, and leads to an in-frame deletion within the prelamin A mRNA and the production of a dominant negative lamin A protein, known as progerin. Here we show that HGPS cells experience genome-wide alterations in patterns of H3K27me3 deposition, changes in the associations of genomic loci with nuclear lamin A/C, and, at late passages, genome-wide loss of spatial compartmentalization of active and inactive chromatin domains that characterizes chromosome folding in normal cells. more...
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL570
6 Samples
Download data: CEL
Series
Accession:
GSE41751
ID:
200041751
12.

Twist expression in HMLE and breast cancer T47D cells

(Submitter supplied) Twist is a key EMT inducer, expression of Twist will induce EMT in HMLE and breast tumor T47D cells By expressing Twist in HMLE and T47D cells, which lack the expression of Twist, will identify the genes regulated by Twist
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL6244
8 Samples
Download data: CEL, CHP
Series
Accession:
GSE53222
ID:
200053222
13.

Comparison of Hutchinson–Gilford Progeria Syndrome fibroblast cell lines to control fibroblast cell lines

(Submitter supplied) Hutchinson–Gilford progeria syndrome (HGPS) is a rare genetic disease with widespread phenotypic features resembling premature aging. HGPS was recently shown to be caused by dominant mutations in the LMNA gene, resulting in the in-frame deletion of 50 amino acids near the carboxyl terminus of the encoded lamin A protein. Children with this disease typically succumb to myocardial infarction or stroke caused by severe atherosclerosis at an average age of 13 years. more...
Organism:
Homo sapiens
Type:
Expression profiling by array
Datasets:
GDS1503 GDS1504
Platforms:
GPL97 GPL96
36 Samples
Download data: CEL
Series
Accession:
GSE3860
ID:
200003860
14.
Full record GDS1504

Hutchinson-Gilford progeria syndrome: fibroblast (HG-U133B)

Expression profiling of three fibroblast cell lines derived from Hutchinson-Gilford progeria syndrome (HGPS) patients. Identified changes in gene expression may provide clues to potential risk factors or factors influencing disease progression.
Organism:
Homo sapiens
Type:
Expression profiling by array, count, 6 cell line, 2 disease state sets
Platform:
GPL97
Series:
GSE3860
18 Samples
Download data: CEL
DataSet
Accession:
GDS1504
ID:
1504
15.
Full record GDS1503

Hutchinson-Gilford progeria syndrome: fibroblast (HG-U133A)

Expression profiling of three fibroblast cell lines derived from Hutchinson-Gilford progeria syndrome (HGPS) patients. Identified changes in gene expression may provide clues to potential risk factors or factors influencing disease progression.
Organism:
Homo sapiens
Type:
Expression profiling by array, count, 6 cell line, 2 disease state sets
Platform:
GPL96
Series:
GSE3860
18 Samples
Download data: CEL
DataSet
Accession:
GDS1503
ID:
1503
16.

Genome-wide DNA methylation profiling of Progeria and Werner syndrome patients

(Submitter supplied) DNA methylation gradiently changes with age and is likely to be involved in aging-related processes resulting in phenotype changes and increased susceptibility to certain diseases. The Hutchinson-Gilford Progeria Syndrome (HGP) and Werner Syndrome are two premature aging diseases showing features of common aging. Mutations in LMNA and WRN genes were associated to disease onset; however for a subset of patients the underlying causative mechanisms remain elusive. more...
Organism:
Homo sapiens
Type:
Methylation profiling by array
Platform:
GPL13534
16 Samples
Download data: TXT
Series
Accession:
GSE42865
ID:
200042865
Format
Items per page
Sort by

Send to:

Choose Destination

Supplemental Content

db=gds|term=|query=1|qty=2|blobid=MCID_6169f618799dd072b8520c5b|ismultiple=true|min_list=5|max_list=20|def_tree=20|def_list=|def_view=|url=/Taxonomy/backend/subset.cgi?|trace_url=/stat?
   Taxonomic Groups  [List]
Tree placeholder
    Top Organisms  [Tree]

Find related data

Recent activity

Your browsing activity is empty.

Activity recording is turned off.

Turn recording back on

See more...
Support Center