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Links from GEO DataSets

Items: 20

1.
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
2.

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
3.

Reprogramming Hutchinson-Gilford Progeria Syndrome fibroblasts resets epigenomic landscape in patient-derived induced pluripotent stem cells [ChIP-Seq]

(Submitter supplied) Hutchinson-Gilford Progeria Syndrome (HGPS) is a segmental premature aging disorder caused by the accumulation of the truncated form of Lamin A known as Progerin within the nuclear lamina. Cellular hallmarks of HGPS include nuclear blebbing, loss of peripheral heterochromatin, defective epigenetic inheritance, altered gene expression, and senescence. To model HGPS using iPSCs, detailed genome-wide and structural analysis of the epigenetic landscape is required to assess the initiation and progression of the disease.
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL10999
16 Samples
Download data: BED, TXT
Series
Accession:
GSE84356
ID:
200084356
4.

A human iPSC model of Hutchinson Gilford Progeria Syndrome reveals a possible mesenchymal stem cell defect

(Submitter supplied) Hutchinson Gilford Progeria Syndrome (HGPS) is a rare, sporadic genetic disease caused by mutations in the nuclear lamin A gene. In most cases the mutation creates an efficient donor-splice site that generates an altered transcript encoding a truncated lamin A protein, progerin. In vitro studies have indicated that progerin can disrupt nuclear function. HGPS affects mainly mesenchymal lineages but the shortage of patient material has precluded a tissue-wide molecular survey of progerin’s cellular impact. more...
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL6883
23 Samples
Download data: TXT
Series
Accession:
GSE26093
ID:
200026093
5.

Progerin-induced changes in gene expression

(Submitter supplied) The premature aging disease Hutchinson-Gilford Progeria Syndrome (HGPS) is caused by constitutive production of progerin, a mutant form of the nuclear architectural protein lamin A1. Progerin is also sporadically expressed in wild type cells and has been linked to physiological aging. HGPS cells exhibit extensive nuclear defects including abnormal chromatin structure and increased DNA damage. At the organismal level, HGPS affects several tissues particularly of mesenchymal origin. more...
Organism:
Homo sapiens
Type:
Expression profiling by array
Dataset:
GDS3495
Platform:
GPL2895
12 Samples
Download data
Series
Accession:
GSE10123
ID:
200010123
6.
Full record GDS3495

Progerin expression in a hTERT-immortalized skin fibroblast cell line: time course

Analysis of skin fibroblasts induced to express GFP-progerin for up to 10 days. Progerin is a mutant form of lamin A and the causal agent of premature-ageing disease Hutchinson-Gilford Progeria Syndrome (HGPS). Results provide insight into molecular mechanisms underlying this pathological effect.
Organism:
Homo sapiens
Type:
Expression profiling by array, count, 2 protocol, 3 time sets
Platform:
GPL2895
Series:
GSE10123
12 Samples
Download data
7.

Exon array analysis in primary human fibroblasts

(Submitter supplied) Exon usage analysis in in vitro cultured fibroblast cells. To assay the genome-wide splicing changes during cellular senescence, we performed splicing analysis on young and old normal fibroblasts, and in fibroblasts +/- tert (telomerase protein subunit Tert immortalized).
Organism:
Homo sapiens
Type:
Expression profiling by array
Platforms:
GPL5175 GPL5188
34 Samples
Download data: CEL, CHP
Series
Accession:
GSE28863
ID:
200028863
8.

NF-κB activation impairs somatic cell reprogramming in ageing

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.
Organism:
Homo sapiens
Type:
Expression profiling by array
Platforms:
GPL5175 GPL19251 GPL6244
18 Samples
Download data: CEL
Series
Accession:
GSE65173
ID:
200065173
9.

NF-κB activation impairs somatic cell reprogramming in ageing [MSCs]

(Submitter supplied) Transcriptional profiling of human control and Néstor-Guillermo Progeria Syndrome (NGPS) mesenchymal stem cells (MSCs). Somatic cell reprogramming involves rejuvenation of adult cells and relies on the ability to erase age-associated molecular marks. Accordingly, reprogramming efficiency declines with ageing, and age-associated features such as genetic instability, cell senescence or telomere shortening negatively affect this process. more...
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL6244
6 Samples
Download data: CEL
Series
Accession:
GSE65172
ID:
200065172
10.

NF-κB activation impairs somatic cell reprogramming in ageing [IKBA-SR]

(Submitter supplied) Transcriptional profiling of human Néstor-Guillermo Progeria Syndrome (NGPS) fibroblasts control, treated with sodium salicylate or transduced with Ikappa B alpha super-repressor. Somatic cell reprogramming involves rejuvenation of adult cells and relies on the ability to erase age-associated molecular marks. Accordingly, reprogramming efficiency declines with ageing, and age-associated features such as genetic instability, cell senescence or telomere shortening negatively affect this process. more...
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL19251
3 Samples
Download data: CEL
Series
Accession:
GSE65171
ID:
200065171
11.

NF-κB activation impairs somatic cell reprogramming in ageing [NGPS_iPSCs]

(Submitter supplied) Transcriptional profiling of human control and Néstor-Guillermo Progeria Syndrome (NGPS) fibroblasts and induced pluripotent stem cells (iPSCs). Somatic cell reprogramming involves rejuvenation of adult cells and relies on the ability to erase age-associated molecular marks. Accordingly, reprogramming efficiency declines with ageing, and age-associated features such as genetic instability, cell senescence or telomere shortening negatively affect this process. more...
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL5175
9 Samples
Download data: CEL
Series
Accession:
GSE65170
ID:
200065170
12.

Epigenetic deregulation of lamina-associated domains in Hutchinson-Gilford Progeria Syndrome

(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
Platforms:
GPL20301 GPL11154
17 Samples
Download data
Series
Accession:
GSE150138
ID:
200150138
13.

Epigenetic deregulation of lamina-associated domains in Hutchinson-Gilford Progeria Syndrome (RNA-Seq)

(Submitter supplied) Hutchinson-Gilford Progeria Syndrome (HGPS) is a progeroid disease characterized by the early onset of some classically age-related phenotypes including arthritis, loss of body fat and hair and atherosclerosis. Cells from affected individuals express a mutant version of the nuclear envelope protein Lamin A (termed Progerin) and have previously been shown to exhibit prominent chromatin changes. Here, we identify epigenetic deregulation of lamina-associated domains (LADs) as a central feature in the molecular pathology of HGPS. more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL11154
9 Samples
Download data: TXT
Series
Accession:
GSE150137
ID:
200150137
14.

Epigenetic deregulation of lamina-associated domains in Hutchinson-Gilford Progeria Syndrome (ATAC-Seq)

(Submitter supplied) Hutchinson-Gilford Progeria Syndrome (HGPS) is a progeroid disease characterized by the early onset of some classically age-related phenotypes including arthritis, loss of body fat and hair and atherosclerosis. Cells from affected individuals express a mutant version of the nuclear envelope protein Lamin A (termed Progerin) and have previously been shown to exhibit prominent chromatin changes. Here, we identify epigenetic deregulation of lamina-associated domains (LADs) as a central feature in the molecular pathology of HGPS. more...
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL20301
8 Samples
Download data: XLS
Series
Accession:
GSE150136
ID:
200150136
15.

Epigenetic deregulation of lamina-associated domains in Hutchinson-Gilford Progeria Syndrome

(Submitter supplied) Hutchinson-Gilford Progeria Syndrome (HGPS) is a progeroid disease characterized by the early onset of some classically age-related phenotypes including arthritis, loss of body fat and hair and atherosclerosis. Cells from affected individuals express a mutant version of the nuclear envelope protein Lamin A (termed Progerin) and have previously been shown to exhibit prominent chromatin changes. Here, we identify epigenetic deregulation of lamina-associated domains (LADs) as a central feature in the molecular pathology of HGPS. more...
Organism:
Homo sapiens
Type:
Methylation profiling by genome tiling array
Platform:
GPL23976
15 Samples
Download data: IDAT
Series
Accession:
GSE149960
ID:
200149960
16.

Gene expression profile of HGPS skin fibroblasts upon treatment with JH4

(Submitter supplied) To gain further insight into the biological effects of JH4, we investigated its impact on gene expression profiles. We defined a set of genes such as IL33, BRCA1, BLM, Rad51, IL6, IL8, and TNFSF18 whose expression is restored by JH4 treatment
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL6244
4 Samples
Download data: CEL
Series
Accession:
GSE84147
ID:
200084147
17.

Transcriptional profiling of liver samples from Lmna Gly609Gly knock-in mice

(Submitter supplied) Hutchinson-Gilford Progeria Syndrome (HGPS) is caused by a point mutation in the LMNA gene that activates a cryptic donor splice site and yields a truncated form of prelamin A called progerin. Small amounts of progerin are also produced during normal aging. Studies with mouse models of HGPS have allowed the recent development of the first therapeutic approaches for this disease. However, none of these earlier works have addressed the aberrant and pathogenic LMNA splicing observed in HGPS patients because of the lack of an appropriate mouse model. more...
Organism:
Mus musculus
Type:
Expression profiling by array
Dataset:
GDS4490
Platform:
GPL6246
6 Samples
Download data: CEL
Series
Accession:
GSE32609
ID:
200032609
18.
Full record GDS4490

Lmna G609G knock-in model of Hutchinson-Gilford Progeria Syndrome: liver

Analysis of liver from Lmna Gly609Gly knock-in C57BL/6 females. These mice accumulate progerin and manifest the main clinical features of human Hutchinson-Gilford progeria syndrome (HGPS). Results provide insight into the molecular mechanisms underlying HGPS.
Organism:
Mus musculus
Type:
Expression profiling by array, count, 2 genotype/variation sets
Platform:
GPL6246
Series:
GSE32609
6 Samples
Download data: CEL
DataSet
Accession:
GDS4490
ID:
4490
19.

Human iPSC-based Modeling of Late-Onset Disease using Progerin-induced Aging

(Submitter supplied) Reprogramming somatic cells to induced pluripotent stem cells (iPSCs) sets their identity back to an embryonic age. This presents a fundamental hurdle for modeling late-onset disorders using iPSC-derived cells. We therefore developed a strategy to induce age-like features in multiple iPSC-derived lineages and tested its impact on modeling Parkinson’s disease (PD). We first describe markers that predict fibroblast donor age and observed the loss of these age-related markers following iPSC induction and re-differentiation into fibroblasts. more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL11154
8 Samples
Download data: TXT
Series
Accession:
GSE52431
ID:
200052431
20.

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
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