GEO DataSets

(Submitter supplied) Progerin-expressing mice (HGPS-like) demonstrated increased energy metabolism and lipodystrophy. Increased mitochondrial biogenesis was found in adipose tissue from HGPS-like mice, whereas lamin C-only mice had fewer mitochondria. Thus we analyse which molecular pathways mediated the changes in adipose tissue caused by lamin C and progerin expression and the roles of these pathways in energy metabolism and aging.

Organism:

Mus musculus

Type:

Expression profiling by array

Platform:

GPL6096

9 Samples

Download data: CEL

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.

Organism:

Mus musculus

Type:

Expression profiling by array

Platforms:

GPL6096 GPL6193

18 Samples

Download data: CEL

(Submitter supplied) Progerin-expressing mice (HGPS-like) demonstrated increased energy metabolism and lipodystrophy. Increased mitochondrial biogenesis was found in adipose tissue from HGPS-like mice, whereas lamin C-only mice had fewer mitochondria. Thus we analyse which molecular pathways mediated the changes in adipose tissue caused by lamin C and progerin expression and the roles of these pathways in energy metabolism and aging.

Organism:

Mus musculus

Type:

Expression profiling by array

Platform:

GPL6193

9 Samples

Download data: CEL

(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

(Submitter supplied) Using ATAC seq analysis, we showed that the MEFs with a knockout of Lmna gene (i.e., missing the lamin A/C nuclear scaffolding protein) (Lmna-/- MEFs) display a striking change in chromatin accessibility landscape (peak signals that are both up and down), both within and outside lamina-associated domains (LADs); moreover, there was a clear overrepresentation of peaks with a gain in chromatin accessibility (within and outside LADs) in the Lmna-/- MEFs, and within LADs compared to outside LADs.

Organism:

Mus musculus

Type:

Genome binding/occupancy profiling by high throughput sequencing

Platform:

GPL19057

8 Samples

Download data: WIG

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.

Organism:

Homo sapiens; Mus musculus

Type:

Expression profiling by array

Platforms:

GPL10558 GPL8389

24 Samples

Download data

(Submitter supplied) The A-type lamins (lamin A/C), encoded by the Lmna gene, are important structural components of the nuclear lamina. Lmna mutations lead to degenerative disorders, including the premature aging disease Hutchinson-Gilford progeria syndrome (HGPS). In addition, altered lamin A/C expression is found in various cancers. Reports indicate that lamin A/C plays a role in DNA double strand break repair, but a role in DNA base excision repair (BER) has not been described. more...

Organism:

Homo sapiens

Type:

Expression profiling by array

Platform:

GPL10558

18 Samples

Download data: XLSX

(Submitter supplied) The A-type lamins (lamin A/C), encoded by the Lmna gene, are important structural components of the nuclear lamina. Lmna mutations lead to degenerative disorders, including the premature aging disease Hutchinson-Gilford progeria syndrome (HGPS). In addition, altered lamin A/C expression is found in various cancers. Reports indicate that lamin A/C plays a role in DNA double strand break repair, but a role in DNA base excision repair (BER) has not been described. more...

Organism:

Mus musculus

Type:

Expression profiling by array

Platform:

GPL8389

6 Samples

Download data: TXT

(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

(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

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

(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

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

(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

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

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.

Organism:

Mus musculus

Type:

Expression profiling by array; Expression profiling by high throughput sequencing

Platforms:

GPL13112 GPL20775

22 Samples

Download data: CEL

(Submitter supplied) Hutchinson-Gilford progeria syndrome (HGPS) is the result of a defective form of the lamin A protein called progerin. While progerin is known to disrupt the properties of the nuclear lamina, the underlying mechanisms responsible for the pathophysiology of HGPS remain less clear. Previous studies in our laboratory have shown that progerin expression in murine epidermal basal cells results in impaired stratification and halted development of the skin. more...

Organism:

Mus musculus

Type:

Expression profiling by array

Platform:

GPL20775

12 Samples

Download data: CEL, CSV

(Submitter supplied) Purpose: Hutchinson-Gilford progeria syndrome (HGPS) is the result of a defective form of the lamin A protein called progerin. While progerin is known to disrupt the properties of the nuclear lamina, the underlying mechanisms responsible for the pathophysiology of HGPS remain less clear. Previous studies in our laboratory have shown that progerin expression in murine epidermal basal cells results in impaired stratification and halted development of the skin. more...

Organism:

Mus musculus

Type:

Expression profiling by high throughput sequencing

Platform:

GPL13112

10 Samples

Download data: TXT