GEO DataSets

(Submitter supplied) LMNA encodes nuclear Lamin A/C that tethers lamina-associated domains (LADs) to the nuclear periphery. Mutations in LMNA cause degenerative disorders including the premature aging disorder Hutchinson-Gilford progeria, but the mechanisms are unknown. We report that Ser22-phosphorylated (pS22) Lamin A/C was localized to the nuclear interior in human fibroblasts throughout the cell cycle. pS22-Lamin A/C interacted with a subset of putative active enhancers, not LADs, at locations co-bound by the transcriptional activator c-Jun. more...

Organism:

Homo sapiens

Type:

Expression profiling by high throughput sequencing

Platform:

GPL11154

8 Samples

Download data: TXT

(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; Other

Platforms:

GPL18573 GPL11154

83 Samples

Download data

(Submitter supplied) LMNA encodes nuclear Lamin A/C that tethers lamina-associated domains (LADs) to the nuclear periphery. Mutations in LMNA cause degenerative disorders including the premature aging disorder Hutchinson-Gilford progeria, but the mechanisms are unknown. We report that Ser22-phosphorylated (pS22) Lamin A/C was localized to the nuclear interior in human fibroblasts throughout the cell cycle. pS22-Lamin A/C interacted with a subset of putative active enhancers, not LADs, at locations co-bound by the transcriptional activator c-Jun. more...

Organism:

Homo sapiens

Type:

Genome binding/occupancy profiling by high throughput sequencing

Platform:

GPL18573

2 Samples

Download data: BW

(Submitter supplied) LMNA encodes nuclear Lamin A/C that tethers lamina-associated domains (LADs) to the nuclear periphery. Mutations in LMNA cause degenerative disorders including the premature aging disorder Hutchinson-Gilford progeria, but the mechanisms are unknown. We report that Ser22-phosphorylated (pS22) Lamin A/C was localized to the nuclear interior in human fibroblasts throughout the cell cycle. pS22-Lamin A/C interacted with a subset of putative active enhancers, not LADs, at locations co-bound by the transcriptional activator c-Jun. more...

Organism:

Homo sapiens

Type:

Other

Platform:

GPL18573

2 Samples

Download data: BW

(Submitter supplied) LMNA encodes nuclear Lamin A/C that tethers lamina-associated domains (LADs) to the nuclear periphery. Mutations in LMNA cause degenerative disorders including the premature aging disorder Hutchinson-Gilford progeria, but the mechanisms are unknown. We report that Ser22-phosphorylated (pS22) Lamin A/C was localized to the nuclear interior in human fibroblasts throughout the cell cycle. pS22-Lamin A/C interacted with a subset of putative active enhancers, not LADs, at locations co-bound by the transcriptional activator c-Jun. more...

Organism:

Homo sapiens

Type:

Genome binding/occupancy profiling by high throughput sequencing

Platform:

GPL11154

71 Samples

Download data: BW

(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

(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

(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

(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

(Submitter supplied) LMNA mutation caused reduced expression of IGFBP5 in patient samples

Organism:

Homo sapiens

Type:

Expression profiling by high throughput sequencing

Platform:

GPL18573

9 Samples

Download data: DIFF

(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

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

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

(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) We present a new high-throughput sequencing-based technique, named Sequential Analysis of MacroMolecules accessibilitY (SAMMY-seq), for the genome-wide mapping of chromatin regions separated by differential accessibility. The method is based on the sequential extraction of multiple chromatin fractions, corresponding to increasingly compacted and less accessible chromatin regions, which are mapped along the genome using high-throughput sequencing. more...

Organism:

Homo sapiens

Type:

Genome binding/occupancy profiling by high throughput sequencing; Expression profiling by high throughput sequencing; Other

Platforms:

GPL16791 GPL24676 GPL11154

76 Samples

Download data: BED, BIGWIG, BROADPEAK, BW, TSV

(Submitter supplied) Three-dimensional (3D) genome organization is thought to be important for regulation of gene expression. Chromosome conformation capture-based studies have uncovered ensemble organizational principles such as active (A) and inactive (B) compartmentalization. In addition, large inactive regions of the genome associate with the nuclear lamina, the Lamina Associated Domains (LADs). Here we investigate the dynamic relationship between A/B-compartment organization and the 3D organization of LADs. more...

Organism:

Mus musculus

Type:

Genome binding/occupancy profiling by high throughput sequencing

Platform:

GPL17021

22 Samples

Download data: BED, BW