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Links from GEO DataSets

Items: 20

1.

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
2.

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
3.

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
4.

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
5.

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
6.
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
7.

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
8.

Transcriptional profiling of chemical Dot1L inhibition during reprogramming to induced pluripotent stem cells

(Submitter supplied) Three independent transcriptional profiling experiments were performed to ascertain how Dot1L affects cell fate change. 1) In a timecoure ("Tc"), reprogramming mouse embryonic fibroblasts were treated with DMSO control or Dot1L inhibitor (Dot1Li -SGC0946) for 2 or 4 days. Surprisingly, despite the enrichment of H3K79me2 on thousands of actively transcribed genes, Dot1L inhibition (Dot1Li) results in few changes in steady state mRNA levels during reprogramming, the majority of which are spuriously upregulated. more...
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platforms:
GPL21103 GPL17021
36 Samples
Download data: TXT
Series
Accession:
GSE160580
ID:
200160580
9.

iPSCs from patients with NBS as a model uncovering disease mechanisms and a screening platform for anti-oxidants modifying genomic stability

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.
Organism:
Homo sapiens
Type:
Expression profiling by array
Platforms:
GPL18405 GPL10558
19 Samples
Download data
Series
Accession:
GSE94708
ID:
200094708
10.

iPSCs from patients with NBS as a model uncovering disease mechanisms and a screening platform for anti-oxidants modifying genomic stability [iPSCs]

(Submitter supplied) Nijmegen Breakage Syndrome (NBS) is a rare autosomal recessive genetic disorder, first described 1981 in Nijmegen, Holland. The characteristics of NBS include genomic instability (resulting in early onset of malignancies), premature aging, microcephaly and other growth retardations, immune deficiency, and impaired puberty and fertility in females. The consequence of these manifestations is a severe decrease in average life span, caused by cancer or infection of the respiratory and urinary tract. more...
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL10558
11 Samples
Download data: TXT
Series
Accession:
GSE94707
ID:
200094707
11.

iPSCs from patients with NBS as a model uncovering disease mechanisms and a screening platform for anti-oxidants modifying genomic stability [fibroblasts]

(Submitter supplied) Nijmegen Breakage Syndrome (NBS) is a rare autosomal recessive genetic disorder, first described 1981 in Nijmegen, Holland. The characteristics of NBS include genomic instability (resulting in early onset of malignancies), premature aging, microcephaly and other growth retardations, immune deficiency, and impaired puberty and fertility in females. The consequence of these manifestations is a severe decrease in average life span, caused by cancer or infection of the respiratory and urinary tract. more...
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL18405
8 Samples
Download data: TXT
Series
Accession:
GSE94706
ID:
200094706
12.

c-Jun impedes somatic cell reprogramming by activating mesenchymal core regulators and suppressing pluripotent ones

(Submitter supplied) The somatic cell fate can be converted to tumor or pluripotent ones by ectopic expression of transcription factors in vitro and in vivo. Many oncogenic transcription factors are known to mediate both fates as they share similar proliferative and metabolic properties. Paradoxically, we found c-Jun as the first oncogene that appears to specify a somatic fate, oppose the pluripotent one and impede reprogramming. more...
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing; Genome binding/occupancy profiling by high throughput sequencing
Platforms:
GPL16417 GPL13112
16 Samples
Download data: TXT, XLS
Series
Accession:
GSE50776
ID:
200050776
13.

Permissive epigenomic states endow reprogramming competence to a broad range of transcriptional regulators

(Submitter supplied) Identifying molecular targets that regulate reprogramming competence of transcription factors in donor cells broadens our understanding of reprogramming process. Here, by a chemical screen targeting major epigenetic pathways in human reprogramming, we discovered that inhibiting specific epigenetic roadblocks allows iPSC generation with almost all OCT factors. Amongst these epigenetic pathways was not only DOT1L-mediated H3K79 methylation but also other modifications catalyzed by LSD1, DNMTs and HDACs, and we found that simultaneous inhibition of these pathways not only dramatically enhances reprogramming competence of most OCT factors but in fact enables to dismantle species-dependent reprograming competence of OCT6, NR5A1, NR5A2, TET1 and GATA3. more...
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL18573
12 Samples
Download data: NARROWPEAK
Series
Accession:
GSE149017
ID:
200149017
14.

Single-cell transcriptomic profiling of patient-specific pluripotent stem cell-derived alveolar epithelial type 2 cells expressing the SFTPCI73T mutation and their gene-edited corrected counterparts

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL18573
7 Samples
Download data: H5
Series
Accession:
GSE160801
ID:
200160801
15.

Single cell transcriptomic profiling of day 114 patient-specific pluripotent stem cell-derived alveolar epithelial type 2 cells expressing the SFTPCI73T mutation and their gene-edited corrected counterparts [D114]

(Submitter supplied) We performed transcriptomic profiling of cells derived from human induced pluripotent stem cells (iPSCs) using our previously described distal lung directed differentiation protocol to generate alveolar epithelial type 2 cells (iAEC2s). We used the SPC2 human iPSC line and specifically the SPC2-ST-B2 (SFTPCtdT/WT) and SPC2-ST-C11 (SFTPCI73T/tdT) clones containing a SFTPCtdTomato knock-in reporter. SFTPCtdTomato+ cells were sorted on day 51 of differentiation and maintained without further sorting in self-renewing 3D alveolosphere cultures passaged approximately every 2 weeks through day 114. more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL18573
3 Samples
Download data: H5
Series
Accession:
GSE160800
ID:
200160800
16.

Single cell transcriptomic profiling of day 113 patient-specific pluripotent stem cell-derived alveolar epithelial type 2 cells expressing the SFTPCI73T mutation and their gene-edited corrected counterparts [D113]

(Submitter supplied) We performed transcriptomic profiling of cells derived from human induced pluripotent stem cells (iPSCs) using our previously described distal lung directed differentiation protocol to generate alveolar epithelial type 2 cells (iAEC2s). We used the SPC2 human iPSC line and specifically the SPC2-ST-B2 (SFTPCtdT/WT) and SPC2-ST-C11 (SFTPCI73T/tdT) clones containing a SFTPCtdTomato knock-in reporter. SFTPCtdTomato+ cells were sorted on day 41 and again on day 79 of differentiation. more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL18573
2 Samples
Download data: H5
Series
Accession:
GSE160799
ID:
200160799
17.

Single cell transcriptomic profiling of day 30 patient-specific pluripotent stem cell-derived alveolar epithelial type 2 cells expressing the SFTPCI73T mutation and their gene-edited corrected counterparts [D30]

(Submitter supplied) We performed transcriptomic profiling of cells derived from human induced pluripotent stem cells (iPSCs) using our previously described distal lung directed differentiation protocol to generate alveolar epithelial type 2 cells (iAEC2s). We used the SPC2 human iPSC line and specifically the SPC2-ST-B2 (SFTPCtdT/WT) and SPC2-ST-C11 (SFTPCI73T/tdT) clones containing a SFTPCtdTomato knock-in reporter. Live SFTPCtdTomato+ iAEC2s were sorted on day 30 and encapsulated for scRNA-seq using the 10X Chromium System. more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL18573
2 Samples
Download data: H5
Series
Accession:
GSE160798
ID:
200160798
18.

Context-dependent requirement of H3K9 dimethyltransferase activity during reprogramming to pluripotency

(Submitter supplied) The methylation of histone 3 at lysine 9 (H3K9) is widely regarded as a major roadblock for cellular reprogramming and interference with associated methyltransferases such as EHMT1 and EHMT2 (also known as GLP and G9A) facilitates the derivation of induced pluripotent stem cells (iPSCs). In addition, activation of demethylases by ascorbic acid (AA) has become a common approach to facilitate the extensive epigenetic remodeling required for iPSC formation. more...
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing; Genome binding/occupancy profiling by high throughput sequencing
Platforms:
GPL17021 GPL21103
28 Samples
Download data: BW, TXT
Series
Accession:
GSE130490
ID:
200130490
19.

Microarray data for rejuvenation experiments through reprogramming

(Submitter supplied) Proliferative and replicative senescent fibroblasts from aged human donors were reprogrammed towards pluripotency and re-differentiated in fibroblasts and then further analyzed for rejuvenation assessment.
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL570
11 Samples
Download data: CEL
Series
Accession:
GSE27924
ID:
200027924
20.

Chromatin and signaling pathways in reprogramming

(Submitter supplied) Reprogramming intermediates (pre-iPSCs) were subjected to control DMSO, ascorbic acid (AA), 2i ( MAP kinase inhibitor + GSKinhibitor) or AA+2i conditions to assess conversion to the iinduced pluripotent stem cell state (iPSC) after 10days.
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL13112
12 Samples
Download data: TXT
Series
Accession:
GSE58836
ID:
200058836
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