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TranscriptomicsRecapitulation of human premature aging by using iPSCs from Hutchinson-Gilford progeria syndrome
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...
ORGANISM(S): Homo sapiens 
2011-03-14 | E-GEOD-24487 | biostudies-arrayexpress
TranscriptomicsA human iPSC model of Hutchinson Gilford Progeria Syndrome reveals a possible mesenchymal stem cell defect
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 ha...
ORGANISM(S): Homo sapiens 
2010-12-23 | E-GEOD-26093 | biostudies-arrayexpress
TranscriptomicsTranscription profiling of human Hutchinson-Gilord progeria syndrome fibroblast cell lines with dominant mutation in the LMNA gene and age-matched normal controls
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 en...
ORGANISM(S): Homo sapiens 
2007-12-12 | E-GEOD-3860 | biostudies-arrayexpress
TranscriptomicsTranscription profiling of primary fibroblasts from a family with autosomal recessive Hutchinson-Gilford Progeria Syndrome
Hutchinson-Gilford progeria syndrome (HGPS) is a genetic disorder displaying features reminiscent of premature senescence caused by germline mutations in the LMNA gene encoding lamin A and C, essential components of the nuclear lamina. By studying a family with homozygous LMNA mutation (K542N), we s...
ORGANISM(S): Homo sapiens 
2011-06-27 | E-MEXP-3097 | biostudies-arrayexpress
GenomicsCorrelated alterations in genome organization, histone methylation, and DNA-lamina interactions in Hutchinson-Gilford progeria syndrome (ChIP-seq)
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 ...
ORGANISM(S): Homo sapiens 
2012-10-30 | E-GEOD-41757 | biostudies-arrayexpress
GenomicsCorrelated alterations in genome organization, histone methylation, and DNA-lamina interactions in Hutchinson-Gilford progeria syndrome
This SuperSeries is composed of the following subset Series: GSE41751: Correlated alterations in genome organization, histone methylation, and DNA-lamina interactions in Hutchinson-Gilford progeria syndrome (expression) GSE41757: Correlated alterations in genome organization, histone methylation, an...
ORGANISM(S): Homo sapiens 
2012-10-30 | E-GEOD-41764 | biostudies-arrayexpress
TranscriptomicsEndothelial YAP/TAZ activation is a key mediator of atherosclerosis in Hutchinson-Gilford progeria syndrome
Hutchinson-Gilford progeria syndrome (HGPS) is an extremely rare disease caused by the expression of progerin, an aberrant protein produced by a de novo point mutation in the LMNA gene. HGPS patients show accelerated aging and die prematurely, mainly from atherosclerosis complications. Understanding...
ORGANISM(S): Mus musculus 
2024-10-17 | E-MTAB-13678 | biostudies-arrayexpress
UnknownOutcomes and costs of autologous stem cell mobilization with chemotherapy plus G-CSF vs G-CSF alone.
Not available
S-EPMC3797171 | biostudies-literature
UnknownEnvelope-Specific Adaptive Immunity following Transplantation of Hematopoietic Stem Cells Modified with VSV-G Lentivirus.
Not available
S-EPMC7683283 | biostudies-literature
UnknownBMI1 represses G-quadruplex DNA formation to maintain genomic stability during replication.
Not available
S-EPMC12919260 | biostudies-literature
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