Unknown,Transcriptomics,Genomics,Proteomics

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Exon array analysis in primary human fibroblasts


ABSTRACT: 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). We analyzed primary fibroblasts from 5 healthy subjects at various passages and from 2 Hutchinson-Gilford Progeria Syndrome (HGPS) patients using the Affymetrix Human Exon 1.0 ST platform. Two or three technical replicates were performed.

ORGANISM(S): Homo sapiens

SUBMITTER: Kan Cao 

PROVIDER: E-GEOD-28863 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Publications

Progerin and telomere dysfunction collaborate to trigger cellular senescence in normal human fibroblasts.

Cao Kan K   Blair Cecilia D CD   Faddah Dina A DA   Kieckhaefer Julia E JE   Olive Michelle M   Erdos Michael R MR   Nabel Elizabeth G EG   Collins Francis S FS  

The Journal of clinical investigation 20110613 7


Hutchinson-Gilford progeria syndrome (HGPS), a devastating premature aging disease, is caused by a point mutation in the lamin A gene (LMNA). This mutation constitutively activates a cryptic splice donor site, resulting in a mutant lamin A protein known as progerin. Recent studies have demonstrated that progerin is also produced at low levels in normal human cells and tissues. However, the cause-and-effect relationship between normal aging and progerin production in normal individuals has not ye  ...[more]

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