Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:2.7.7.48 (transcriptase)
 9,479 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Hutchinson Gilford syndrome (progeria [PG]) is a human disease associated with accelerated aging. To elucidate the acceleration mechanism, we first tried to transform a PG-derived cell line by infection of a recombinant adenovirus expressing HPV (human papilloma virus)-E6 and HPV-E7 genes. The transfected PG cells had a greater number of population doublings (PD) (>80), faster doubling time, and less staining of senescence-associated ss-galactosidase than the nontransfected PG cells. The transfected cells also showed markedly more detectable telomerase activity than the nontransformed cells. The expression levels of the genes in the E6-transduced and E7-transduced cell line were then compared with those of the nontransfected cell line using an mRNA differential display method, following reverse-transcriptase polymerase chain reaction analysis. Expression of huntingtin interacting protein-1 (HIP-1) gene was found to be increased not only in PG cells but also in fibroblast cells from aged healthy donors. Thus, HIP-1 might be a molecular assistant in the pathogenesis of the cellular senescent process in the human cells tested.
 ...
PMID:Increased expression of the Huntingtin interacting protein-1 gene in cells from Hutchinson Gilford Syndrome (Progeria) patients and aged donors. 1457 Aug 52

Hutchinson-Gilford progeria syndrome (HGPS; MIM 176670) is a rare disease characterized by accelerated aging. In this study, light and immunofluorescence microscopy were used to assess morphological changes, measures of cell growth kinetics and gene expression profiles in HGPS cells and normal fibroblasts in culture. A filtering strategy was developed based on differentially expressed transcripts seen consistently across three culture stages based on cell passage number. This filtering strategy produced a list of 66 unique differentially expressed genes, of which approximately 40% were upregulated in HGPS cells compared to normal fibroblasts. The increased mRNA expression in HGPS cells that was seen for one gene defined using this strategy--namely ANK3--was validated using quantitative reverse-transcriptase amplification, Western analysis and immunofluorescence microscopy, all of which showed significantly increased ankyrin G expression. These findings demonstrate differences in morphology, growth kinetics and mRNA expression profiles in HGPS cells compared to normal fibroblasts in culture, including increased expression of ANK3/ankyrin G. Furthermore, other genes that co-clustered with ANK3 might provide mechanistic clues regarding senescence in cultured HGPS cells.
 ...
PMID:Ankyrin G overexpression in Hutchinson-Gilford progeria syndrome fibroblasts identified through biological filtering of expression profiles. 1703 32