ArticlePloS one2014
Expression of the genetic suppressor element 24.2 (GSE24.2) decreases DNA damage and oxidative stress in X-linked dyskeratosis congenita cells.
Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 32 citations in OpenAlex.
- Structural switches: intracellular G-quadruplexes modulate DNA repair and genome maintenance inmBio · 2025Article
- A Review of Telomere Attrition in Cancer and Aging: Current Molecular Insights and Future Therapeutic Approaches.Cancers · 2025Review
- Clinical mutations in the TERT and TERC genes coding for telomerase components induced oxidative stress, DNA damage at telomeres and cell apoptosis besides decreased telomerase activity.Human molecular genetics · 2024Article
- Exploring the Causal Relationship Between Telomere Biology and Alzheimer's Disease.Molecular neurobiology · 2023Review
- Multisystemic Manifestations in Rare Diseases: The Experience of Dyskeratosis Congenita.Genes · 2022Review
- GSE4-loaded nanoparticles a potential therapy for lung fibrosis that enhances pneumocyte growth, reduces apoptosis and DNA damage.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2021Article
- Generation of dyskeratosis congenita-like hematopoietic stem cells through the stable inhibition of DKC1.Stem cell research & therapy · 2021Article
- Article
- GSE4 peptide suppresses oxidative and telomere deficiencies in ataxia telangiectasia patient cells.Cell death and differentiation · 2019Article
- Idiopathic Pulmonary Fibrosis (IPF): An Overview.Journal of clinical medicine · 2018Review
- Acute telomerase components depletion triggers oxidative stress as an early event previous to telomeric shortening.Redox biology · 2018Article
- Robust DNA Damage Response and Elevated Reactive Oxygen Species in TINF2-Mutated Dyskeratosis Congenita Cells.PloS one · 2016Article
- Article
Corrections and comments
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Authors and funding
11 authors at 6 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The predominant X-linked form of Dyskeratosis congenita results from mutations in DKC1, which encodes dyskerin, a protein required for ribosomal RNA modification that is also a component of the telomerase complex. We have previously found that expression of an internal fragment of dyskerin (GSE24.2) rescues telomerase activity in X-linked dyskeratosis congenita (X-DC) patient cells. Here we have found that an increased basal and induced DNA damage response occurred in X-DC cells in comparison with normal cells. DNA damage that is also localized in telomeres results in increased heterochromatin formation and senescence. Expression of a cDNA coding for GSE24.2 rescues both global and telomeric DNA damage. Furthermore, transfection of bacterial purified or a chemically synthesized GSE24.2 peptide is able to rescue basal DNA damage in X-DC cells. We have also observed an increase in oxidative stress in X-DC cells and expression of GSE24.2 was able to diminish it. Altogether our data indicated that supplying GSE24.2, either from a cDNA vector or as a peptide reduces the pathogenic effects of Dkc1 mutations and suggests a novel therapeutic approach.
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