ArticleAging cell2007
Telomere restoration and extension of proliferative lifespan in dyskeratosis congenita fibroblasts.
Article in Aging cell, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
40 citing papers in PubMed, 69 citations in OpenAlex.
- Multiple cell types support productive infection and dynamic translocation of infectious Ebola virus to the surface of human skin.Science advances · 2025Article
- Fibroblast-Adipocyte Lineage Cell Interactions Result in Differential Production of Extracellular Matrix Proteins.Cellular and molecular bioengineering · 2024Article
- Thioredoxin (Trx): A redox target and modulator of cellular senescence and aging-related diseases.Redox biology · 2024Review
- CRISPR screen identifies CEBPB as contributor to dyskeratosis congenita fibroblast senescence via augmented inflammatory gene response.G3 (Bethesda, Md.) · 2023Article
- Effect of gait training using rhythmic auditory stimulation on gait speed in older adults admitted to convalescent rehabilitation wards: A study protocol for a pilot randomized controlled clinical trial.Contemporary clinical trials communications · 2023Article
- Tieing together loose ends: telomere instability in cancer and aging.Molecular oncology · 2022Review
- Nuclear export restricts Gdown1 to a mitotic function.Nucleic acids research · 2022Article
- Telomerase RNA processing: Implications for human health and disease.Stem cells (Dayton, Ohio) · 2020Review
- Human Adipocyte Conditioned Medium Promotes In Vitro Fibroblast Conversion to Myofibroblasts.Scientific reports · 2020Article
- Small-Molecule PAPD5 Inhibitors Restore Telomerase Activity in Patient Stem Cells.Cell stem cell · 2020Article
- Pathogenic TERT promoter variants in telomere diseases.Genetics in medicine : official journal of the American College of Medical Genetics · 2019Article
- Loss of MCU prevents mitochondrial fusion in GScience signaling · 2019Article
- AGO2 promotes telomerase activity and interaction between the telomerase components TERT and TERC.EMBO reports · 2019Article
- Evaluation and Management of Hematopoietic Failure in Dyskeratosis Congenita.Hematology/oncology clinics of North America · 2018Review
- The potential of non-myeloablative heterochronous autologous hematopoietic stem cell transplantation for extending a healthy life span.GeroScience · 2018Review
- A novel TERC CR4/CR5 domain mutation causes telomere disease via decreased TERT binding.Blood · 2016Article
- Posttranscriptional manipulation of TERC reverses molecular hallmarks of telomere disease.The Journal of clinical investigation · 2016Article
- New prospects for targeting telomerase beyond the telomere.Nature reviews. Cancer · 2016Review
- Robust DNA Damage Response and Elevated Reactive Oxygen Species in TINF2-Mutated Dyskeratosis Congenita Cells.PloS one · 2016Article
- Poly(A)-specific ribonuclease (PARN) mediates 3'-end maturation of the telomerase RNA component.Nature genetics · 2015Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 3 institutions in 3 countries.
Funding
Abstract
Dyskeratosis congenita (DC), an inherited bone marrow failure syndrome, is caused by defects in telomerase. Somatic cells from DC patients have shortened telomeres and clinical symptoms are most pronounced in organs with a high cell turnover, including those involved in hematopoiesis and skin function. We previously identified an autosomal dominant (AD) form of DC that is caused by mutations in the telomerase RNA component (TER). In this study, we evaluated whether retroviral expression of TER and/or telomerase reverse transcriptase (TERT), the catalytic component of telomerase, could extend telomere length and rescue AD DC cells from a phenotype characteristic of early senescence. Exogenous TER expression, without TERT, could not activate telomerase in AD DC skin fibroblasts. Transduction of TERT alone, however, provided AD DC cells with sufficient telomerase activity to extend average telomere length and proliferative capacity. Interestingly, we found that expression of TER and TERT together resulted in extension of lifespan and higher levels of telomerase and longer telomeres than expression of TERT alone in both AD DC and normal cells. Our results provide evidence that AD DC cells can be rescued from defects in telomere maintenance and proliferation, and that coexpression of TERT and TER together provides a more efficient means to elongate telomeres than expression of TERT alone. Similar strategies may be useful for ameliorating the detrimental effects of telomere shortening in AD DC and other diseases associated with telomerase or telomere defects.
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What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.