ArticleAging2014
Methylated TRF2 associates with the nuclear matrix and serves as a potential biomarker for cellular senescence.
Article in Aging, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers, 1 of them a synthesis that pooled it.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
10 citing papers in PubMed, 1 synthesis or guideline pooled it, 13 citations in OpenAlex.
- The biomedical application of inorganic metal nanoparticles in aging and aging-associated diseases.Journal of advanced research · 2025Pooled it
- Telomeres expand sphere of influence: emerging molecular impact of telomeres in non-telomeric functions.Trends in genetics : TIG · 2023Review
- Cellular aging beyond cellular senescence: Markers of senescence prior to cell cycle arrest in vitro and in vivo.Aging cell · 2021Review
- The Long Linker Region of Telomere-Binding Protein TRF2 Is Responsible for Interactions with Lamins.International journal of molecular sciences · 2021Article
- Cockayne syndrome group B protein regulates DNA double-strand break repair and checkpoint activation.The EMBO journal · 2015Article
- Article
- Transcriptional outcome of telomere signalling.Nature reviews. Genetics · 2014Review
- Expression level of hTERT is regulated by somatic mutation and common single nucleotide polymorphism at promoter region in glioblastoma.Oncotarget · 2014Article
- BRG1, the ATPase subunit of SWI/SNF chromatin remodeling complex, interacts with HDAC2 to modulate telomerase expression in human cancer cells.Cell cycle (Georgetown, Tex.) · 2014Article
- The basic N-terminal domain of TRF2 limits recombination endonuclease action at human telomeres.Cell cycle (Georgetown, Tex.) · 2014Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Methylation of N-terminal arginines of the shelterin component TRF2 is important for cellular proliferation. While TRF2 is found at telomeres, where it plays an essential role in maintaining telomere integrity, little is known about the cellular localization of methylated TRF2. Here we report that the majority of methylated TRF2 is resistant to extraction by high salt buffer and DNase I treatment, indicating that methylated TRF2 is tightly associated with the nuclear matrix. We show that methylated TRF2 drastically alters its nuclear staining as normal human primary fibroblast cells approach and enter replicative senescence. This altered nuclear staining, which is found to be overwhelmingly associated with misshapen nuclei and abnormal nuclear matrix folds, can be suppressed by hTERT and it is barely detectable in transformed and cancer cell lines. We find that dysfunctional telomeres and DNA damage, both of which are potent inducers of cellular senescence, promote the altered nuclear staining of methylated TRF2, which is dependent upon the ATM-mediated DNA damage response. Collectively, these results suggest that the altered nuclear staining of methylated TRF2 may represent ATM-mediated nuclear structural alteration associated with cellular senescence. Our data further imply that methylated TRF2 can serve as a potential biomarker for cellular senescence.
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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.