ArticleAging2011
p53 governs telomere regulation feedback too, via TRF2.
Article in Aging, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
23 citing papers in PubMed, 39 citations in OpenAlex.
- ARMH4 accelerates aging by maintaining a positive-feedback growth signaling circuit.Nature communications · 2025Article
- Cellular Aging and Senescence in Cancer: A Holistic Review of Cellular Fate Determinants.Aging and disease · 2024Review
- Abnormal function of telomere protein TRF2 induces cell mutation and the effects of environmental tumor‑promoting factors (Review).Oncology reports · 2021Review
- Review
- Improving Age-Related Cognitive Decline through Dietary Interventions Targeting Mitochondrial Dysfunction.International journal of molecular sciences · 2021Review
- Estrogen Replacement Therapy Induces Antioxidant and Longevity-Related Genes in Women after Medically Induced Menopause.Oxidative medicine and cellular longevity · 2021Article
- Retrotransposon-derived p53 binding sites enhance telomere maintenance and genome protection.BioEssays : news and reviews in molecular, cellular and developmental biology · 2016Review
- Gastrokine 1 induces senescence and apoptosis through regulating telomere length in gastric cancer.Oncotarget · 2014Article
- The basic N-terminal domain of TRF2 limits recombination endonuclease action at human telomeres.Cell cycle (Georgetown, Tex.) · 2014Article
- Dysregulation of the mTOR pathway in p53-deficient mice.Cancer biology & therapy · 2013Article
- Nature vs nurture: interplay between the genetic control of telomere length and environmental factors.Cell cycle (Georgetown, Tex.) · 2013Article
- QTL mapping of leukocyte telomere length in American Indians: the Strong Heart Family Study.Aging · 2013Article
- Telomerase downregulation induces proapoptotic genes expression and initializes breast cancer cells apoptosis followed by DNA fragmentation in a cell type dependent manner.Molecular biology reports · 2013Article
- Oxidative stress, DNA damage, and the telomeric complex as therapeutic targets in acute neurodegeneration.Neurochemistry international · 2013Review
- p53 expression controls prostate cancer sensitivity to chemotherapy and the MDM2 inhibitor Nutlin-3.Cell cycle (Georgetown, Tex.) · 2012Article
- p63 the guardian of human reproduction.Cell cycle (Georgetown, Tex.) · 2012Review
- Review
- Tissue-specific expression of p73 C-terminal isoforms in mice.Cell cycle (Georgetown, Tex.) · 2012Article
- Potential anti-aging agents suppress the level of constitutive mTOR- and DNA damage- signaling.Aging · 2012Article
- Controversial aspects of oncogene-induced senescence.Cell cycle (Georgetown, Tex.) · 2012Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
p53 takes critical part in a number of positive and negative feedback loops to regulate carcinogenesis, aging and other biological processes. Uncapped or dysfunctional telomeres are an endogenous DNA damage that activates ATM kinase (ataxia telangiectasia mutated) and then p53 to induce cellular senescence or apoptosis. Our recent study shows that p53, a downstream effector of the telomere damage signaling, also functions upstream of the telomere‐capping protein complex by inhibiting one of its components, TRF2 (telomeric repeat binding factor 2). Since TRF2 inhibition leads to ATM activation, a novel positive feedback loop exists to amplify uncapped telomere‐induced, p53‐mediated cellular responses. Siah1 (seven in absentia homolog 1), a p53‐inducible E3 ubiquitin ligase, plays a key role in this feedback regulation by targeting TRF2 for ubiquitination and proteasomal degradation. Biological significance and therapeutic implications of this study are discussed.
Indexed as
Identifiers
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.