ArticleeLife2014
Coordinated control of senescence by lncRNA and a novel T-box3 co-repressor complex.
Article in eLife, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 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
58 citing papers in PubMed, 87 citations in OpenAlex.
- Genetic loci responsible for atrioventricular block in children.Frontiers in cell and developmental biology · 2026Review
- The T-Box Transcription Factors TBX2 and TBX3 Are Molecular Targets of Piroctone Olamine in the Treatment of Pancreatic Cancer.Journal of cellular and molecular medicine · 2025Article
- ALKBH5 Stabilized NCells · 2023Article
- Article
- Iron overload induces cerebral endothelial senescence in aged mice and in primary culture in a sex-dependent manner.Aging cell · 2023Article
- Integrative GWAS and co-localisation analysis suggests novel genes associated with age-related multimorbidity.Scientific data · 2023Article
- Knockdown of long noncoding RNA SAN rejuvenates aged adipose-derived stem cells via miR-143-3p/ADD3 axis.Stem cell research & therapy · 2023Article
- Biomarkers of aging.Science China. Life sciences · 2023Review
- Dynamic chromatin accessibility tuning by the long noncoding RNA ELDR accelerates chondrocyte senescence and osteoarthritis.American journal of human genetics · 2023Article
- Noncoding RNAs: Novel Targets for Opioid Tolerance.Current neuropharmacology · 2023Review
- Indisulam exerts anticancer effects via modulation of transcription, translation and alternative splicing on human cervical cancer cells.American journal of cancer research · 2023Article
- The mechanisms and diagnostic potential of lncRNAs, miRNAs, and their related signaling pathways in cervical cancer.Frontiers in cell and developmental biology · 2023Review
- Review
- Tumor-Promoting Actions of HNRNP A1 in HCC Are Associated with Cell Cycle, Mitochondrial Dynamics, and Necroptosis.International journal of molecular sciences · 2022Article
- MicroRNAs, Long Non-Coding RNAs, and Circular RNAs in the Redox Control of Cell Senescence.Antioxidants (Basel, Switzerland) · 2022Review
- nc886, a Non-Coding RNA, Is a New Biomarker and Epigenetic Mediator of Cellular Senescence in Fibroblasts.International journal of molecular sciences · 2021Article
- The Role of Long Non-Coding RNAs in Endometriosis.International journal of molecular sciences · 2021Review
- RNA-binding protein 39: a promising therapeutic target for cancer.Cell death discovery · 2021Review
- Regulatory role of long non-coding RNA UCA1 in signaling pathways and its clinical applications.Oncology letters · 2021Review
- HES5 Activates Long Noncoding RNA UCA1 to Induce Colorectal Cancer Progression by Modulating miR-185/NOTCH3 Signaling.Gastroenterology research and practice · 2021Article
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 2 institutions in 1 country.
Funding
Abstract
Cellular senescence is a crucial tumor suppressor mechanism. We discovered a CAPERα/TBX3 repressor complex required to prevent senescence in primary cells and mouse embryos. Critical, previously unknown roles for CAPERα in controlling cell proliferation are manifest in an obligatory interaction with TBX3 to regulate chromatin structure and repress transcription of CDKN2A-p16INK and the RB pathway. The IncRNA UCA1 is a direct target of CAPERα/TBX3 repression whose overexpression is sufficient to induce senescence. In proliferating cells, we found that hnRNPA1 binds and destabilizes CDKN2A-p16INK mRNA whereas during senescence, UCA1 sequesters hnRNPA1 and thus stabilizes CDKN2A-p16INK. Thus CAPERα/TBX3 and UCA1 constitute a coordinated, reinforcing mechanism to regulate both CDKN2A-p16INK transcription and mRNA stability. Dissociation of the CAPERα/TBX3 co-repressor during oncogenic stress activates UCA1, revealing a novel mechanism for oncogene-induced senescence. Our elucidation of CAPERα and UCA1 functions in vivo provides new insights into senescence induction, and the oncogenic and developmental properties of TBX3.
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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.