ArticleNature cell biology2012
Senescence is an endogenous trigger for microRNA-directed transcriptional gene silencing in human cells.
Article in Nature cell biology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 147 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
147 citing papers in PubMed, 249 citations in OpenAlex.
- Cytokine-induced senescence in tumors is based on sustained activation of STAT1- and NFκB-dependent gene regulatory signatures.GeroScience · 2026Article
- Ago1 is required for the regulation of mitochondrial translation under heat stress in Schizosaccharomyces pombe.The Journal of biological chemistry · 2026Article
- The paradox of nuclear miRNAs: Mechanisms, therapeutic potential, and future directions.Non-coding RNA research · 2026Review
- A selective enrichment and specific probe terminal mediated strategy for highly sensitive detection of microRNAs.Nature communications · 2026Article
- MicroRNA chemical modifications in post-transcriptional gene silencing and human diseases.Molecular therapy. Nucleic acids · 2025Review
- Redefining the concept of erythrocyte senescence: is eryptosis fundamentally different from erythrocyte senescence.GeroScience · 2025Review
- Nuclear Argonaute:miRNA complexes recognize target sequences within chromatin-associated RNA and silence gene expression.Nucleic acids research · 2025Article
- The roles of subcellular Argonaute 2 in cardiovascular diseases.Journal of translational internal medicine · 2025Article
- The subcellular topology of the RNAi machinery is multifaceted and reveals adherens junctions as an epithelial hub.Scientific reports · 2025Article
- Non-coding RNAs in BRAF-mutant melanoma: targets, indicators, and therapeutic potential.Naunyn-Schmiedeberg's archives of pharmacology · 2025Review
- Identification of Oncogene-Induced Senescence-Associated MicroRNAs.Methods in molecular biology (Clifton, N.J.) · 2025Article
- miR-96-5p expression is sufficient to induce and maintain the senescent cell fate in the absence of stress.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Elucidation of how the Mir-23-27-24 cluster regulates development and aging.Experimental & molecular medicine · 2024Review
- Nuclear miRNAs: Gene Regulation Activities.International journal of molecular sciences · 2024Review
- RNA-RNA interactions between respiratory syncytial virus and miR-26 and miR-27 are associated with regulation of cell cycle and antiviral immunity.Nucleic acids research · 2024Article
- Nuclear AGO2 promotes myocardial remodeling by activating ANKRD1 transcription in failing hearts.Molecular therapy : the journal of the American Society of Gene Therapy · 2024Article
- Nuclear localization of Argonaute 2 is affected by cell density and may relieve repression by microRNAs.Nucleic acids research · 2024Article
- Noncanonical functions of microRNAs in the nucleus.Acta biochimica et biophysica Sinica · 2024Review
- Transcription factor network dynamics during the commitment to oncogene-induced senescence.Frontiers in epigenetics and epigenomics · 2024Article
- Coordinated Regulation of Myonuclear DNA Methylation, mRNA, and miRNA Levels Associates With the Metabolic Response to Rapid Synergist Ablation-Induced Skeletal Muscle Hypertrophy in Female Mice.Function (Oxford, England) · 2024Article
87 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 5 institutions in 2 countries.
Funding
Abstract
Cellular senescence is a tumour-suppressor mechanism that is triggered by cancer-initiating or promoting events in mammalian cells. The molecular underpinnings for this stable arrest involve transcriptional repression of proliferation-promoting genes regulated by the retinoblastoma (RB1)/E2F repressor complex. Here, we demonstrate that AGO2, RB1 and microRNAs (miRNAs), as exemplified here by let-7, physically and functionally interact to repress RB1/E2F-target genes in senescence, a process that we call senescence-associated transcriptional gene silencing (SA-TGS). Herein, AGO2 acts as the effector protein for let-7-directed implementation of silent-state chromatin modifications at target promoters, and inhibition of the let-7/AGO2 effector complex perturbs the timely execution of senescence. Thus, we identify cellular senescence as the an endogenous signal of miRNA/AGO2-mediated TGS in human cells. Our results suggest that miRNA/AGO2-mediated SA-TGS may contribute to tumour suppression by stably repressing proliferation-promoting genes in premalignant cancer cells.
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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.