ArticleGenes & development2008
CPEB regulation of human cellular senescence, energy metabolism, and p53 mRNA translation.
Article in Genes & development, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 90 papers, 2 of them syntheses 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.
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Who cites it
90 citing papers in PubMed, 2 syntheses or guidelines pooled it, 136 citations in OpenAlex.
- Genome-wide association studies and Mendelian randomization analyses provide insights into the causes of early-onset colorectal cancer.Annals of oncology : official journal of the European Society for Medical Oncology · 2024Pooled it
- Translational control of cell growth and malignancy by the CPEBs.Nature reviews. Cancer · 2013Pooled it
- Targeting RNA binding proteins with small-molecule inhibitors: Advances, challenges, and therapeutic opportunities.Acta pharmaceutica Sinica. B · 2026Review
- Oligonucleotides targeting the 3' splice site downstream of a microexon as an innovative therapy for autism.NAR molecular medicine · 2025Article
- Gene-Expression Programs in Salivary Gland Adenoid Cystic Carcinoma Analyzed Using Single-Cell and Spatial Transcriptomics.bioRxiv : the preprint server for biology · 2025Article
- Cytoplasmic regulation of the poly(A) tail length as a potential therapeutic target.RNA (New York, N.Y.) · 2025Review
- Metabolic regulation in adult and aging skeletal muscle stem cells.Genes & development · 2025Review
- Exploiting Translation Machinery for Cancer Therapy: Translation Factors as Promising Targets.International journal of molecular sciences · 2024Review
- Article
- Cytoplasmic Polyadenylation Element Binding Protein 1 and Atherosclerosis: Prospective Target and New Insights.Current vascular pharmacology · 2024Review
- Article
- Advanced age is associated with changes in alveolar macrophages and their responses to the stress of traumatic injury.Journal of leukocyte biology · 2022Article
- Pathogenic Roles of RNA-Binding Proteins in Sarcomas.Cancers · 2022Review
- Orb-dependent polyadenylation contributes to PLP expression and centrosome scaffold assembly.Development (Cambridge, England) · 2022Article
- Oppositional poly(A) tail length regulation by FMRP and CPEB1.RNA (New York, N.Y.) · 2022Article
- Protein synthesis control in cancer: selectivity and therapeutic targeting.The EMBO journal · 2022Review
- Enterobacteria impair host p53 tumor suppressor activity through mRNA destabilization.Oncogene · 2022Article
- CPEB1 directs muscle stem cell activation by reprogramming the translational landscape.Nature communications · 2022Article
- Reciprocal modulation of long noncoding RNA EMS and p53 regulates tumorigenesis.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- Protein of a thousand faces: The tumor-suppressive and oncogenic responses of p53.Frontiers in molecular biosciences · 2022Review
30 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
2 authors at 1 institution in 1 country.
Funding
Abstract
Cytoplasmic polyadenylation element-binding protein (CPEB) stimulates polyadenylation and translation in germ cells and neurons. Here, we show that CPEB-regulated translation is essential for the senescence of human diploid fibroblasts. Knockdown of CPEB causes skin and lung cells to bypass the M1 crisis stage of senescence; reintroduction of CPEB into the knockdown cells restores a senescence-like phenotype. Knockdown cells that have bypassed senescence undergo little telomere erosion. Surprisingly, knockdown of exogenous CPEB that induced a senescence-like phenotype results in the resumption of cell growth. CPEB knockdown cells have fewer mitochondria than wild-type cells and resemble transformed cells by having reduced respiration and reactive oxygen species (ROS), normal ATP levels, and enhanced rates of glycolysis. p53 mRNA contains cytoplasmic polyadenylation elements in its 3' untranslated region (UTR), which promote polyadenylation. In CPEB knockdown cells, p53 mRNA has an abnormally short poly(A) tail and a reduced translational efficiency, resulting in an approximately 50% decrease in p53 protein levels. An shRNA-directed reduction in p53 protein by about 50% also results in extended cellular life span, reduced respiration and ROS, and increased glycolysis. Together, these results suggest that CPEB controls senescence and bioenergetics in human cells at least in part by modulating p53 mRNA polyadenylation-induced translation.
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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.