ArticleNature cell biology2017
Circadian- and UPR-dependent control of CPEB4 mediates a translational response to counteract hepatic steatosis under ER stress.
Article in Nature cell biology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers.
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Who cites it
51 citing papers in PubMed, 79 citations in OpenAlex.
- mTOR signaling contributes to system-driven rhythmic gene expression in mouse liver.Science advances · 2026Article
- Posttranscriptional reprogramming controls MASLD progression through chronic ER stress adaptation.Science advances · 2026Article
- Stress-Induced Down-Regulation of CPEB4 Disrupts Sodium Channel Regulation and Myocardial Excitability.JACC. Basic to translational science · 2026Article
- Metabolic dysfunction‑associated steatotic liver disease: Pathogenesis, model and treatment (Review).International journal of molecular medicine · 2025Review
- Article
- Hepatocyte FAM210A deficiency disrupts mitochondrial function and triggers juvenile steatosis with compensatory repair in adulthood.bioRxiv : the preprint server for biology · 2025Article
- Circadian rhythms in metabolism and mental health: a reciprocal regulatory network with implications for metabolic and neuropsychiatric disorders.Current opinion in physiology · 2025Review
- Review of roles of RNA-binding proteins on NAFLD and the related pharmaceutical measures.Biomolecules & biomedicine · 2025Review
- Homeostasis control in health and disease by the unfolded protein response.Nature reviews. Molecular cell biology · 2025Review
- CPEB4 modulates liver cancer progression by translationally regulating hepcidin expression and sensitivity to ferroptosis.JHEP reports : innovation in hepatology · 2025Article
- Cytoplasmic regulation of the poly(A) tail length as a potential therapeutic target.RNA (New York, N.Y.) · 2025Review
- Spatial transcriptomics of healthy and fibrotic human liver at single-cell resolution.Nature communications · 2025Article
- Review
- Clock-dependent chromatin accessibility rhythms regulate circadian transcription.PLoS genetics · 2024Article
- Tissue-specific mechanisms of fat metabolism that focus on insulin actions.Journal of advanced research · 2023Review
- Identification of novel genes associated with exercise and calorie restriction effects in skeletal muscle.Aging · 2023Article
- Antitumor T-cell function requires CPEB4-mediated adaptation to chronic endoplasmic reticulum stress.The EMBO journal · 2023Article
- Control of immediate early gene expression by CPEB4-repressor complex-mediated mRNA degradation.Genome biology · 2022Article
- Comparative analyses of vertebrate CPEB proteins define two subfamilies with coordinated yet distinct functions in post-transcriptional gene regulation.Genome biology · 2022Article
- Macrophage inflammation resolution requires CPEB4-directed offsetting of mRNA degradation.eLife · 2022Article
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9 authors at 5 institutions in 1 country.
Funding
Abstract
The cytoplasmic polyadenylation element-binding (CPEB) proteins regulate pre-mRNA processing and translation of CPE-containing mRNAs in early embryonic development and synaptic activity. However, specific functions in adult organisms are poorly understood. Here we show that CPEB4 is required for adaptation to high-fat-diet- and ageing-induced endoplasmic reticulum (ER) stress, and subsequent hepatosteatosis. Stress-activated liver CPEB4 expression is dual-mode regulated. First, Cpeb4 mRNA transcription is controlled by the circadian clock, and then its translation is regulated by the unfolded protein response (UPR) through upstream open reading frames within the 5'UTR. Thus, the CPEB4 protein is synthesized only following ER stress but the induction amplitude is circadian. In turn, CPEB4 activates a second wave of UPR translation required to maintain ER and mitochondrial homeostasis. Our results suggest that combined transcriptional and translational Cpeb4 regulation generates a 'circadian mediator', which coordinates hepatic UPR activity with periods of high ER-protein-folding demand. Accordingly, CPEB4 deficiency results in non-alcoholic fatty liver disease.
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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.