ArticleThe EMBO journal2020
CLUH granules coordinate translation of mitochondrial proteins with mTORC1 signaling and mitophagy.
Article in The EMBO journal, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.
What it found
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Who cites it
37 citing papers in PubMed, 83 citations in OpenAlex.
- Brucea javanica Oil Emulsion Promotes Breast Cancer Cell Autophagy and Apoptosis by Regulating PAX6 mRNA Stability Through the hsa_circ_0001589/G3BP1 Axis.Clinical and experimental pharmacology & physiology · 2026Article
- Specific SLC25 carriers regulate mitochondrial protein synthesis.Science advances · 2026Article
- Review
- mTOR signaling networks: mechanistic insights and translational frontiers in disease therapeutics.Signal transduction and targeted therapy · 2025Review
- Clu1/Clu form mitochondria-associated granules upon metabolic transitions and regulate mitochondrial protein translation via ribosome interactions.PLoS genetics · 2025Article
- Drosophila Clu ribonucleoprotein particle dynamics rely on the availability of functional Clu and translating ribosomes.Journal of cell science · 2025Article
- Whole-Genome Sequencing Unveils the Uniqueness of Yushu Yaks (International journal of molecular sciences · 2025Article
- RNA-binding proteins as versatile metabolic regulators.npj metabolic health and disease · 2025Article
- Mitochondrial protein deacetylation by SIRT3 in osteoclasts promotes bone resorption with aging in female mice.Molecular metabolism · 2024Article
- Inhibition of K63 ubiquitination by G-Protein pathway suppressor 2 (GPS2) regulates mitochondria-associated translation.Pharmacological research · 2024Article
- CLUH maintains functional mitochondria and translation in motoneuronal axons and prevents peripheral neuropathy.Science advances · 2024Article
- Biologically informed NeuralODEs for genome-wide regulatory dynamics.Genome biology · 2024Article
- Nutrient-dependent regulation of a stable intron modulates germline mitochondrial quality control.Nature communications · 2024Article
- IPCellular & molecular biology letters · 2024Article
- HMGCS2 serves as a potential biomarker for inhibition of renal clear cell carcinoma growth.Scientific reports · 2023Article
- RNA binding protein: coordinated expression between the nuclear and mitochondrial genomes in tumors.Journal of translational medicine · 2023Review
- CLUH functions as a negative regulator of inflammation in human macrophages and determines ulcerative colitis pathogenesis.JCI insight · 2023Article
- Endogenous TOM20 Proximity Labeling: A Swiss-Knife for the Study of Mitochondrial Proteins in Human Cells.International journal of molecular sciences · 2023Article
- G3BP1 coordinates lysophagy activity to protect against compression-induced cell ferroptosis during intervertebral disc degeneration.Cell proliferation · 2023Article
- Multi-Omics Profiling of Hypertrophic Cardiomyopathy Reveals Altered Mechanisms in Mitochondrial Dynamics and Excitation-Contraction Coupling.International journal of molecular sciences · 2023Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
Abstract
Mitochondria house anabolic and catabolic processes that must be balanced and adjusted to meet cellular demands. The RNA-binding protein CLUH (clustered mitochondria homolog) binds mRNAs of nuclear-encoded mitochondrial proteins and is highly expressed in the liver, where it regulates metabolic plasticity. Here, we show that in primary hepatocytes, CLUH coalesces in specific ribonucleoprotein particles that define the translational fate of target mRNAs, such as Pcx, Hadha, and Hmgcs2, to match nutrient availability. Moreover, CLUH granules play signaling roles, by recruiting mTOR kinase and the RNA-binding proteins G3BP1 and G3BP2. Upon starvation, CLUH regulates translation of Hmgcs2, involved in ketogenesis, inhibits mTORC1 activation and mitochondrial anabolic pathways, and promotes mitochondrial turnover, thus allowing efficient reprograming of metabolic function. In the absence of CLUH, a mitophagy block causes mitochondrial clustering that is rescued by rapamycin treatment or depletion of G3BP1 and G3BP2. Our data demonstrate that metabolic adaptation of liver mitochondria to nutrient availability depends on a compartmentalized CLUH-dependent post-transcriptional mechanism that controls both mTORC1 and G3BP signaling and ensures survival.
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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.