ArticleNucleic acids research2018
Deacetylation of NAT10 by Sirt1 promotes the transition from rRNA biogenesis to autophagy upon energy stress.
Article in Nucleic acids research, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 76 papers.
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Who cites it
76 citing papers in PubMed, 111 citations in OpenAlex.
- RNA N4-acetylcytidine modification in health and cancer: molecular mechanisms, cellular plasticity, and therapeutic opportunities.Biomarker research · 2026Review
- DUSP12 Regulates NAT10-Mediated RNA Acetylation to Modulate DNA Repair and Therapeutic Response in Hepatocellular Carcinoma.MedComm · 2026Article
- NAT10 aggravates psoriasis by promoting keratinocytes fatty acid synthesis via stable FASN transcription.Journal of pharmaceutical analysis · 2026Article
- The functions, mechanisms and clinical relevance of RNA and protein acetyltransferase NAT10: a comprehensive review.Cell biology and toxicology · 2026Review
- RNA acetylation modification ac4C: An emerging regulatory hub of RNA metabolism disruption in Alzheimer's disease.Molecular biology reports · 2026Review
- Article
- mTOR-NAA10-C7orf50 axis senses nutritional status to coordinate ribosome biogenesis and autophagy.Science advances · 2026Article
- NAT10 drives ovarian cancer progression via NLRP3 mRNA ac4C modification.Discover oncology · 2026Article
- RNA N4-acetylcytidine modification in human cancers: from molecular function to oncogenic mechanisms.iScience · 2026Review
- The NAT10/acCell communication and signaling : CCS · 2026Review
- NAT10 regulates heart development and function by maintaining the expression of genes related to fatty acid β-oxidation and heart contraction.Cell death and differentiation · 2026Article
- Targeting the SIRT1-NAT10-GABABR1 Axis: A Novel Epitranscriptomic Approach to Mitigate Sevoflurane-Induced Cognitive Impairment in Aging.CNS neuroscience & therapeutics · 2026Article
- NAT10-Mediated ac4C-Modification Exacerbates Ferroptosis by Stabilizing HMOX1 in Deep Vein Thrombosis.Arteriosclerosis, thrombosis, and vascular biology · 2026Article
- Epitranscriptomic control of epithelial-mesenchymal transition in cancer: mechanisms, plasticity, and therapeutic opportunities.Frontiers in cell and developmental biology · 2026Review
- Long non-coding RNA LINC01532 sustains redox homeostasis and accelerates lenvatinib resistance in hepatocellular carcinoma.Journal of advanced research · 2025Article
- Pre-rRNAs control mitosis by maintaining chromosomal segregation through protecting SMC2 from AURKA-mediated phosphorylation.Cell death & disease · 2025Article
- NAT10-mediated ac4C modification of Lipin1 mRNA contributes to the pathogenesis of PWMI.JCI insight · 2025Article
- Nicotinamide boosts oocyte quantity and quality by promoting N4-acetylation modification in lupus mice.Science advances · 2025Article
- Emerging role of N-acetyltransferase 10 in diseases: RNA ac4C modification and beyond.Molecular biomedicine · 2025Review
- Hederagenin promotes SIRT6 to attenuate epidural scar formation by aggravating PRMT1 deacetylation.Bone & joint research · 2025Article
16 more citing papers are in PubMed but not listed here.
Corrections and comments
- Erratum issued
Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Anabolism and catabolism are tightly regulated according to the cellular energy supply. Upon energy stress, ribosomal RNA (rRNA) biogenesis is inhibited, and autophagy is induced. However, the mechanism linking rRNA biogenesis and autophagy is unclear. Here, we demonstrate that the nucleolar protein NAT10 plays a role in the transition between rRNA biogenesis and autophagy. Under normal conditions, NAT10 is acetylated to activate rRNA biogenesis and inhibit autophagy induction. Mechanistic studies demonstrate that NAT10 binds to and acetylates the autophagy regulator Che-1 at K228 to suppress the Che-1-mediated transcriptional activation of downstream genes Redd1 and Deptor under adequate energy supply conditions. Upon energy stress, NAT10 is deacetylated by Sirt1, leading to suppression of NAT10-activated rRNA biogenesis. In addition, deacetylation of NAT10 abolishes the NAT10-mediated transcriptional repression of Che-1, leading to the release of autophagy inhibition. Collectively, we demonstrate that the acetylation status of NAT10 is important for the anabolism-catabolism transition in response to energy stress, providing a novel mechanism by which nucleolar proteins control rRNA synthesis and autophagy in response to the cellular energy supply.
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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.