ArticleCellular and molecular gastroenterology and hepatology2025
Inhibition of Ribosome Biogenesis In Vivo Causes p53-Dependent Death and p53-Independent Dysfunction.
Article in Cellular and molecular gastroenterology and hepatology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- NAT10 governs development through the Xrp1-mediated stress response rather than its RNA acetylation activity.Science advances · 2026Article
- Stress-Responsive Protein IFRD1 Protects Assembled Ribosomes via a Ribosome-Salvaging Mechanism.bioRxiv : the preprint server for biology · 2026Article
- Wdr4 regulates ribosome biogenesis and intestinal homeostasis via let-7.EMBO reports · 2026Article
- Decoding Ribosome Stress: How NAT10 Influences Pancreatic Acinar Cell Survival and Cancer Development.Cellular and molecular gastroenterology and hepatology · 2025Article
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9 authors.
Funding
Abstract
BACKGROUND &
aimsAlthough it is well-known that ribosomes are critical for cell function, and their synthesis (known as ribosome biogenesis [RiBi]) is energy-intensive, surprisingly little is known about RiBi in vivo in adult tissue.
methodsUsing a mouse model with conditional deletion of Nat10, an essential gene for RiBi and subsequent translation of mRNA, we investigated the effects of RiBi blockade in vivo, with a focus on pancreatic acinar cells during homeostasis and tumorigenesis.
resultsWe observed an unexpected latency of several weeks between Nat10 deletion and onset of structural and functional abnormalities and p53-dependent acinar cell death. Although deletion of Trp53 rescued acinar cells from apoptotic cell death, Nat10
conclusionsTogether, our results provide initial insights into how differentiated cells respond to defects in RiBi and translation in vivo in various physiological contexts.
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