ArticleAging cell2019
Inhibition of nucleolar stress response by Sirt1: A potential mechanism of acetylation-independent regulation of p53 accumulation.
Article in Aging cell, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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.
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Who cites it
9 citing papers in PubMed, 22 citations in OpenAlex.
- Molecular mechanisms of SIRT1 in regulating ageing and related intervention strategies.Molecular biology reports · 2026Review
- Molecular basis of CX-5461-induced DNA damage response in primary vascular smooth muscle cells.Heliyon · 2024Article
- Oxidative stress impairs the Nur77-Sirt1 axis resulting in a decline in organism homeostasis during aging.Aging cell · 2023Article
- Ercc2/Xpd deficiency results in failure of digestive organ growth in zebrafish with elevated nucleolar stress.iScience · 2022Article
- Cellular senescence and abdominal aortic aneurysm: From pathogenesis to therapeutics.Frontiers in cardiovascular medicine · 2022Review
- SIRT7-dependent deacetylation of NPM promotes p53 stabilization following UV-induced genotoxic stress.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- Sirt-1 Regulates Physiological Process and Exerts Protective Effects against Oxidative Stress.BioMed research international · 2021Article
- Article
- Inhibition of nucleolar stress response by Sirt1: A potential mechanism of acetylation-independent regulation of p53 accumulation.Aging cell · 2019Article
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 2 countries.
Funding
Abstract
The mammalian Sirt1 deacetylase is generally thought to be a nuclear protein, but some pilot studies have suggested that Sirt1 may also be involved in orchestrating nucleolar functions. Here, we show that nucleolar stress response is a ubiquitous cellular reaction that can be induced by different types of stress conditions, and Sirt1 is an endogenous suppressor of nucleolar stress response. Using stable isotope labeling by amino acids in cell culture approach, we have identified a physical interaction of between Sirt1 and the nucleolar protein nucleophosmin, and this protein-protein interaction appears to be necessary for Sirt1 inhibition on nucleolar stress, whereas the deacetylase activity of Sirt1 is not strictly required. Based on the reported prerequisite role of nucleolar stress response in stress-induced p53 protein accumulation, we have also provided evidence suggesting that Sirt1-mediated inhibition on nucleolar stress response may represent a novel mechanism by which Sirt1 can modulate intracellular p53 accumulation independent of lysine deacetylation. This process may represent an alternative mechanism by which Sirt1 regulates functions of the p53 pathway.
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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.