ArticleiScience2025
A bacterial genotoxin reveals a p53-proteasome-LC3 regulatory axis that drives the suppression of autophagy in cells experiencing sublethal DNA damage.
Article in iScience, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 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
2 citing papers in PubMed.
- Proton Radiation-Induced Cognitive Impairment via Disruption of Hippocampal Neuronal Mitophagic Homeostasis.Biomolecules · 2026Article
- The Gut-Prostate Axis: Decoding the Interplay of Environmental Factors, Microbial Metabolites, and Hormonal Regulation in Prostate Cancer Pathogenesis.Technology in cancer research & treatmentReview
Corrections and comments
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Authors and funding
15 authors.
Funding
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Abstract
Macroautophagy is thought to have a critical role in shaping and refining cellular proteostasis in eukaryotic cells recovering from DNA damage. Autophagy activation has been previously reported in DNA-damaged cells, often in association with increased cellular cytotoxicity. However, we now report a mechanism by which autophagy is suppressed in the absence of cytotoxicity within cells exposed to bacterial toxin-, chemical-, or radiation-mediated sources of genotoxicity. Specifically, our studies demonstrate the DNA damage response-dependent stabilization of the tumor suppressor p53, which is both required and sufficient for regulating the ubiquitination and proteasome-dependent reduction in cellular pools of microtubule-associated protein 1 light chain 3 (LC3A/B), a key precursor of autophagosome biogenesis and maturation, in both epithelial cells and an
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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 Socratic graph.