ArticleAutophagy2012
Autophagy is induced through the ROS-TP53-DRAM1 pathway in response to mitochondrial protein synthesis inhibition.
Article in Autophagy, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.
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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
38 citing papers in PubMed, 63 citations in OpenAlex.
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- Ergothioneine Improves the Quality of Boar Sperm DuringAnimals : an open access journal from MDPI · 2025Article
- Decoding SFRP2 progenitors in sustaining tooth growth at single-cell resolution.Stem cell research & therapy · 2025Article
- A potential XGBoost Diagnostic Score forFrontiers in immunology · 2025Article
- Mitochonic acid 5 increases boar sperm quality by mitigating mitochondrial dysfunction.Frontiers in cell and developmental biology · 2025Article
- The p53 target DRAM1 modulates calcium homeostasis and ER stress by promoting contact between lysosomes and the ER through STIM1.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- AMPK/MTOR/TP53 Signaling Pathway Regulation by Calcitonin Gene-Related Peptide Reduces Oxygen-Induced Lung Damage in Neonatal Rats through Autophagy Promotion.Inflammation · 2024Article
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- Transcriptomic analysis of bovine endometrial epithelial cells in response to interferon tau and hormone stimulation.Frontiers in veterinary science · 2024Article
- Deciphering the molecular and cellular atlas of immune cells in septic patients with different bacterial infections.Journal of translational medicine · 2023Review
- Role of CELF2 in ferroptosis: Potential targets for cancer therapy (Review).International journal of molecular medicine · 2023Review
- GTPase Era at the heart of ribosome assembly.Frontiers in molecular biosciences · 2023Review
- Dynamical modeling of miR-34a, miR-449a, and miR-16 reveals numerous DDR signaling pathways regulating senescence, autophagy, and apoptosis in HeLa cells.Scientific reports · 2022Article
- The crosstalk between reactive oxygen species and noncoding RNAs: from cancer code to drug role.Molecular cancer · 2022Review
- Quantitative Proteomics Analysis of Berberine-Treated Colon Cancer Cells Reveals Potential Therapy Targets.Biology · 2021Article
- DRAM1 plays a tumor suppressor role in NSCLC cells by promoting lysosomal degradation of EGFR.Cell death & disease · 2020Article
- Autophagy suppresses resveratrol-induced apoptosis in renal cell carcinoma 786-O cells.Oncology letters · 2020Article
- Intra-articular Injection of Chloramphenicol Reduces Articular Cartilage Degeneration in a Rabbit Model of Osteoarthritis.Clinical orthopaedics and related research · 2019Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mitoribosome in mammalian cells is responsible for synthesis of 13 mtDNA-encoded proteins, which are integral parts of four mitochondrial respiratory chain complexes (I, III, IV and V). ERAL1 is a nuclear-encoded GTPase important for the formation of the 28S small mitoribosomal subunit. Here, we demonstrate that knockdown of ERAL1 by RNA interference inhibits mitochondrial protein synthesis and promotes reactive oxygen species (ROS) generation, leading to autophagic vacuolization in HeLa cells. Cells that lack ERAL1 expression showed a significant conversion of LC3-I to LC3-II and an enhanced accumulation of autophagic vacuoles carrying the LC3 marker, all of which were blocked by the autophagy inhibitor 3-MA as well as by the ROS scavenger NAC. Inhibition of mitochondrial protein synthesis either by ERAL1 siRNA or chloramphenicol (CAP), a specific inhibitor of mitoribosomes, induced autophagy in HTC-116 TP53 (+/+) cells, but not in HTC-116 TP53 (-/-) cells, indicating that tumor protein 53 (TP53) is essential for the autophagy induction. The ROS elevation resulting from mitochondrial protein synthesis inhibition induced TP53 expression at transcriptional levels by enhancing TP53 promoter activity, and increased TP53 protein stability by suppressing TP53 ubiquitination through MAPK14/p38 MAPK-mediated TP53 phosphorylation. Upregulation of TP53 and its downstream target gene DRAM1, but not CDKN1A/p21, was required for the autophagy induction in ERAL1 siRNA or CAP-treated cells. Altogether, these data indicate that autophagy is induced through the ROS-TP53-DRAM1 pathway in response to mitochondrial protein synthesis inhibition.
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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.