ArticleCell cycle (Georgetown, Tex.)2013
mTORC1 and p53: clash of the gods?
Article in Cell cycle (Georgetown, Tex.), 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
57 citing papers in PubMed, 97 citations in OpenAlex.
- mTORC1 suppression by Trp53 mutation drives resistance to immune checkpoint blockade.Cell death & disease · 2026Article
- Endothelial F3-mediated autolysosome and lipid metabolism promote resistance to anti-VEGFA therapy in metastatic colorectal cancer.Autophagy · 2025Article
- Basal metabolic rate shapes the development and progression of hepatocellular carcinoma.BMC cancer · 2025Article
- Review
- The Role of p53 Mutations in Early and Late Response to Mitotic Aberrations.Biomolecules · 2025Review
- The multifaceted role of mitochondria in autism spectrum disorder.Molecular psychiatry · 2025Review
- R-loop formation contributes to mTORC1 activation-dependent DNA replication stress induced by p53 deficiency.Acta biochimica et biophysica Sinica · 2024Article
- Article
- Resistance to PRMT5-targeted therapy in mantle cell lymphoma.Blood advances · 2024Article
- Activation of mTOR signaling in adult lung microvascular progenitor cells accelerates lung aging.The Journal of clinical investigation · 2023Article
- TP53 somatic mutations in Asian breast cancer are associated with subtype-specific effects.Breast cancer research : BCR · 2023Article
- Claspin is Required for Growth Recovery from Serum Starvation through Regulating the PI3K-PDK1-mTOR Pathway in Mammalian Cells.Molecular and cellular biology · 2023Article
- Visual barcodes for clonal-multiplexing of live microscopy-based assays.Nature communications · 2022Article
- p53 at the crossroad of DNA replication and ribosome biogenesis stress pathways.Cell death and differentiation · 2022Review
- Pharmacological CDK4/6 inhibition reveals a p53-dependent senescent state with restricted toxicity.The EMBO journal · 2022Article
- Transcriptional changes in dendritic cells underlying allergen specific induced tolerance in a mouse model.Scientific reports · 2022Article
- The role of the mTOR pathway in diabetic retinopathy.Frontiers in medicine · 2022Review
- Bruton tyrosine kinase inhibitors as potential therapeutic agents for COVID-19: A review.Metabolism open · 2021Article
- Synthetic mRNAs; Their Analogue Caps and Contribution to Disease.Diseases (Basel, Switzerland) · 2021Review
- Protein mimetic amyloid inhibitor potently abrogates cancer-associated mutant p53 aggregation and restores tumor suppressor function.Nature communications · 2021Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
A balance must be struck between cell growth and stress responses to ensure that cells proliferate without accumulating damaged DNA. This balance means that optimal cell proliferation requires the integration of pro-growth and stress-response pathways. mTOR (mechanistic target of rapamycin) is a pleiotropic kinase found in complex 1 (mTORC1).The mTORC1 pathway governs a response to mitogenic signals with high energy levels to promote protein synthesis and cell growth. In contrast, the p53DNA damage response pathway is the arbiter of cell proliferation, restraining mTORC1 under conditions of genotoxic stress. Recent studies suggest a complicated integration of these pathways to ensure successful cell growth and proliferation without compromising genome maintenance. Deciphering this integration could be key to understanding the potential clinical usefulness of mTORC1 inhibitors like rapamycin. Here we discuss how these p53-mTORC1 interactions might play a role in the suppression of cancer and perhaps the development of cellular senescence and organismal aging.
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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.