ArticleOncotarget2015
p53 and rapamycin are additive.
Article in Oncotarget, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
31 citing papers in PubMed, 1 synthesis or guideline pooled it, 35 citations in OpenAlex.
- Rapamycin, Not Metformin, Mirrors Dietary Restriction-Driven Lifespan Extension in Vertebrates: A Meta-Analysis.Aging cell · 2025Pooled it
- Integrating evolutionary theory into a framework for the mechanistic evaluation of candidate anti-aging interventions.Frontiers in aging · 2026Article
- Extreme exercise in males is linked to mTOR signalling and onset of amyotrophic lateral sclerosis.Brain : a journal of neurology · 2025Article
- Review
- Cellular Senescence in Endometrium: A Pivotal Regulator in Physiological Remodeling and Pathological Disorders.International journal of biological sciences · 2025Review
- mTOR and SGLT-2 Inhibitors: Their Synergistic Effect on Age-Related Processes.International journal of molecular sciences · 2024Review
- Rapamycin, the only drug that has been consistently demonstrated to increase mammalian longevity. An update.Experimental gerontology · 2023Review
- Targeting the biology of aging with mTOR inhibitors.Nature aging · 2023Review
- Adult progenitor rejuvenation with embryonic factors.Cell proliferation · 2023Article
- Cell senescence, rapamycin and hyperfunction theory of aging.Cell cycle (Georgetown, Tex.) · 2022Review
- As expected, based on rapamycin-like p53-mediated gerosuppression, mTOR inhibition acts as a checkpoint in p53-mediated tumor suppression.Oncoscience · 2022Article
- Senolytics reduce coronavirus-related mortality in old mice.Science (New York, N.Y.) · 2021Article
- Effect of rapamycin on aging and age-related diseases-past and future.GeroScience · 2021Review
- Article
- Unlike dietary restriction, rapamycin fails to extend lifespan and reduce transcription stress in progeroid DNA repair-deficient mice.Aging cell · 2021Article
- Pulmonary Artery Smooth Muscle Cell Senescence Promotes the Proliferation of PASMCs by Paracrine IL-6 in Hypoxia-Induced Pulmonary Hypertension.Frontiers in physiology · 2021Article
- Senolytic drugs: from discovery to translation.Journal of internal medicine · 2020Review
- Correlative imaging of ionic transport and electronic structure in nano LiChemical communications (Cambridge, England) · 2020Article
- Is Rapamycin a Dietary Restriction Mimetic?The journals of gerontology. Series A, Biological sciences and medical sciences · 2020Review
- Mechanistic target of rapamycin signaling in mouse models of accelerated aging.The journals of gerontology. Series A, Biological sciences and medical sciences · 2020Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
14 authors at 3 institutions in 1 country.
Funding
Abstract
Mechanistic target of rapamycin (mTOR) is a kinase found in a complex (mTORC1) that enables macromolecular synthesis and cell growth and is implicated in cancer etiology. The rapamycin-FK506 binding protein 12 (FKBP12) complex allosterically inhibits mTORC1. In response to stress, p53 inhibits mTORC1 through a separate pathway involving cell signaling and amino acid sensing. Thus, these different mechanisms could be additive. Here we show that p53 improved the ability of rapamycin to: 1) extend mouse life span, 2) suppress ionizing radiation (IR)-induced senescence-associated secretory phenotype (SASP) and 3) increase the levels of amino acids and citric acid in mouse embryonic stem (ES) cells. This additive effect could have implications for cancer treatment since rapamycin and p53 are anti-oncogenic.
Indexed as
Identifiers
What OpenQuestion holds
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.