ArticleFASEB journal : official publication of the Federation of American Societies for Experimental Biology2017
Liver p53 is stabilized upon starvation and required for amino acid catabolism and gluconeogenesis.
Article in FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT04259879 (Evaluation of p21 Induction and Molecular Pathways Related to Short-term Fasting Response), which is not on this map. Cited by 48 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.
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.
Evaluation of p21 Induction and Molecular Pathways Related to Short-term Fasting Response
Who cites it
48 citing papers in PubMed, 67 citations in OpenAlex.
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- Harnessing p53 for targeted cancer therapy: new advances and future directions.Transcription · 2025Review
- Systemic and transcriptional response to intermittent fasting and fasting-mimicking diet in mice.BMC biology · 2024Article
- Skeletal muscle p53-depletion uncovers a mechanism of fuel usage suppression that enables efficient energy conservation.Journal of cachexia, sarcopenia and muscle · 2024Article
- Adipocyte p53 coordinates the response to intermittent fasting by regulating adipose tissue immune cell landscape.Nature communications · 2024Article
- Doxorubicin Attenuates Free Fatty Acid-Induced Lipid Accumulation via Stimulation of p53 in HepG2 Cells.Biomolecules & therapeutics · 2024Article
- Low glucose metabolite 3-phosphoglycerate switches PHGDH from serine synthesis to p53 activation to control cell fate.Cell research · 2023Article
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- Protective Effects ofInternational journal of molecular sciences · 2023Article
- Liver regeneration after partial hepatectomy is improved in the absence of aryl hydrocarbon receptor.Scientific reports · 2022Article
- Fasting induces a highly resilient deep quiescent state in muscle stem cells via ketone body signaling.Cell metabolism · 2022Article
- Complementary omics strategies to dissect p53 signaling networks under nutrient stress.Cellular and molecular life sciences : CMLS · 2022Article
- Fasting improves therapeutic response in hepatocellular carcinoma through p53-dependent metabolic synergism.Science advances · 2022Article
- p53 Regulates a miRNA-Fructose Transporter Axis in Brown Adipose Tissue Under Fasting.Frontiers in genetics · 2022Article
- Tumor Suppressor Par-4 Regulates Complement Factor C3 and Obesity.Frontiers in oncology · 2022Article
- Sestrins' Expression in the Liver Is Not Altered by Short-Term Calorie Restriction in Young and Old Rats.Gerontology · 2022Article
- O-GlcNAcylated p53 in the liver modulates hepatic glucose production.Nature communications · 2021Article
- Hepatic transcriptional responses to fasting and feeding.Genes & development · 2021Review
Corrections and comments
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Authors and funding
15 authors at 5 institutions in 3 countries.
Funding
Abstract
The ability to adapt cellular metabolism to nutrient availability is critical for survival. The liver plays a central role in the adaptation to starvation by switching from glucose-consuming processes and lipid synthesis to providing energy substrates like glucose to the organism. Here we report a previously unrecognized role of the tumor suppressor p53 in the physiologic adaptation to food withdrawal. We found that starvation robustly increases p53 protein in mouse liver. This induction was posttranscriptional and mediated by a hepatocyte-autonomous and AMP-activated protein kinase-dependent mechanism. p53 stabilization was required for the adaptive expression of genes involved in amino acid catabolism. Indeed, acute deletion of p53 in livers of adult mice impaired hepatic glycogen storage and induced steatosis. Upon food withdrawal, p53-deleted mice became hypoglycemic and showed defects in the starvation-associated utilization of hepatic amino acids. In summary, we provide novel evidence for a p53-dependent integration of acute changes of cellular energy status and the metabolic adaptation to starvation. Because of its tumor suppressor function, p53 stabilization by starvation could have implications for both metabolic and oncological diseases of the liver.-Prokesch, A., Graef, F. A., Madl, T., Kahlhofer, J., Heidenreich, S., Schumann, A., Moyschewitz, E., Pristoynik, P., Blaschitz, A., Knauer, M., Muenzner, M., Bogner-Strauss, J. G., Dohr, G., Schulz, T. J., Schupp, M. Liver p53 is stabilized upon starvation and required for amino acid catabolism and gluconeogenesis.
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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.