ArticleNature communications2021
O-GlcNAcylated p53 in the liver modulates hepatic glucose production.
Article in Nature communications, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.
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Who cites it
36 citing papers in PubMed, 72 citations in OpenAlex.
- OGT regulates histone demethylation and alleviates osteoarthritis progression by O-GlcNAcylation of KDM6B.Journal of advanced research · 2026Article
- The Dynamic Alliance of p53 and Metabolism in the Tumor Microenvironment Shapes Tumor Evolution.BioEssays : news and reviews in molecular, cellular and developmental biology · 2026Review
- Hepatic HuR modulates glucose metabolism through the C/EBPβ/PCK1 pathway.Molecular metabolism · 2026Article
- Sepsis induced coagulopathy (SIC): is it monolithic?Thrombosis journal · 2026Article
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- Inducible skeletal muscle-specific p53 deletion alleviates high-fat diet-induced insulin resistance by modulating mitochondria-associated membrane in obese mice.Redox biology · 2025Article
- Bioactive Component Screening and Mechanistic Study of the Anti-Diabetic Activity ofCurrent issues in molecular biology · 2025Article
- Aberrant activation of p53-TRIB3 axis contributes to diabetic myocardial insulin resistance and sulforaphane protection.Journal of advanced research · 2025Article
- Flavonoid-Rich Extracts from Chuju (Foods (Basel, Switzerland) · 2025Article
- Curcumin attenuates liver injury by modulating the AGE-RAGE axis and metabolic homeostasis in high-fat diet/streptozotocin-induced type 2 diabetic mice.Frontiers in nutrition · 2025Article
- PCK1 as a target for cancer therapy: from metabolic reprogramming to immune microenvironment remodeling.Cell death discovery · 2024Review
- Preclinical validation of human recombinant glutamate-oxaloacetate transaminase for the treatment of acute ischemic stroke.iScience · 2024Article
- Causal Effects of Oxidative Stress on Diabetes Mellitus and Microvascular Complications: Insights Integrating Genome-Wide Mendelian Randomization, DNA Methylation, and Proteome.Antioxidants (Basel, Switzerland) · 2024Article
- Comparative Brain Proteomic Analysis between Sham and Cerebral Ischemia Experimental Groups.International journal of molecular sciences · 2024Article
- Post-Translational Modifications and Diabetes.Biomolecules · 2024Review
- Astrocytic insulin receptor controls circadian behavior via dopamine signaling in a sexually dimorphic manner.Nature communications · 2023Article
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- Neddylation of phosphoenolpyruvate carboxykinase 1 controls glucose metabolism.Cell metabolism · 2023Article
- Review
Corrections and comments
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Authors and funding
43 authors at 13 institutions in 5 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
p53 regulates several signaling pathways to maintain the metabolic homeostasis of cells and modulates the cellular response to stress. Deficiency or excess of nutrients causes cellular metabolic stress, and we hypothesized that p53 could be linked to glucose maintenance. We show here that upon starvation hepatic p53 is stabilized by O-GlcNAcylation and plays an essential role in the physiological regulation of glucose homeostasis. More specifically, p53 binds to PCK1 promoter and regulates its transcriptional activation, thereby controlling hepatic glucose production. Mice lacking p53 in the liver show a reduced gluconeogenic response during calorie restriction. Glucagon, adrenaline and glucocorticoids augment protein levels of p53, and administration of these hormones to p53 deficient human hepatocytes and to liver-specific p53 deficient mice fails to increase glucose levels. Moreover, insulin decreases p53 levels, and over-expression of p53 impairs insulin sensitivity. Finally, protein levels of p53, as well as genes responsible of O-GlcNAcylation are elevated in the liver of type 2 diabetic patients and positively correlate with glucose and HOMA-IR. Overall these results indicate that the O-GlcNAcylation of p53 plays an unsuspected key role regulating in vivo glucose homeostasis.
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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 OpenQuestion graph.