ArticleCell death and differentiation2014
AMPK couples p73 with p53 in cell fate decision.
Article in Cell death and differentiation, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
29 citing papers in PubMed, 44 citations in OpenAlex.
- AMPK-mediated HCN4 channel phosphorylation contributes to age-related intrinsic bradycardia.The Journal of general physiology · 2026Article
- AMPK at the interface of nutrient sensing, metabolic flux and energy homeostasis.Nature metabolism · 2026Review
- Doxorubicin Attenuates Free Fatty Acid-Induced Lipid Accumulation via Stimulation of p53 in HepG2 Cells.Biomolecules & therapeutics · 2024Article
- The Competition of Yin and Yang: Exploring the Role of Wild-Type and Mutant p53 in Tumor Progression.Biomedicines · 2023Article
- Mechanisms of cancer cell death induction by paclitaxel: an updated review.Apoptosis : an international journal on programmed cell death · 2022Review
- P63 and P73 Activation in Cancers with p53 Mutation.Biomedicines · 2022Review
- Oxidative Pentose Phosphate Pathway Enzyme 6-Phosphogluconate Dehydrogenase Plays a Key Role in Breast Cancer Metabolism.Biology · 2021Article
- AMP-activated protein kinase contributes to cisplatin-induced renal epithelial cell apoptosis and acute kidney injury.American journal of physiology. Renal physiology · 2020Article
- MicroRNA-708 modulates Hepatic Stellate Cells activation and enhances extracellular matrix accumulation via direct targeting TMEM88.Journal of cellular and molecular medicine · 2020Article
- Glucose-dependent GPER1 expression modulates tamoxifen-induced IGFBP-1 accumulation.Journal of molecular endocrinology · 2019Article
- Role of p53 Family Proteins in Metformin Anti-Cancer Activities.Journal of Cancer · 2019Review
- AMPK: Regulation of Metabolic Dynamics in the Context of Autophagy.International journal of molecular sciences · 2018Review
- Cancer driver mutations in endometriosis: Variations on the major theme of fibrogenesis.Reproductive medicine and biology · 2018Review
- AMPK β1 reduces tumor progression and improves survival in p53 null mice.Molecular oncology · 2017Article
- Ultraconserved long non-coding RNA uc.63 in breast cancer.Oncotarget · 2017Article
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- Activation of PPARγ/P53 signaling is required for curcumin to induce hepatic stellate cell senescence.Cell death & disease · 2016Article
- p73 promotes glioblastoma cell invasion by directly activating POSTN (periostin) expression.Oncotarget · 2016Article
- P53 functional abnormality in mesenchymal stem cells promotes osteosarcoma development.Cell death & disease · 2016Review
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 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The p53 family of proteins has an important role in determining cell fate in response to different types of stress, such as DNA damage, hypoxia, or oncogenic stress. In recent years, p53 has also been shown to respond to metabolic stress, and to be induced by the AMP-activated protein kinase (AMPK), a central cellular energy sensor. A bioinformatic analysis revealed three putative AMPK phopshorylation sites in p73, a p53 tumor suppressor paralog. In vitro and in vivo assays confirmed that AMPK phosphorylates p73 on a novel residue, S426. Following specific pharmacologic stimulation of AMPK in cells, p73 protein half-life was prolonged leading to p73 accumulation in the nucleus. We show that p73 escaped the E3 ligase Itch resulting in reduced p73 ubiquitination and proteasomal degradation. Furthermore, chronic activation of AMPK led to apoptosis that was p73 dependent, but only in p53-expressing cells. Surprisingly, we found that p73 was required for p53 stabilization and accumulation under AMPK activation, but was dispensable under DNA damage. Our findings couple p73 with p53 in determining cell fate under AMPK-induced metabolic stress.
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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 Socratic graph.