ArticleNature communications2015
SUMOylation of AMPKα1 by PIAS4 specifically regulates mTORC1 signalling.
Article in Nature communications, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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Who cites it
28 citing papers in PubMed, 45 citations in OpenAlex.
- SUMOylation is destined for regulatory T cell-related immune dysregulation.Cell death discovery · 2026Review
- AMPK at the interface of nutrient sensing, metabolic flux and energy homeostasis.Nature metabolism · 2026Review
- Gain of Alternative Allele Expression of LINC02449 at rs149707223 in Schizophrenia and Bipolar Disorder: Inducing Synaptic Transmission and Behavioral Deficits in Mice.Nature communications · 2025Article
- Tanshinone IIA destabilizes SLC7A11 by regulating PIAS4-mediated SUMOylation of SLC7A11 through KDM1A, and promotes ferroptosis in breast cancer.Journal of advanced research · 2025Article
- Post-translational modifications orchestrate mTOR-driven cell death in cardiovascular disease.Frontiers in cardiovascular medicine · 2025Review
- SUMO modifies GβL and mediates mTOR signaling.The Journal of biological chemistry · 2024Article
- Review
- SUMO Proteomics Analyses Identify Protein Inhibitor of Activated STAT-Mediated Regulatory Networks Involved in Cell Cycle and Cell Proliferation.Journal of proteome research · 2023Article
- Function and regulation of ubiquitin-like SUMO system in heart.Frontiers in cell and developmental biology · 2023Review
- Cardiac-targeted PIASy gene silencing mediates deSUMOylation of caveolin-3 and prevents ischemia/reperfusion-induced NaMilitary Medical Research · 2022Article
- AMPK signaling and its targeting in cancer progression and treatment.Seminars in cancer biology · 2022Review
- Cancer-Associated Dysregulation of Sumo Regulators: Proteases and Ligases.International journal of molecular sciences · 2022Review
- The protease SENP2 controls hepatic gluconeogenesis by regulating the SUMOylation of the fuel sensor AMPKα.The Journal of biological chemistry · 2022Article
- SUMOylation activates large tumour suppressor 1 to maintain the tissue homeostasis during Hippo signalling.Oncogene · 2021Article
- Review
- Lessons from Comparison of Hypoxia Signaling in Plants and Mammals.Plants (Basel, Switzerland) · 2021Review
- An immunohistochemical panel of three small ubiquitin-like modifier genes predicts outcomes of patients with triple-negative breast cancer.Gland surgery · 2021Article
- Post-Translational Modifications of the Energy Guardian AMP-Activated Protein Kinase.International journal of molecular sciences · 2021Review
- SUMOylation Wrestles With the Occurrence and Development of Breast Cancer.Frontiers in oncology · 2021Review
- SUMO: From Bench to Bedside.Physiological reviews · 2020Review
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
AMP-activated protein kinase (AMPK) inhibits several anabolic pathways such as fatty acid and protein synthesis, and identification of AMPK substrate specificity would be useful to understand its role in particular cellular processes and develop strategies to modulate AMPK activity in a substrate-specific manner. Here we show that SUMOylation of AMPKα1 attenuates AMPK activation specifically towards mTORC1 signalling. SUMOylation is also important for rapid inactivation of AMPK, to allow prompt restoration of mTORC1 signalling. PIAS4 and its SUMO E3 ligase activity are specifically required for the AMPKα1 SUMOylation and the inhibition of AMPKα1 activity towards mTORC1 signalling. The activity of a SUMOylation-deficient AMPKα1 mutant is higher than the wild type towards mTORC1 signalling when reconstituted in AMPKα-deficient cells. PIAS4 depletion reduced growth of breast cancer cells, specifically when combined with direct AMPK activator A769662, suggesting that inhibiting AMPKα1 SUMOylation can be explored to modulate AMPK activation and thereby suppress cancer cell growth.
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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.