ArticleNature communications2018
Loss of the E3 ubiquitin ligase MKRN1 represses diet-induced metabolic syndrome through AMPK activation.
Article in Nature communications, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers.
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Who cites it
50 citing papers in PubMed, 70 citations in OpenAlex.
- M1-linked ubiquitination by LUBAC regulates AMPK signalling and the response to energetic stress.Cell death and differentiation · 2026Article
- Identification of MKRN1 as a key modulator of the p53-MDM2 feedback loop.Cell death and differentiation · 2026Article
- Endothelial KSR2 regulated by genetic variation protects against atherosclerosis through AMPKα1 stabilization.Theranostics · 2026Article
- Low expression of MKRN1 promotes leukemia cell proliferation.European journal of medical research · 2025Article
- Ubiquitination and ubiquitin-like modifications in metabolic dysfunction-associated steatotic liver disease: mechanisms and implications.BMB reports · 2025Review
- FOXM1 Protects Against Myocardial Ischemia-Reperfusion Injury in Rodent and Porcine Models by Suppressing MKRN1-Dependent LKB1 Ubiquitination.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- The emerging role of E3 ubiquitin ligases and deubiquitinases in metabolic dysfunction-associated steatotic liver disease.Journal of translational medicine · 2025Review
- The ubiquitin-proteasome system: A potential target for the MASLD.Acta pharmaceutica Sinica. B · 2025Review
- E3 ligase FBXW7 suppresses brown fat expansion and browning of white fat.EMBO reports · 2025Article
- Ebastine-mediated destabilization of E3 ligase MKRN1 protects against metabolic dysfunction-associated steatohepatitis.Cellular and molecular life sciences : CMLS · 2025Article
- Research progress on AMPK in the pathogenesis and treatment of MASLD.Frontiers in immunology · 2025Review
- Decoding temporal thermogenesis: coregulator selectivity and transcriptional control in brown and beige adipocytes.Adipocyte · 2024Article
- Erythropoietin regulates energy metabolism through EPO-EpoR-RUNX1 axis.Nature communications · 2024Article
- Ventromedial hypothalamic nucleus subset stimulates tissue thermogenesis via preoptic area outputs.Molecular metabolism · 2024Article
- Ubiquitin ligase RNF20 coordinates sequential adipose thermogenesis with brown and beige fat-specific substrates.Nature communications · 2024Article
- Exploring molecular mechanisms of exercise on metabolic syndrome: a bibliometric and visualization study using CiteSpace.Frontiers in endocrinology · 2024Review
- Ubiquitination and Metabolic Disease.Advances in experimental medicine and biology · 2024Review
- Single-cell RNA sequencing to reveal non-parenchymal cell heterogeneity and immune network of acetaminophen-induced liver injury in mice.Archives of toxicology · 2023Article
- Targeting protein modifications in metabolic diseases: molecular mechanisms and targeted therapies.Signal transduction and targeted therapy · 2023Review
- Construction of a ternary component chip with enhanced desorption efficiency for laser desorption/ionization mass spectrometry based metabolic fingerprinting.Frontiers in bioengineering and biotechnology · 2023Article
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Authors and funding
22 authors at 7 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
AMP-activated protein kinase (AMPK) plays a key role in controlling energy metabolism in response to physiological and nutritional status. Although AMPK activation has been proposed as a promising molecular target for treating obesity and its related comorbidities, the use of pharmacological AMPK activators has been met with contradictory therapeutic challenges. Here we show a regulatory mechanism for AMPK through its ubiquitination and degradation by the E3 ubiquitin ligase makorin ring finger protein 1 (MKRN1). MKRN1 depletion promotes glucose consumption and suppresses lipid accumulation due to AMPK stabilisation and activation. Accordingly, MKRN1-null mice show chronic AMPK activation in both liver and adipose tissue, resulting in significant suppression of diet-induced metabolic syndrome. We demonstrate also its therapeutic effect by administering shRNA targeting MKRN1 into obese mice that reverses non-alcoholic fatty liver disease. We suggest that ubiquitin-dependent AMPK degradation represents a target therapeutic strategy for metabolic disorders.
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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.