ArticleThe Journal of cell biology2014
Trim32 reduces PI3K-Akt-FoxO signaling in muscle atrophy by promoting plakoglobin-PI3K dissociation.
Article in The Journal of cell biology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 60 papers.
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Who cites it
60 citing papers in PubMed, 98 citations in OpenAlex.
- Upregulated TRIM32 correlates with enhanced cell proliferation and poor prognosis in hepatocellular carcinoma.Molecular and cellular biochemistry · 2016Trial
- Skeletal muscle adaptation to microgravity: how altered mechanical cues drive catabolic signaling.EMBO reports · 2026Review
- Mechanisms of protein degradation in atrophying muscles: What have we learned during the past decade?The Journal of biological chemistry · 2026Review
- Optineurin binding to the novel interacting partner Junction plakoglobin prevents muscle atrophy in mice.PLoS biology · 2026Article
- Adipocyte-specific ablation of plakoglobin in mice does not affect adiposity but results in sexual-dimorphic effects on weight gain.Physiological reports · 2025Article
- Combating muscle atrophy: emerging therapeutic targets that are fiber-type-specific.The FEBS journal · 2025Review
- Activation of SIK1 by phanginin A regulates skeletal muscle glucose uptake by phosphorylating HADC4/5/7 and enhancing GLUT4 expression and translocation.Natural products and bioprospecting · 2025Article
- RNA signaling in skeletal muscle: the central role of microRNAs and exosomal microRNAs.Frontiers in cell and developmental biology · 2025Review
- Analysis of lncRNAs and Their Regulatory Network in Skeletal Muscle Development of the Yangtze River Delta White Goat.Animals : an open access journal from MDPI · 2024Article
- Ubiquitination Insight from Spinal Muscular Atrophy-From Pathogenesis to Therapy: A Muscle Perspective.International journal of molecular sciences · 2024Review
- The role of PI3K/Akt signaling pathway in chronic kidney disease.International urology and nephrology · 2024Review
- Adipose stem cell‑derived exosomes promote high glucose-induced wound healing by regulating the TRIM32/STING axis.Archives of dermatological research · 2024Article
- Immunoglobulin heavy constant gamma 1 silencing decreases tonicity-responsive enhancer-binding protein expression to alleviate diabetic nephropathy.Journal of diabetes investigation · 2024Article
- Polyphenols alleviate metabolic disorders: the role of ubiquitin-proteasome system.Frontiers in nutrition · 2024Review
- Molecular Mechanisms and the Interplay of Important Chronic Obstructive Pulmonary Disease Biomarkers Reveals Novel Therapeutic Targets.ACS omega · 2023Review
- A critical discussion on the relationship between E3 ubiquitin ligases, protein degradation, and skeletal muscle wasting: it's not that simple.American journal of physiology. Cell physiology · 2023Review
- Targeting E3 ubiquitin ligases and their adaptors as a therapeutic strategy for metabolic diseases.Experimental & molecular medicine · 2023Review
- Review
- Bibliometric and visual analysis of diabetes mellitus and pyroptosis from 2011 to 2022.European journal of medical research · 2023Article
- Targeting protein modifications in metabolic diseases: molecular mechanisms and targeted therapies.Signal transduction and targeted therapy · 2023Review
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Activation of the PI3K-Akt-FoxO pathway induces cell growth, whereas its inhibition reduces cell survival and, in muscle, causes atrophy. Here, we report a novel mechanism that suppresses PI3K-Akt-FoxO signaling. Although skeletal muscle lacks desmosomes, it contains multiple desmosomal components, including plakoglobin. In normal muscle plakoglobin binds the insulin receptor and PI3K subunit p85 and promotes PI3K-Akt-FoxO signaling. During atrophy, however, its interaction with PI3K-p85 is reduced by the ubiquitin ligase Trim32 (tripartite motif containing protein 32). Inhibition of Trim32 enhanced plakoglobin binding to PI3K-p85 and promoted PI3K-Akt-FoxO signaling. Surprisingly, plakoglobin overexpression alone enhanced PI3K-Akt-FoxO signaling. Furthermore, Trim32 inhibition in normal muscle increased PI3K-Akt-FoxO signaling, enhanced glucose uptake, and induced fiber growth, whereas plakoglobin down-regulation reduced PI3K-Akt-FoxO signaling, decreased glucose uptake, and caused atrophy. Thus, by promoting plakoglobin-PI3K dissociation, Trim32 reduces PI3K-Akt-FoxO signaling in normal and atrophying muscle. This mechanism probably contributes to insulin resistance during fasting and catabolic diseases and perhaps to the myopathies and cardiomyopathies seen with Trim32 and plakoglobin mutations.
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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.