ArticleExperimental & molecular medicine2018
An MG53-IRS1-interaction disruptor ameliorates insulin resistance.
Article in Experimental & molecular medicine, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 14 citations in OpenAlex.
- Emerging perspectives in proteostasis: bridging mechanisms and therapeutics for human diseases.Signal transduction and targeted therapy · 2026Review
- Ubiquitination modifications as central regulators of metabolic dysfunction in type 2 diabetes mellitus.Frontiers in endocrinology · 2026Review
- Tumor-derived MG53 aggravates gastrointestinal cancer cachexia related muscle atrophy by inhibiting the TLR4/PI3K/AKT/FOXO3a signaling pathway.Frontiers in oncology · 2026Article
- Review
- Trim72 is a major host factor protecting against lethal Candida albicans infection.PLoS pathogens · 2024Article
- Hypoglycemic Effect of Edible Fungi Polysaccharides Depends on Their Metabolites from the Fermentation of Human Fecal Microbiota.Foods (Basel, Switzerland) · 2023Article
- Targeting E3 ubiquitin ligases and their adaptors as a therapeutic strategy for metabolic diseases.Experimental & molecular medicine · 2023Review
- Is MG53 a potential therapeutic target for cancer?Frontiers in endocrinology · 2023Review
- Rosuvastatin exerts cardioprotective effect in lipopolysaccharide-mediated injury of cardiomyocytes in an MG53-dependent manner.BMC cardiovascular disorders · 2022Article
- Application of Low-Intensity Laser in the Treatment of Skeletal Muscle Injury in Runners.Emergency medicine international · 2022Article
- Characterization of DNA Methylation and Screening of Epigenetic Markers in Polycystic Ovary Syndrome.Frontiers in cell and developmental biology · 2021Article
- Mini Review: Opposing Pathologies in Cancer and Alzheimer's Disease: Does the PI3K/Akt Pathway Provide Clues?Frontiers in endocrinology · 2020Review
Corrections and comments
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Authors and funding
10 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mitsugumin 53 (MG53) is an E3 ligase that induces insulin receptor substrate-1 (IRS-1) ubiquitination and degradation in skeletal muscle. We previously demonstrated that the pharmaceutical disruption of the MG53-IRS-1 interaction improves insulin sensitivity by abrogating IRS-1 ubiquitination and increasing IRS-1 levels in C2C12 myotubes. Here, we developed a novel MG53-IRS-1 interaction disruptor (MID-00935) that ameliorates insulin resistance in diet-induced obese (DIO) mice. MID-00935 disrupted the molecular interaction of MG53 and IRS-1, abrogated MG53-induced IRS-1 ubiquitination and degradation and improved insulin signaling in C2C12 myotubes. Oral administration of MID-00935 increased insulin-induced IRS-1, Akt, and Erk phosphorylation via increasing IRS-1 levels in the skeletal muscle of DIO mice. In DIO mice, MID-00935 treatment lowered fasting blood glucose levels and improved glucose disposal in glucose and insulin tolerance tests. These results suggest that MID-00935 may be a potential muscle-targeting drug candidate for treating insulin resistance.
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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.