ArticleThe Journal of biological chemistry2014
Mitsugumin 53 (MG53) ligase ubiquitinates focal adhesion kinase during skeletal myogenesis.
Article in The Journal of biological chemistry, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
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Who cites it
35 citing papers in PubMed, 64 citations in OpenAlex.
- NINJ1 ubiquitination by TRIM72 protects against plasma membrane rupture and AKI-CKD progression.Cell death and differentiation · 2026Article
- MG53, a Regenerative Myokine Linking Skeletal Muscle to Cardiac Repair.Biomolecules · 2026Review
- Mitsugumin 53 Inhibits Angiogenesis Through Regulating Focal Adhesion Turnover and Tip Cell Formation.Journal of cellular and molecular medicine · 2025Article
- Recombinant human mitsugumin 53: a potential therapeutic agent for multiple diseases.Frontiers in pharmacology · 2025Review
- TRIM72 inhibits cell migration and epithelial-mesenchymal transition by attenuating FAK/akt signaling in colorectal cancer.Heliyon · 2024Article
- TRIM72 restricts lyssavirus infection by inducing K48-linked ubiquitination and proteasome degradation of the matrix protein.PLoS pathogens · 2024Article
- Multisite phosphorylation dictates selective E2-E3 pairing as revealed by Ubc8/UBE2H-GID/CTLH assemblies.Molecular cell · 2024Article
- MG53/TRIM72: multi-organ repair protein and beyond.Frontiers in physiology · 2024Review
- Long non-coding RNA NRSN2-AS1 promotes ovarian cancer progression through targeting PTK2/β-catenin pathway.Cell death & disease · 2023Article
- Structural basis for TRIM72 oligomerization during membrane damage repair.Nature communications · 2023Article
- The Effects of Antioxidants and Pulsed Magnetic Fields on Slow and Fast Skeletal Muscle Atrophy Induced by Streptozotocin: A Preclinical Study.Journal of diabetes research · 2023Article
- FAK in Cancer: From Mechanisms to Therapeutic Strategies.International journal of molecular sciences · 2022Review
- MG53 Inhibits Necroptosis Through Ubiquitination-Dependent RIPK1 Degradation for Cardiac Protection Following Ischemia/Reperfusion Injury.Frontiers in cardiovascular medicine · 2022Article
- Dickkopf-1 Inhibition Reactivates Wnt/β-Catenin Signaling in Rhabdomyosarcoma, Induces Myogenic Markers In Vitro and Impairs Tumor Cell Survival In Vivo.International journal of molecular sciences · 2021Article
- MG53 suppresses tumor progression and stress granule formation by modulating G3BP2 activity in non-small cell lung cancer.Molecular cancer · 2021Article
- MG53 inhibits angiogenesis through regulating focal adhesion kinase signalling.Journal of cellular and molecular medicine · 2021Article
- Biochemical characterization of TRIM72 E3 ligase and its interaction with the insulin receptor substrate 1.Biochemistry and biophysics reports · 2020Article
- Multi-Cellular Functions of MG53 in Muscle Calcium Signaling and Regeneration.Frontiers in physiology · 2020Review
- A knock-in mutation at cysteine 144 of TRIM72 is cardioprotective and reduces myocardial TRIM72 release.Journal of molecular and cellular cardiology · 2019Article
- Sustained elevation of MG53 in the bloodstream increases tissue regenerative capacity without compromising metabolic function.Nature communications · 2019Article
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The striated muscle-specific mitsugumin 53 (MG53) is a novel E3 ligase that induces the ubiquitination of insulin receptor substrate 1 (IRS-1) during skeletal myogenesis, negatively regulating insulin-like growth factor and insulin signaling. Here we show that focal adhesion kinase (FAK) is the second target of MG53 during skeletal myogenesis. The FAK protein level gradually decreased, whereas its mRNA level was constant during myogenesis in C2C12 cells and MyoD-overexpressing mouse embryonic fibroblasts. The FAK protein was associated with the E2 enzyme UBE2H and the E3 enzyme MG53 in endogenous and exogenous immunoprecipitation experiments. FAK ubiquitination and degradation was induced by MG53 overexpression in myoblasts but abolished by MG53 or UBE2H knockdown in myotubes. Because RING-disrupted MG53 mutants (C14A and ΔR) did not induce FAK ubiquitination and degradation, the RING domain was determined to be required for MG53-induced FAK ubiquitination. Taken together, these data indicate that MG53 induces FAK ubiquitination with the aid of UBE2H during skeletal myogenesis.
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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.