Affinage

TRIM72

Tripartite motif-containing protein 72 · UniProt Q6ZMU5

Length
477 aa
Mass
52.7 kDa
Annotated
2026-06-10
100 papers in source corpus 43 papers cited in narrative 43 extracted findings
Cross-family judge vs UniProt: Affinage preferred faithfulness: 8/8 claims corpus-supported (100%)

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

TRIM72 (MG53) is a muscle-enriched TRIM-family protein that nucleates the cell-membrane repair machinery at sites of sarcolemmal injury and doubles as a redox-regulated RING E3 ubiquitin ligase controlling metabolic and survival signaling (PMID:19043407, PMID:23354051). In its repair role, MG53 associates with intracellular vesicles through binding to phosphatidylserine and other negatively charged lipids, and upon membrane wounding the resulting oxidative environment drives its oligomerization — an obligatory step requiring Cys242 disulfide formation and the LZ1 leucine-zipper motif of the coiled-coil domain — to translocate vesicles to the lesion (PMID:19043407, PMID:21525429). Recruitment to the injury site is cholesterol-dependent and uses PTRF/cavin-1 as a docking protein, with Zn2+ binding to the RING and B-box motifs and the motor activity of nonmuscle myosin IIA required for assembly, while caveolin-3, dysferlin, and Ca2+-facilitated vesicle fusion complete the repair patch (PMID:19380584, PMID:20466981, PMID:21343302, PMID:22253476, PMID:25869134). Crystallographic and cryo-electron tomography analyses show that phosphatidylserine-membrane engagement licenses higher-order MG53 assembly on the bilayer, which in turn activates its RING-dependent ubiquitination activity (PMID:36944613, PMID:37770719). As an E3 ligase acting with the E2 enzyme UBE2H, MG53 ubiquitinates and degrades the insulin receptor and IRS-1 to suppress insulin signaling and myogenesis, and its ligase activity is gated by GSK3β-mediated phosphorylation at Ser255 (PMID:23354051, PMID:23965929, PMID:36337049). The same activity targets a broad substrate set including FAK, AMPKα, RIPK1, and cyclin D1, linking MG53 to glucose handling, necroptosis suppression, and cell-cycle control (PMID:24344130, PMID:33400924, PMID:35711363, PMID:37414783). MG53 is also secreted as a glucose-sensitive myokine/cardiokine through PKC-δ Y311 phosphorylation, and circulating MG53 binds the insulin-receptor extracellular domain as an allosteric blocker, functioning as a multi-organ tissue-repair and metabolic factor (PMID:30586741, PMID:32677469). Genetic ablation studies establish MG53 as essential for membrane resealing in skeletal and cardiac muscle and kidney, and for ischemic pre-/postconditioning cardioprotection via caveolin-3–PI3K tethering and the RISK pathway (PMID:20516375, PMID:21285295, PMID:25787762).

Mechanistic history

Synthesis pass · year-by-year structured walk · 12 steps
  1. 2008 High

    Established that MG53 is the nucleator of an acute cell-membrane repair response, answering how striated muscle reseals wounds and linking the process to vesicle lipid binding and oxidative triggering.

    Evidence Live imaging of GFP-MG53, lipid-binding assays, KO mice, and dye-entry repair assays in muscle fibers; plus imaging/knockdown showing vesicle budding and caveolin-3 interaction

    PMID:19029292 PMID:19043407

    Open questions at the time
    • Molecular basis of oxidation sensing not yet defined
    • Composition of the repair patch beyond vesicle recruitment unresolved
  2. 2009 High

    Defined the membrane-repair partner complex, showing MG53 traffics dysferlin and depends on caveolin-3 localization, explaining why Cav3 mutations cause defective repair.

    Evidence Reciprocal Co-IP, dominant-negative Cav3 mutants, live imaging with repair readouts in skeletal muscle

    PMID:19380584

    Open questions at the time
    • Stoichiometry and order of complex assembly unresolved
    • Direct vs indirect MG53-dysferlin contact not fully mapped
  3. 2010 High

    Extended MG53 function to the heart and to insulin signaling, establishing its role in ischemic preconditioning via caveolin-3/PI3K-RISK and as a negative regulator of IRS-1/myogenesis.

    Evidence KO mice with Langendorff perfusion, cholesterol depletion/repletion imaging, Co-IP, and IRS-1 raft-association/promoter analysis

    PMID:20139895 PMID:20466981 PMID:20516375

    Open questions at the time
    • Whether IRS-1 regulation in 2010 was degradative was not yet defined
    • Cholesterol-sensing receptor for MG53 not identified
  4. 2011 High

    Dissected the molecular requirements for injury-site translocation — a docking protein and the redox-dependent oligomerization chemistry — and mapped domain-specific tethering of Cav3 and PI3K.

    Evidence PTRF knockdown/rescue imaging, LZ1/Cys242 mutagenesis with cross-linking and live imaging, and domain-deletion Co-IP with postconditioning assays

    PMID:21285295 PMID:21343302 PMID:21525429

    Open questions at the time
    • How PTRF/cholesterol couples to oligomerization mechanistically unclear
    • Reversibility of disulfide-driven assembly not addressed
  5. 2012 Medium

    Resolved the cytoskeletal and Ca2+-dependent steps of repair and quantified MG53 lipid affinities, showing NM-IIA-driven vesicle transport and Ca2+-dependent dysferlin-dimer association.

    Evidence NM-IIA Co-IP/knockdown/rescue with imaging, dysferlin C2A-mutant pulldowns, and in vitro lipid-binding Kd measurements

    PMID:22253476 PMID:22281009 PMID:23145354

    Open questions at the time
    • PLoS Currents/BMB findings from single labs with limited follow-up
    • Physiological lipid-conformation switching not validated in vivo
  6. 2013 High

    Identified MG53 as a bona fide E3 ubiquitin ligase, naming UBE2H as its E2 and IR, IRS-1, and FAK as degradation substrates, thereby mechanistically linking MG53 to insulin resistance and myogenesis.

    Evidence In vitro ubiquitination reconstitution, RING-domain mutagenesis, transgenic and KO mice with metabolic challenge, reciprocal Co-IP

    PMID:23354051 PMID:23965929 PMID:24344130

    Open questions at the time
    • Ubiquitin linkage type for IR/IRS1 not fully specified in these studies
    • Trigger coupling membrane assembly to ligase activity not yet defined
  7. 2014 High

    Showed that cysteine redox chemistry regulates MG53 stability, with S-nitrosylation at C144 protecting against oxidation-induced degradation and limiting I/R damage.

    Evidence C144S mutagenesis, GSNO/H2O2 treatment, and Langendorff I/R with infarct measurement

    PMID:24487118

    Open questions at the time
    • Endogenous nitrosylation machinery not identified
    • Interplay between C144 SNO and Cys242 oligomerization not resolved
  8. 2015 High

    Defined Zn2+ as a cofactor for repair assembly and extended MG53's repair/protective roles to kidney and dermal wound healing as a secreted/recombinant therapeutic.

    Evidence RING/B-box Zn-binding mutagenesis with chelation, KO mice in renal I/R and dermal injury models, rhMG53 treatment, TGF-β readouts

    PMID:25637627 PMID:25787762 PMID:25869134 PMID:26306047 PMID:26637632

    Open questions at the time
    • Mechanism of extracellular Zn2+ entry into the repair process unclear
    • How secreted MG53 reaches distant injury sites not fully defined
  9. 2019 High

    Established MG53 as a circulating myokine/cardiokine and an allosteric insulin-receptor blocker, providing a humoral mechanism for systemic insulin resistance distinct from intracellular degradation.

    Evidence Perfused muscle/heart, surface plasmon resonance and Co-IP for IR-ectodomain binding, transgenic mice, and neutralizing antibody therapy in db/db mice; plus G3BP2 stress-granule interaction in NSCLC

    PMID:30586741 PMID:34521423

    Open questions at the time
    • Secretion route of a transmembrane-less protein incompletely defined here
    • Relative contribution of circulating vs intracellular MG53 to disease unclear
  10. 2020 High

    Identified the secretion trigger (PKC-δ Y311 phosphorylation) and broadened MG53 ligase/regulatory functions to AMPKα degradation and innate-immune suppression.

    Evidence Y311 phospho-mutants and proteomics for secretion, in vitro ubiquitination with AMPKα phosphomimetics, and macrophage KO/RyR-dependency infection models

    PMID:32677469 PMID:32681036 PMID:33400924

    Open questions at the time
    • Vesicular vs non-conventional secretion machinery not fully resolved
    • Immune findings rest on single-lab models
  11. 2022 High

    Pinpointed GSK3β-Ser255 phosphorylation as the switch gating E3 ligase activity independently of membrane repair, and expanded substrate range to RIPK1/RIP3, cardiolipin-mediated mitochondrial targeting, and post-translational stabilizing modifications.

    Evidence IP-MS phosphosite mapping, GSK3β kinase assay, S255A knock-in mice in diabetic I/R; ubiquitination site mapping for RIPK1; cardiolipin binding and mitophagy reporters; K130 succinylation Co-IP

    PMID:35679798 PMID:35711363 PMID:36337049 PMID:37527538 PMID:37848382

    Open questions at the time
    • Several substrate/modification studies are single-lab
    • How Ser255 phosphorylation structurally activates the RING not defined
  12. 2023 High

    Provided the structural basis for membrane-coupled activation, showing phosphatidylserine engagement licenses higher-order assembly that activates RING E3 activity, and consolidated MG53's tumor-suppressive substrate network.

    Evidence Crystal structures of BCC-SPRY and near-complete RBCC-SPRY, cryo-ET subtomogram averaging, structure-guided mutagenesis with in vitro ubiquitination; cyclin D1, p53, RAC1, MGMT degradation assays with tumor models

    PMID:34788479 PMID:34958003 PMID:35858925 PMID:36944613 PMID:37414783 PMID:37770719 PMID:39111582

    Open questions at the time
    • Cancer substrate findings largely single-lab
    • Full-length apo vs membrane-bound conformational transition not captured at atomic resolution

Open questions

Synthesis pass · forward-looking unresolved questions
  • It remains unresolved how the membrane-repair scaffold function and the substrate-selective E3 ligase function are coordinately controlled in vivo, and what governs the choice among MG53's many reported substrates in different tissues.
  • No unified model linking membrane assembly to substrate choice
  • Tissue-specific substrate prioritization undefined
  • In vivo relevance of many single-lab cancer substrates untested across labs

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0016874 ligase activity 7 GO:0140096 catalytic activity, acting on a protein 4 GO:0008289 lipid binding 3 GO:0060090 molecular adaptor activity 2 GO:0098772 molecular function regulator activity 1
Localization
GO:0005576 extracellular region 3 GO:0005886 plasma membrane 3 GO:0031410 cytoplasmic vesicle 2 GO:0005634 nucleus 1 GO:0005739 mitochondrion 1
Pathway
R-HSA-392499 Metabolism of proteins 4 GO:0140096 catalytic activity, acting on a protein 3 R-HSA-162582 Signal Transduction 3 R-HSA-5357801 Programmed Cell Death 3 R-HSA-1640170 Cell Cycle 1
Partners
CAV1CAV3DYSFG3BP2MYH9PTRFRELAUBE2H
Complex memberships
MG53-UBE2H E2-E3 ubiquitination complexMG53-dysferlin-caveolin-3 membrane repair complex

Evidence

Reading pass · 43 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
2008 MG53 (TRIM72) is a muscle-specific TRIM family protein that associates with intracellular vesicles via binding to phosphatidylserine, traffics to and fuses with the sarcolemmal membrane, and nucleates assembly of the cell membrane repair machinery. Oxidative stress upon membrane injury triggers MG53 oligomerization, recruiting MG53-containing vesicles to injury sites; subsequent extracellular Ca2+ entry facilitates vesicle fusion to reseal the membrane. Live cell imaging of GFP-MG53, lipid-binding assays, MG53 knockout mice, treadmill exercise/membrane repair assays, dye-entry into isolated muscle fibers Nature cell biology High 19043407
2008 MG53 regulates membrane budding and exocytosis in striated muscle; it is tightly associated with intracellular vesicles without a transmembrane segment and its activity is regulated by functional interaction with caveolin-3. RNAi knockdown impedes myoblast differentiation whereas overexpression enhances vesicle trafficking to and budding from the sarcolemmal membrane. Live cell confocal imaging of GFP-MG53, RNAi knockdown, co-expression studies, domain analysis The Journal of biological chemistry High 19029292
2009 MG53 interacts physically with dysferlin and caveolin-3 (Cav3) to form a molecular complex essential for membrane repair in skeletal muscle. MG53 mediates active trafficking of intracellular vesicles to the sarcolemma and is required for movement of dysferlin to injury sites during repair patch formation. Cav3 mutations (P104L, R26Q) that retain Cav3 in the Golgi result in aberrant localization of both MG53 and dysferlin, leading to defective membrane repair. Co-immunoprecipitation, live cell imaging, dominant-negative Cav3 mutant expression, membrane repair assays The Journal of biological chemistry High 19380584
2010 MG53 is essential for cardiac ischemic preconditioning (IPC)-mediated cardioprotection. MG53 mediates interaction between caveolin-3 and the p85 subunit of PI3K, leading to activation of the reperfusion injury salvage kinase (RISK) pathway (PI3K-Akt-GSK3β and ERK1/2) without altering the SAFE (JAK-STAT3) pathway. MG53-deficient mice show increased myocardial vulnerability to ischemia/reperfusion injury and abolished IPC protection. MG53 knockout mice, Langendorff heart perfusion, neonatal cardiomyocyte overexpression/knockdown, Co-IP, kinase activity assays Circulation High 20516375
2010 MG53-mediated cardiac membrane repair operates through a cholesterol-dependent mechanism: depletion of membrane cholesterol abolishes injury-induced MG53 translocation to damage sites, while cholesterol recovery restores it. Oxidation of MG53 confers stability to the membrane repair patch but does not initiate MG53 translocation. MG53 ablation prevents sarcolemmal resealing after laser-induced damage in intact heart. Infrared laser membrane damage in intact hearts, cholesterol depletion/repletion experiments, MG53 KO mice, live cell imaging Circulation research High 20466981
2010 TRIM72 (MG53) negatively regulates skeletal myogenesis by associating with insulin receptor substrate-1 (IRS-1) in sarcolemmal lipid rafts, suppressing IGF-induced IRS-1 activation. TRIM72 overexpression prevents C2C12 myogenesis; TRIM72 silencing or knockout enhances myogenesis and Akt activation. TRIM72 transcription is driven by MyoD/Akt-dependent activation of two proximal E-boxes in the TRIM72 promoter. Adenoviral overexpression, RNAi knockdown, TRIM72−/− satellite cells, Co-IP, promoter analysis Cell death and differentiation High 20139895
2011 Polymerase I and transcript release factor (PTRF/cavin-1) acts as a docking protein for MG53 at membrane injury sites, potentially by binding exposed membrane cholesterol. Cells lacking PTRF show defective MG53 trafficking to injury sites; a disease-associated PTRF mutation causes aberrant nuclear localization of PTRF and disrupts MG53 membrane repair function. RNAi knockdown of PTRF, PTRF overexpression rescue, live cell imaging, PTRF mutant expression, membrane repair assays The Journal of biological chemistry High 21343302
2011 Redox-dependent MG53 oligomerization through leucine zipper motif LZ1 (residues L176/L183/L190/V197) in the coiled-coil domain is essential for translocation to membrane injury sites. Cys242 oxidation (disulfide bond formation) is an obligatory step; LZ1 mutations (but not LZ2) diminish redox-dependent oligomerization and impair MG53 translocation. Alkylation of cysteine residues in vivo prevents MG53 movement to injury sites. Site-directed mutagenesis, chemical cross-linking, GFP-MG53 live cell imaging, alkylating reagent treatment, mechanical membrane damage assays American journal of physiology. Cell physiology High 21525429
2011 MG53 participates in ischemic postconditioning (PostC)-mediated cardioprotection through the RISK signaling pathway. Structure-function analysis shows MG53 TRIM domain (aa1–284) physically interacts with Cav3 but not p85-PI3K, while the SPRY domain (aa285–477) interacts with p85-PI3K but not Cav3, establishing that MG53 tethers Cav3 and PI3K via its N- and C-termini respectively to activate RISK. MG53-KO mouse Langendorff perfusion, domain deletion constructs, Co-IP with isolated domains, PostC protocol Cardiovascular research High 21285295
2012 Nonmuscle myosin IIA (NM-IIA) physically interacts with MG53 and is required for vesicle trafficking during cell membrane repair. NM-IIA-deficient cells fail to translocate MG53 to injury sites; rescue of NM-IIA restores MG53-mediated repair. Pharmacological alteration of NM-IIA motor function also compromises membrane repair. Co-immunoprecipitation, NM-IIA knockdown/rescue, pharmacological inhibition of NM-IIA, live cell imaging of MG53 translocation, dye-entry membrane repair assay FASEB journal High 22253476
2012 The C2A domain of dysferlin is important for Ca2+-dependent association with MG53 dimers. Wild-type dysferlin associates with MG53 dimers in a Ca2+-dependent manner; MG53 oligomers associate with both wild-type and C2A-mutant dysferlin in a Ca2+-independent manner. A pathogenic C2A missense mutation (W52R) inhibits the association with MG53 dimers. Co-expression of C242A-MG53 (dimer but not oligomer form) impairs recruitment of both MG53 and dysferlin to sarcolemmal injury sites. Immunoprecipitation, pulldown assays, Ca2+-dependency experiments, live cell imaging of dysferlin and MG53 behavior during sarcolemmal wounding, pathogenic and engineered MG53 mutants PLoS currents Medium 23145354
2013 MG53 functions as an E3 ubiquitin ligase mediating ubiquitin-dependent degradation of the insulin receptor (IR) and insulin receptor substrate-1 (IRS1) in skeletal muscle. MG53 overexpression is sufficient to trigger muscle insulin resistance and metabolic syndrome in mice; ablation of MG53 preserves IR, IRS1, and insulin signaling integrity and prevents diet-induced metabolic syndrome. MG53 transgenic and knockout mice, ubiquitination assays, IR/IRS1 degradation assays, glucose/insulin tolerance tests, Western blotting Nature High 23354051
2013 MG53 is an E3 ubiquitin ligase that induces IRS-1 ubiquitination with the aid of E2-conjugating enzyme UBE2H. Disruption of MG53 E3-ligase function (RING domain mutations) abolishes IRS-1 ubiquitination and enhances skeletal myogenesis. Elevated IRS-1 in MG53−/− skeletal muscle protects from high-fat/high-sucrose diet-induced insulin resistance. E3-ligase domain mutations, ubiquitination assays, MG53−/− mice, high-fat/high-sucrose diet challenge, Co-IP for UBE2H-MG53-IRS1 complex Nature communications High 23965929
2013 MG53 ubiquitinates focal adhesion kinase (FAK) using E2 enzyme UBE2H during skeletal myogenesis, reducing FAK protein levels without affecting mRNA. The RING domain of MG53 is required for FAK ubiquitination; RING-disrupted mutants (C14A and ΔR) abolish FAK ubiquitination and degradation. Endogenous and exogenous Co-IP for MG53-UBE2H-FAK complex, overexpression/knockdown ubiquitination assays, RING domain mutants in myoblasts and myotubes The Journal of biological chemistry High 24344130
2014 S-nitrosylation of TRIM72 at cysteine 144 (C144) by S-nitrosoglutathione (GSNO) prevents oxidation-induced protein degradation and promotes cell survival. C144S mutation renders TRIM72 resistant to H2O2-induced degradation, whereas GSNO treatment preserves wild-type TRIM72 levels and blocks ischemia/reperfusion-induced decrease in TRIM72, reducing infarct size. C144 SNO competes with irreversible oxidation to protect protein stability. C144S site-directed mutagenesis, H2O2 treatment, GSNO treatment, Langendorff-perfused heart I/R model, infarct size measurement, Western blotting for protein stability Journal of molecular and cellular cardiology High 24487118
2015 Zinc (Zn2+) binding to the RING and B-box motifs of MG53 is indispensable for assembly of the cell membrane repair machinery. Extracellular Zn2+ entry is essential for translocation of MG53-containing vesicles to acute membrane injury sites; this effect is abolished in mg53−/− muscle fibers. Mutagenesis of Zn2+-binding residues in RING and B-box abolishes MG53-mediated membrane repair. Live cell imaging, Zn2+ chelation and supplementation, MG53 KO muscle fibers, RING and B-box mutagenesis, membrane repair assays The Journal of biological chemistry High 25869134
2015 MG53 translocates to acute injury sites on renal proximal tubular epithelial (PTE) cells, forms a repair patch, and binds phosphatidylserine at injury sites. MG53-deficient mice develop pronounced tubulointerstitial injury and increased susceptibility to ischemia/reperfusion-induced acute kidney injury. Live cell imaging of MG53 translocation, MG53 KO mice, I/R and nephrotoxin injury models, histology, serum creatinine/BUN measurement, rhMG53 treatment Science translational medicine High 25787762
2015 MG53 interferes with TGF-β-dependent activation of myofibroblast differentiation during wound healing, down-regulating α-smooth muscle actin and extracellular matrix proteins, thereby reducing scarring. MG53-deficient mice show delayed wound healing, abnormal scarring, and collagen overproduction. MG53 also facilitates fibroblast migration in response to scratch wounding. MG53 KO mice, scratch wound assay, TGF-β stimulation with rhMG53 treatment, Western blotting for α-SMA and ECM proteins, rodent dermal injury models The Journal of biological chemistry Medium 26306047
2015 MG53 transcriptional upregulation of peroxisome proliferator-activated receptor alpha (PPARα) and its target genes in cardiomyocytes leads to lipid accumulation and lipotoxicity. MG53 transgenic mice develop diabetic cardiomyopathy with insulin resistance, lipid accumulation, hypertrophy, and fibrosis via dual mechanisms: PPARα upregulation and destabilization of IR and IRS1. Cardiac-specific MG53 transgenic mice, echocardiography, lipid assays, Western blotting for IR/IRS1, PPARα target gene expression, histology Circulation Medium 25637627
2018 TRIM72 undergoes mono-ADP-ribosylation at arginine residues (R207, R260) by ADP-ribosyltransferase 1 (ART1), and this modification is reversed by ARH1. ADP-ribosylated TRIM72 levels are elevated in ARH1-deficient mice after I/R injury. Mutant TRIM72 (R207K/R260K) that cannot be ADP-ribosylated interferes with assembly of TRIM72 repair complexes at laser-induced injury sites, and mono-ADP-ribosylation inhibitors block TRIM72 oligomerization. ARH1-deficient mice, C2C12 knockdown/scratch assay, mutant TRIM72 live cell imaging, mono-ADP-ribosylation inhibitors (vitamin K1, novobiocin), Co-IP from heart lysates JCI insight Medium 30429362
2019 MG53 acts as a glucose-sensitive myokine/cardiokine secreted from striated muscle in response to high glucose or high insulin. Circulating MG53 binds the extracellular domain of the insulin receptor and acts as an allosteric blocker of insulin signaling. Neutralizing circulating MG53 with monoclonal antibodies has therapeutic effects in diabetic db/db mice. Perfused rodent heart/skeletal muscle, Co-immunoprecipitation and surface plasmon resonance for MG53-insulin receptor extracellular domain interaction, cardiac-specific MG53 transgenic mice, monoclonal antibody neutralization in db/db mice Circulation High 30586741
2019 MG53 modulates G3BP2 activity in non-small cell lung cancer through physical interaction via the TRIM domain of MG53, inducing nuclear translocation of G3BP2 and blocking stress granule formation. Loss of MG53 promotes lung cancer progression; MG53 anti-proliferative effects on NSCLC cells are abolished with G3BP2 knockout. Co-immunoprecipitation for MG53-G3BP2 interaction, shRNA knockdown, live cell imaging, xenograft and allograft tumor models, domain mapping Molecular cancer Medium 34521423
2020 High glucose represses AMPK signaling via MG53 E3-ubiquitin-ligase-mediated AMPKα ubiquitination and degradation. Specifically, high-glucose-stimulated ROS signals AKT to phosphorylate AMPKα at S485/491, which recruits MG53 and triggers ubiquitination and proteasomal degradation of AMPKα. High glucose also deactivates AMPK by ROS-dependent suppression of AMPKα T172 phosphorylation. In vitro ubiquitination assays, phosphomimetic AMPKα mutants, ROS manipulation, AKT inhibitors, MG53 knockdown/overexpression, co-immunoprecipitation Molecular cell High 33400924
2020 MG53 is expressed in human macrophages and suppresses type I interferon (IFNβ) production upon viral infection by inhibiting RyR-mediated intracellular calcium oscillation and subsequent NFκB signaling activation. MG53 knockdown in macrophages increases IFNβ upon infection; MG53 KO mice infected with influenza show elevated IFNβ and increased morbidity. MG53 inhibits IFNβ induction in an RyR-dependent manner. MG53 knockdown in macrophages, MG53 KO mouse infection model, calcium imaging, RyR inhibitor rescue, NFκB reporter assays Nature communications Medium 32681036
2020 Cardiac ischemic preconditioning promotes MG53 secretion through H2O2-evoked activation of protein kinase C-δ (PKC-δ). Specifically, IPC-induced myocardial MG53 secretion is mediated by H2O2-triggered phosphorylation of PKC-δ at Y311, which is necessary and sufficient to facilitate MG53 secretion from cardiomyocytes without causing membrane leakage. Proteomic analysis, pharmacological and genetic manipulation of PKC-δ, Y311 phospho-mutants, rodent in vivo and isolated perfused heart models, neonatal cardiomyocyte culture Circulation High 32677469
2021 MG53 inhibits necroptosis by acting as an E3 ubiquitin ligase that adds ubiquitin chains to RIPK1 at residues K316, K604, and K627, promoting proteasome-mediated RIPK1 degradation. ROS generated during I/R injury promote interaction between MG53 and RIPK1. N-acetylcysteine disrupts the MG53-RIPK1 interaction and abolishes MG53-mediated cardioprotection. Co-immunoprecipitation, CRISPR/Cas9 and mutagenesis to identify ubiquitination sites, Western blotting, antioxidant treatment, hiPSC-derived cardiomyocyte H/R model, I/R mouse model Frontiers in cardiovascular medicine Medium 35711363
2021 MG53 interacts physically with the p65 subunit of NF-κB and can enter the nuclei of proximal tubular epithelial cells to directly suppress NF-κB activation, thereby reducing inflammation and kidney fibrosis. Co-IP of MG53 with p65, nuclear fractionation, MG53 KO and overexpression, unilateral ureteral obstruction model, histology for fibrosis Kidney international Medium 34757120
2021 MG53 interacts with NF-κB pathway components TAK1 and IκBα (by Co-IP) and regulates NF-κB activity, thereby controlling KChIP2 transcription (confirmed by ChIP showing NF-κB binding to KChIP2 gene 5' regulatory region) and the fast transient outward K+ current (Ito,f) in cardiomyocytes. MG53 knockout reduces KChIP2/Ito,f; MG53 overexpression increases it. Co-immunoprecipitation (MG53 with TAK1 and IκBα), chromatin immunoprecipitation for NF-κB at KChIP2 promoter, MG53 KO mice, adenoviral overexpression/knockdown, patch-clamp electrophysiology, pressure-overload cardiac hypertrophy model Circulation Medium 30760025
2022 MG53 binds to cardiolipin (CL), a mitochondria-specific lipid, and translocates to mitochondria after ischemic injury. rhMG53 treatment reduces superoxide generation and inhibits mitophagy in cardiomyocytes, preserving mitochondrial integrity. Lipid-binding assay for cardiolipin, fluorescent imaging of MG53 localization to mitochondria in vivo/in vitro, mt-mKeima mitophagy reporter, superoxide detection Redox biology Medium 35679798
2022 MG53 phosphorylation at serine 255 (S255) by GSK3β is a prerequisite for MG53 E3 ligase activity. Elevated S255 phosphorylation in metabolic disorder models enhances E3 ligase activity, forming a vicious cycle with IR-IRS1-GSK3β-MG53. The S255A mutant eliminates E3 ligase activity while retaining cell-protective membrane repair function, providing cardioprotection in diabetic mice without adverse metabolic effects. Immunoprecipitation-mass spectrometry to identify phosphosite, in vitro kinase assay with GSK3β, S255A site-directed mutagenesis, knock-in mice, db/db diabetic mouse I/R model Circulation research High 36337049
2022 MG53 binds to p53 and promotes its ubiquitination and proteasomal degradation, reducing apoptosis and elevating proliferation in trophoblasts. CVMSC-derived exosomes upregulate TRIM72/MG53 expression, which in turn degrades p53. Co-immunoprecipitation for TRIM72-p53 interaction, ubiquitination assay, luciferase reporter, Western blotting, mRNA sequencing FASEB journal Medium 34788479
2022 MG53 succinylation at K130 suppresses its ubiquitination at the same residue and stabilizes MG53 protein. SIRT7 inhibits and KAT3B promotes succinylation of MG53 at K130; SIRT7 aggravates and KAT3B alleviates MG53-mediated protection against hypoxia/reoxygenation-induced cardiomyocyte injury. The relationship between MG53 and KAT3B or SIRT7 was confirmed by co-IP. Co-immunoprecipitation for MG53-KAT3B and MG53-SIRT7 interactions, IP for succinylation and ubiquitination levels, site-specific mutagenesis at K130 Clinical and experimental hypertension Medium 37848382
2023 Complete crystal structure of Mus musculus TRIM72 (BCC-SPRY domains) reveals the molecular basis of TRIM72 oligomerization, which is closely linked to disulfide bond formation. Phosphatidylserine-enriched membrane interaction is necessary for oligomeric assembly and ubiquitination activity of TRIM72. Cryo-electron tomography and subtomogram averaging elucidated a higher-order TRIM72 assembly on the phospholipid bilayer. TRIM72 also interacts with several other negatively charged lipids beyond phosphatidylserine. Cryo-electron tomography and subtomogram averaging, crystal structure of BCC-SPRY domains, structure-guided mutagenesis, biochemical ubiquitination assays, lipid binding assays Nature communications High 36944613
2023 Crystal structure of mouse TRIM72 (complete RING-B-box-coiled-coil-SPRY model) shows that phosphatidylserine-membrane interaction is necessary for oligomeric assembly and ubiquitination activity. Structure-function study on the membrane identifies key interdomain contacts for RING E3 ligase activation through higher-order assembly on membranes. Cryo-EM structure of full-length TRIM72, biochemical ubiquitination assays, phosphatidylserine binding assays, domain mutagenesis Nature structural & molecular biology High 37770719
2023 MG53 E3 ligase activity mediates K48-linked ubiquitination and proteasomal degradation of cyclin D1, causing G1 cell cycle arrest and suppression of cancer cell proliferation in colorectal and gastric cancer. In vitro ubiquitination assays, K48-linkage specific ubiquitin experiments, MG53 overexpression/knockdown in cancer cells, xenograft tumor models, AOM/DSS colorectal cancer model Signal transduction and targeted therapy Medium 37414783
2023 MG53 directly binds p53 tumor suppressor to regulate its ubiquitination and degradation via the RING E3 ligase domain, thereby preventing DOX-induced ferroptosis by maintaining SLC7A11 and GPX4 levels through the p53/SLC7A11/GPX4 pathway. Co-IP for MG53-p53 interaction, ubiquitination assay, MG53 overexpression and p53 knockdown in cardiomyocytes, in vivo DIC mouse model, cardiac function assessment Free radical biology & medicine Medium 39111582
2023 p55γ recruits MG53 as the E3 ligase to mediate ubiquitin-dependent degradation of RIP3, thereby suppressing ischemia-induced myocardial necroptosis. p55γ directly binds and degrades RIP3 in an MG53-dependent manner; IPC-mediated suppression of necroptosis is attenuated in p55γ-deficient hearts. Co-IP and pulldown assays for p55γ-MG53-RIP3 complex, p55γ transgenic and KO mice, mass spectrometry, ChIP for Hif1α at p55γ promoter, in vivo LAD ligation I/R model Cardiovascular research Medium 37527538
2022 MG53 catalyzes K48-linked polyubiquitination of RAC1 at Lys5 via its coiled-coil domain direct interaction with RAC1, suppressing RAC1 activity and the RAC1-MAPK signaling axis in hepatocellular carcinoma cells. Co-IP for MG53-RAC1 interaction, domain deletion mutants, in vitro ubiquitination assay, K48-specific ubiquitin chains, RAC1 activity assay, xenograft models Oncogenesis Medium 35858925
2022 TRIM72 interacts with and ubiquitinates MGMT (O6-methylguanine DNA methyl transferase) for proteasomal degradation. TRIM72 knockdown increases MGMT protein levels while reducing its ubiquitination; ectopic TRIM72 expression sensitizes uveal melanoma cells to dacarbazine treatment. Co-IP for TRIM72-MGMT interaction, ubiquitination assay, shRNA knockdown, overexpression in UM cells, Western blotting Cancer biomarkers Medium 34958003
2018 TRIM72 physically interacts with complement receptor CRIg in alveolar macrophages (confirmed by pulldown, Co-IP, and gradient binding assays) and inhibits CRIg-mediated phagosome formation, suppressing complement receptor-mediated phagocytosis. Genetic ablation of TRIM72 leads to improved pathogen clearance, reduced cytokine storm, and improved survival in murine pneumonia models. Pulldown assay, Co-immunoprecipitation, gradient binding assay, TRIM72 KO mice, AM adoptive transfer, in vivo Pseudomonas aeruginosa pneumonia model American journal of respiratory cell and molecular biology Medium 29268030
2015 TRIM72 interacts with caveolin-1 (Cav1) in lung epithelial cells; deletion of any functional domain (RING, B-box, coiled-coil, or PRY-SPRY) abolishes the physical TRIM72-Cav1 interaction. TRIM72 loss reduces Cav1 at the plasma membrane and markedly attenuates caveolar endocytosis; TRIM72 overexpression selectively increases caveolar endocytosis. TRIM72 KO and Cav1 KO mice show increased lung cell death after injurious ventilation, with double KO being most severe. Co-immunoprecipitation with domain deletion mutants, caveolar endocytosis assays, lentiviral overexpression, TRIM72 KO and Cav1 KO mice, injurious ventilation model American journal of physiology. Lung cellular and molecular physiology Medium 26637632
2015 MG53 translocates to injury sites on renal proximal tubular cells and binds phosphatidylserine to protect against contrast-induced membrane injury. MG53 translocation from serum to injury sites was shown by immunoblot and immunohistochemical staining in vivo. In vivo rat CI-AKI model with immunoblot and IHC for MG53 translocation, rhMG53 treatment, phosphatidylserine binding confirmation in RPT cells Acta pharmacologica Sinica Low 32424239
2012 TRIM72 binds various lipids in vitro including phosphatidylserine, palmitate, and stearate with Kd values in the nanomolar to submicromolar range. TRIM72 can be dynamically converted by stimuli (fluorescence-quenching changes in conformation reduce lipid binding affinity), suggesting regulated lipid-binding during sarcolemmal repair. In vitro lipid binding assay with fluorescence measurements, Kd determination, time-resolved fluorescence BMB reports Medium 22281009

Source papers

Stage 0 corpus · 100 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2008 MG53 nucleates assembly of cell membrane repair machinery. Nature cell biology 414 19043407
2013 Central role of E3 ubiquitin ligase MG53 in insulin resistance and metabolic disorders. Nature 252 23354051
2009 Membrane repair defects in muscular dystrophy are linked to altered interaction between MG53, caveolin-3, and dysferlin. The Journal of biological chemistry 239 19380584
2012 Recombinant MG53 protein modulates therapeutic cell membrane repair in treatment of muscular dystrophy. Science translational medicine 187 22723464
2010 MG53 constitutes a primary determinant of cardiac ischemic preconditioning. Circulation 182 20516375
2013 MG53-induced IRS-1 ubiquitination negatively regulates skeletal myogenesis and insulin signalling. Nature communications 148 23965929
2010 Cardioprotection of ischemia/reperfusion injury by cholesterol-dependent MG53-mediated membrane repair. Circulation research 145 20466981
2015 MG53-mediated cell membrane repair protects against acute kidney injury. Science translational medicine 128 25787762
2015 Upregulation of MG53 induces diabetic cardiomyopathy through transcriptional activation of peroxisome proliferation-activated receptor α. Circulation 127 25637627
2021 Negative regulation of AMPK signaling by high glucose via E3 ubiquitin ligase MG53. Molecular cell 122 33400924
2014 Treatment of acute lung injury by targeting MG53-mediated cell membrane repair. Nature communications 122 25034454
2008 MG53 regulates membrane budding and exocytosis in muscle cells. The Journal of biological chemistry 111 19029292
2014 Cardioprotection of recombinant human MG53 protein in a porcine model of ischemia and reperfusion injury. Journal of molecular and cellular cardiology 107 25533937
2019 Glucose-Sensitive Myokine/Cardiokine MG53 Regulates Systemic Insulin Response and Metabolic Homeostasis. Circulation 97 30586741
2011 Polymerase transcriptase release factor (PTRF) anchors MG53 protein to cell injury site for initiation of membrane repair. The Journal of biological chemistry 92 21343302
2012 Enhancing muscle membrane repair by gene delivery of MG53 ameliorates muscular dystrophy and heart failure in δ-Sarcoglycan-deficient hamsters. Molecular therapy : the journal of the American Society of Gene Therapy 79 22314291
2011 MG53 participates in ischaemic postconditioning through the RISK signalling pathway. Cardiovascular research 79 21285295
2010 TRIM72 negatively regulates myogenesis via targeting insulin receptor substrate-1. Cell death and differentiation 72 20139895
2015 Modulation of wound healing and scar formation by MG53 protein-mediated cell membrane repair. The Journal of biological chemistry 70 26306047
2022 MG53 preserves mitochondrial integrity of cardiomyocytes during ischemia reperfusion-induced oxidative stress. Redox biology 67 35679798
2019 Sustained elevation of MG53 in the bloodstream increases tissue regenerative capacity without compromising metabolic function. Nature communications 65 31604915
2011 Redox-dependent oligomerization through a leucine zipper motif is essential for MG53-mediated cell membrane repair. American journal of physiology. Cell physiology 63 21525429
2021 MG53 suppresses tumor progression and stress granule formation by modulating G3BP2 activity in non-small cell lung cancer. Molecular cancer 62 34521423
2009 Mitsugumin 53 (MG53) facilitates vesicle trafficking in striated muscle to contribute to cell membrane repair. Communicative & integrative biology 62 19641737
2012 Nonmuscle myosin IIA facilitates vesicle trafficking for MG53-mediated cell membrane repair. FASEB journal : official publication of the Federation of American Societies for Experimental Biology 61 22253476
2019 MG53 attenuates lipopolysaccharide-induced neurotoxicity and neuroinflammation via inhibiting TLR4/NF-κB pathway in vitro and in vivo. Progress in neuro-psychopharmacology & biological psychiatry 58 31260721
2016 MG53 permeates through blood-brain barrier to protect ischemic brain injury. Oncotarget 58 26967557
2014 S-nitrosylation of TRIM72 at cysteine 144 is critical for protection against oxidation-induced protein degradation and cell death. Journal of molecular and cellular cardiology 58 24487118
2020 MG53 suppresses interferon-β and inflammation via regulation of ryanodine receptor-mediated intracellular calcium signaling. Nature communications 53 32681036
2013 Mitsugumin 53 (MG53) ligase ubiquitinates focal adhesion kinase during skeletal myogenesis. The Journal of biological chemistry 46 24344130
2020 MG53 Does Not Manifest the Development of Diabetes in db/db Mice. Diabetes 45 32139593
2020 Cardiac Ischemic Preconditioning Promotes MG53 Secretion Through H2O2-Activated Protein Kinase C-δ Signaling. Circulation 45 32677469
2019 MG53 promotes corneal wound healing and mitigates fibrotic remodeling in rodents. Communications biology 45 30793049
2021 MG53 suppresses NF-κB activation to mitigate age-related heart failure. JCI insight 44 34292883
2019 MG53, A Novel Regulator of KChIP2 and Ito,f, Plays a Critical Role in Electrophysiological Remodeling in Cardiac Hypertrophy. Circulation 44 30760025
2017 Treatment with Recombinant Human MG53 Protein Increases Membrane Integrity in a Mouse Model of Limb Girdle Muscular Dystrophy 2B. Molecular therapy : the journal of the American Society of Gene Therapy 44 28750735
2017 MG53 anchored by dysferlin to cell membrane reduces hepatocyte apoptosis which induced by ischaemia/reperfusion injury in vivo and in vitro. Journal of cellular and molecular medicine 43 28401647
2013 Hypercholesterolemia blocked sevoflurane-induced cardioprotection against ischemia-reperfusion injury by alteration of the MG53/RISK/GSK3β signaling. International journal of cardiology 43 23856444
2021 MG53, A Tissue Repair Protein with Broad Applications in Regenerative Medicine. Cells 41 33440658
2022 MG53 protein rejuvenates hUC-MSCs and facilitates their therapeutic effects in AD mice by activating Nrf2 signaling pathway. Redox biology 37 35525026
2019 TRIM72 contributes to cardiac fibrosis via regulating STAT3/Notch-1 signaling. Journal of cellular physiology 37 30820965
2014 TRIM72 is required for effective repair of alveolar epithelial cell wounding. American journal of physiology. Lung cellular and molecular physiology 35 25106429
2022 Mesenchymal stem cells-derived exosomes prevent sepsis-induced myocardial injury by a CircRTN4/miR-497-5p/MG53 pathway. Biochemical and biophysical research communications 34 35724457
2015 Amelioration of ischemia-reperfusion-induced muscle injury by the recombinant human MG53 protein. Muscle & nerve 34 25703692
2024 MG53 inhibits ferroptosis by targeting the p53/SLC7A11/GPX4 pathway to alleviate doxorubicin-induced cardiotoxicity. Free radical biology & medicine 33 39111582
2020 MG53 Protects against Sepsis-Induced Myocardial Dysfunction by Upregulating Peroxisome Proliferator-Activated Receptor-α. Oxidative medicine and cellular longevity 33 32908637
2010 TRIM72, a novel negative feedback regulator of myogenesis, is transcriptionally activated by the synergism of MyoD (or myogenin) and MEF2. Biochemical and biophysical research communications 32 20399744
2017 MG53: Biological Function and Potential as a Therapeutic Target. Molecular pharmacology 31 28432201
2015 Zinc Binding to MG53 Protein Facilitates Repair of Injury to Cell Membranes. The Journal of biological chemistry 31 25869134
2012 The C2A domain in dysferlin is important for association with MG53 (TRIM72). PLoS currents 31 23145354
2021 The cell membrane repair protein MG53 modulates transcription factor NF-κB signaling to control kidney fibrosis. Kidney international 30 34757120
2023 E3 ligase MG53 suppresses tumor growth by degrading cyclin D1. Signal transduction and targeted therapy 29 37414783
2021 Membrane-delimited signaling and cytosolic action of MG53 preserve hepatocyte integrity during drug-induced liver injury. Journal of hepatology 29 34736969
2020 MG53 protects against contrast-induced acute kidney injury by reducing cell membrane damage and apoptosis. Acta pharmacologica Sinica 27 32424239
2023 Structure and activation of the RING E3 ubiquitin ligase TRIM72 on the membrane. Nature structural & molecular biology 26 37770719
2021 Muscle multiorgan crosstalk with MG53 as a myokine for tissue repair and regeneration. Current opinion in pharmacology 26 34052525
2016 Dual function of MG53 in membrane repair and insulin signaling. BMB reports 26 27174502
2013 Compensation of the AKT signaling by ERK signaling in transgenic mice hearts overexpressing TRIM72. Experimental cell research 26 23567182
2022 MG53 Inhibits Necroptosis Through Ubiquitination-Dependent RIPK1 Degradation for Cardiac Protection Following Ischemia/Reperfusion Injury. Frontiers in cardiovascular medicine 23 35711363
2022 The E3 ubiquitin ligase MG53 inhibits hepatocellular carcinoma by targeting RAC1 signaling. Oncogenesis 23 35858925
2021 Cardiac effects and clinical applications of MG53. Cell & bioscience 23 34183055
2018 Inhibition of Macrophage Complement Receptor CRIg by TRIM72 Polarizes Innate Immunity of the Lung. American journal of respiratory cell and molecular biology 23 29268030
2018 Inhaled TRIM72 Protein Protects Ventilation Injury to the Lung through Injury-guided Cell Repair. American journal of respiratory cell and molecular biology 23 29958015
2023 Structural basis for TRIM72 oligomerization during membrane damage repair. Nature communications 22 36944613
2022 Blocking MG53S255 Phosphorylation Protects Diabetic Heart From Ischemic Injury. Circulation research 22 36337049
2020 TRIM72 promotes alveolar epithelial cell membrane repair and ameliorates lung fibrosis. Respiratory research 22 32471489
2020 MG53 Protects hUC-MSCs against Inflammatory Damage and Synergistically Enhances Their Efficacy in Neuroinflammation Injured Brain through Inhibiting NLRP3/Caspase-1/IL-1β Axis. ACS chemical neuroscience 22 32786312
2018 Role of a TRIM72 ADP-ribosylation cycle in myocardial injury and membrane repair. JCI insight 22 30429362
2015 TRIM72 modulates caveolar endocytosis in repair of lung cells. American journal of physiology. Lung cellular and molecular physiology 22 26637632
2023 p55γ degrades RIP3 via MG53 to suppress ischaemia-induced myocardial necroptosis and mediates cardioprotection of preconditioning. Cardiovascular research 21 37527538
2022 MG53 E3 Ligase-Dead Mutant Protects Diabetic Hearts From Acute Ischemic/Reperfusion Injury and Ameliorates Diet-Induced Cardiometabolic Damage. Diabetes 21 34844991
2017 MG53 is dispensable for T-tubule maturation but critical for maintaining T-tubule integrity following cardiac stress. Journal of molecular and cellular cardiology 21 28822805
2021 MG53 is not a critical regulator of insulin signaling pathway in skeletal muscle. PloS one 20 33566837
2023 TRIM72 Alleviates Muscle Inflammation in mdx Mice via Promoting Mitophagy-Mediated NLRP3 Inflammasome Inactivation. Oxidative medicine and cellular longevity 19 36713032
2023 MG53 alleviates hypoxia/reoxygenation-induced cardiomyocyte injury by succinylation and ubiquitination modification. Clinical and experimental hypertension (New York, N.Y. : 1993) 19 37848382
2021 MG53 as a Novel Therapeutic Protein to Treat Acute Lung Injury. Military medicine 19 33499468
2020 Autoantibodies targeting TRIM72 compromise membrane repair and contribute to inflammatory myopathy. The Journal of clinical investigation 19 32687067
2017 Potential role of MG53 in the regulation of transforming-growth-factor-β1-induced atrial fibrosis and vulnerability to atrial fibrillation. Experimental cell research 18 29233682
2024 MG53/TRIM72: multi-organ repair protein and beyond. Frontiers in physiology 17 38681139
2022 MG53 attenuates nitrogen mustard-induced acute lung injury. Journal of cellular and molecular medicine 17 35199443
2019 MG53 Inhibits the Progression of Tongue Cancer Cells through Regulating PI3K-AKT Signaling Pathway: Evidence from 3D Cell Culture and Animal Model. Small (Weinheim an der Bergstrasse, Germany) 17 30690890
2021 MG53 inhibits angiogenesis through regulating focal adhesion kinase signalling. Journal of cellular and molecular medicine 16 34240802
2018 Serum Levels of TRIM72 Are Lower among Patients with Colon Cancer: Identification of a Potential Diagnostic Marker. The Tohoku journal of experimental medicine 16 29806630
2011 Visualization of MG53-mediated cell membrane repair using in vivo and in vitro systems. Journal of visualized experiments : JoVE 16 21750489
2023 Potentilla anserina polysaccharide alleviates cadmium-induced oxidative stress and apoptosis of H9c2 cells by regulating the MG53-mediated RISK pathway. Chinese journal of natural medicines 15 37120246
2021 MG53 Preserves Neuromuscular Junction Integrity and Alleviates ALS Disease Progression. Antioxidants (Basel, Switzerland) 15 34679657
2020 LncRNA AK045171 protects the heart from cardiac hypertrophy by regulating the SP1/MG53 signalling pathway. Aging 15 32087602
2020 Serum MG53/TRIM72 Is Associated With the Presence and Severity of Coronary Artery Disease and Acute Myocardial Infarction. Frontiers in physiology 15 33391037
2016 MG53-IRS-1 (Mitsugumin 53-Insulin Receptor Substrate-1) Interaction Disruptor Sensitizes Insulin Signaling in Skeletal Muscle. The Journal of biological chemistry 15 27810898
2020 MG53/CAV1 regulates transforming growth factor-β1 signaling-induced atrial fibrosis in atrial fibrillation. Cell cycle (Georgetown, Tex.) 14 33000676
2019 TRIM72 Immunohistochemical Expression Can Predict Relapse in Colorectal Carcinoma. Pathology oncology research : POR 14 30852740
2012 Lipid-binding properties of TRIM72. BMB reports 14 22281009
2024 MLL1 promotes placental trophoblast ferroptosis and aggravates preeclampsia symptoms through epigenetic regulation of RBM15/TRIM72/ADAM9 axis. Biology direct 13 39709463
2023 MG53 ameliorates nerve injury induced neuropathic pain through the regulation of Nrf2/HO-1 signaling in rats. Behavioural brain research 13 37169128
2022 Ubiquitination and degradation of MGMT by TRIM72 increases the sensitivity of uveal melanoma cells to Dacarbazine treatment. Cancer biomarkers : section A of Disease markers 13 34958003
2021 Chorionic villus-derived mesenchymal stem cells induce E3 ligase TRIM72 expression and regulate cell behaviors through ubiquitination of p53 in trophoblasts. FASEB journal : official publication of the Federation of American Societies for Experimental Biology 13 34788479
2019 N-acetylcysteine prevents oxidized low-density lipoprotein-induced reduction of MG53 and enhances MG53 protective effect on bone marrow stem cells. Journal of cellular and molecular medicine 13 31742908
2014 Effect of recombinant human MG53 protein on tourniquet-induced ischemia-reperfusion injury in rat muscle. Muscle & nerve 13 24395153
2022 Protective role of MG53 against ischemia/reperfusion injury on multiple organs: A narrative review. Frontiers in physiology 12 36479346
2018 An MG53-IRS1-interaction disruptor ameliorates insulin resistance. Experimental & molecular medicine 12 29884820

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