ArticleHuman molecular genetics2015
The E3 ubiquitin ligase TRIM32 regulates myoblast proliferation by controlling turnover of NDRG2.
Article in Human molecular genetics, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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Who cites it
30 citing papers in PubMed, 41 citations in OpenAlex.
- Investigating genotype-phenotype correlation of limb-girdle muscular dystrophy R8: association of clinical severity, protein biological function and protein oligomerization.Acta neuropathologica communications · 2025Article
- Erythropoietin regulates energy metabolism through EPO-EpoR-RUNX1 axis.Nature communications · 2024Article
- Epigenetics of Genes Preferentially Expressed in Dissimilar Cell Populations: Myoblasts and Cerebellum.Epigenomes · 2024Article
- Review
- Review
- E3 ligase Deltex2 accelerates myoblast proliferation and inhibits myoblast differentiation by targeting Pax7 and MyoD, respectively.Acta biochimica et biophysica Sinica · 2023Article
- Integrated transcriptomic and proteomic analysis reveals potential targets for heart regeneration.Biomolecules & biomedicine · 2023Article
- Identification of Ubiquitination-Associated Proteins Using 2D-DIGE.Methods in molecular biology (Clifton, N.J.) · 2023Article
- Mammalian Target of Rapamycin (mTOR) Signaling at the Crossroad of Muscle Fiber Fate in Sarcopenia.International journal of molecular sciences · 2022Review
- Molecular and cellular basis of genetically inherited skeletal muscle disorders.Nature reviews. Molecular cell biology · 2021Review
- Review
- TRIM32: A Multifunctional Protein Involved in Muscle Homeostasis, Glucose Metabolism, and Tumorigenesis.Biomolecules · 2021Review
- Ubiquitin Ligases at the Heart of Skeletal Muscle Atrophy Control.Molecules (Basel, Switzerland) · 2021Review
- Article
- Biochemical characterization of TRIM72 E3 ligase and its interaction with the insulin receptor substrate 1.Biochemistry and biophysics reports · 2020Article
- Impaired Regeneration in Dystrophic Muscle-New Target for Therapy.Frontiers in molecular neuroscience · 2020Article
- TRIM proteins in neuroblastoma.Bioscience reports · 2019Review
- ER Stress Induces Cell Cycle Arrest at the G2/M Phase Through eIF2α Phosphorylation and GADD45α.International journal of molecular sciences · 2019Article
- Characterization of Contractile Proteins from Skeletal Muscle Using Gel-Based Top-Down Proteomics.Proteomes · 2019Review
- Autophagy induction in atrophic muscle cells requires ULK1 activation by TRIM32 through unanchored K63-linked polyubiquitin chains.Science advances · 2019Article
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Limb girdle muscular dystrophy 2H is caused by mutations in the gene encoding the E3 ubiquitin ligase, TRIM32. Previously, we generated and characterized a Trim32 knockout mouse (T32KO) that displays both neurogenic and myopathic features. The myopathy in these mice is attributable to impaired muscle growth, associated with satellite cell senescence and premature sarcopenia. This satellite cell senescence is due to accumulation of the SUMO ligase PIASy, a substrate of TRIM32. The goal of this investigation was to identify additional substrates of TRIM32 using 2D fluorescence difference gel electrophoresis (2D-DIGE) in order to further explore its role in skeletal muscle. Because TRIM32 is an E3 ubiquitin ligase, we reasoned that TRIM32's substrates would accumulate in its absence. 2D-DIGE identified 19 proteins that accumulate in muscles from the T32KO mouse. We focused on two of these proteins, NDRG2 and TRIM72, due to their putative roles in myoblast proliferation and myogenesis. Follow-up analysis confirmed that both proteins were ubiquitinated by TRIM32 in vitro; however, only NDRG2 accumulated in skeletal muscle and myoblasts in the absence of TRIM32. NDRG2 overexpression in myoblasts led to reduced cell proliferation and delayed cell cycle withdrawal during differentiation. Thus, we identified NDRG2 as a novel target for TRIM32; these findings further corroborate the hypothesis that TRIM32 is involved in control of myogenic cells proliferation and differentiation.
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