ArticleHuman molecular genetics2009
TRIM32 is an E3 ubiquitin ligase for dysbindin.
Article in Human molecular genetics, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 83 papers.
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Who cites it
83 citing papers in PubMed, 144 citations in OpenAlex.
- West Nile Virus Exploits miR-155-5p-Mediated Regulation of TRIM32-IκBα Axis to Evade NF-κB-Mediated Innate Immune Responses in Human Microglial Cells.Molecular neurobiology · 2026Article
- TRIM32-mediated ubiquitination of STING promotes glycolysis and tumor progression.Cell death and differentiation · 2026Article
- TRIM28 and TRIM32: multifaceted regulators of innate immunity and antiviral defence.Immunologic research · 2026Review
- Emerging Role and Potential Therapeutic Application of TRIM Proteins in Cardiovascular Diseases.Biomolecules · 2026Review
- Supercharging-enhanced nDIA-MS enables global profiling of drug-induced proteome solubility shifts.Nature communications · 2026Article
- Degrons: defining the rules of protein degradation.Nature reviews. Molecular cell biology · 2025Review
- Investigating genotype-phenotype correlation of limb-girdle muscular dystrophy R8: association of clinical severity, protein biological function and protein oligomerization.Acta neuropathologica communications · 2025Article
- Research on the Effect and Mechanism of Selenium on Colorectal Cancer Through TRIM32.Biological trace element research · 2025Article
- TRIM32 inhibits Venezuelan equine encephalitis virus infection by targeting a late step in viral entry.PLoS pathogens · 2024Article
- TRIM32 inhibits Venezuelan Equine Encephalitis Virus Infection by targeting a late step in viral entry.bioRxiv : the preprint server for biology · 2024Article
- Review
- TRIM32 biallelic defects cause limb-girdle muscular dystrophy R8: identification of two novel mutations and investigation of genotype-phenotype correlation.Skeletal muscle · 2023Article
- Modelling renal defects in Bardet-Biedl syndrome patients using human iPS cells.Frontiers in cell and developmental biology · 2023Article
- Misfolding of fukutin-related protein (FKRP) variants in congenital and limb girdle muscular dystrophies.Frontiers in molecular biosciences · 2023Article
- The Notch signaling pathway in skeletal muscle health and disease.Muscle & nerve · 2022Review
- RING-finger E3 ligases regulatory network in PI3K/AKT-mediated glucose metabolism.Cell death discovery · 2022Review
- The E3 ligase Thin controls homeostatic plasticity through neurotransmitter release repression.eLife · 2022Article
- BBSome: a New Player in Hypertension and Other Cardiovascular Risks.Hypertension (Dallas, Tex. : 1979) · 2022Review
- Article
- Tumor suppressor p53 cross-talks with TRIM family proteins.Genes & diseases · 2021Review
23 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Mutations in the gene encoding tripartite motif protein 32 (TRIM32) cause two seemingly diverse diseases: limb-girdle muscular dystrophy type 2H (LGMD2H) or sarcotubular myopathy (STM) and Bardet-Biedl syndrome type 11(BBS11). Although TRIM32 is involved in protein ubiquitination, its substrates and the molecular consequences of disease-causing mutations are poorly understood. In this paper, we show that TRIM32 is a widely expressed ubiquitin ligase that is localized to the Z-line in skeletal muscle. Using the yeast two-hybrid system, we found that TRIM32 binds and ubiquitinates dysbindin, a protein implicated in the genetic aetiology of schizophrenia, augmenting its degradation. Small-interfering RNA-mediated knock-down of TRIM32 in myoblasts resulted in elevated levels of dysbindin. Importantly, the LGMD2H/STM-associated TRIM32 mutations, D487N and R394H impair ubiquitin ligase activity towards dysbindin and were mislocalized in heterologous cells. These mutants were able to self-associate and also co-immunoprecipitated with wild-type TRIM32 in transfected cells. Furthermore, the D487N mutant could bind to both dysbindin and its E2 enzyme but was defective in monoubiquitination. In contrast, the BBS11 mutant P130S did not show any biochemical differences compared with the wild-type protein. Our data identify TRIM32 as a regulator of dysbindin and demonstrate that the LGMD2H/STM mutations may impair substrate ubiquitination.
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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.