ArticleeLife2021
TRIM37 prevents formation of centriolar protein assemblies by regulating Centrobin.
Article in eLife, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 29 citations in OpenAlex.
- Cumulative microscopy reveals cellular states in fibroblasts from patients with genetic disorders.EMBO reports · 2026Article
- CDK1 and CEP97 cooperatively control centriole length to orchestrate ciliogenesis and developmental patterning.Genes & development · 2026Article
- Sensing centrosome amplification: the interface between centriole duplication and autophagy.Nature communications · 2026Article
- Mulibrey Nanism: Clinical Spectrum and Molecular Pathogenesis.International journal of molecular sciences · 2026Review
- Development of the fluorescent probe CenSpark for labeling centrioles and cilia.Nature chemical biology · 2026Article
- Centriolar satellites regulatebioRxiv : the preprint server for biology · 2026Article
- TRIM37 recognizes a bipartite degron to ubiquitinate centrosome substrates.bioRxiv : the preprint server for biology · 2025Article
- A GPER-PKA-Centrin axis regulates centrosome numbers and centriole integrity in colon cancer cells.Communications biology · 2025Article
- PLK4: Master Regulator of Centriole Duplication and Its Therapeutic Potential.Cytoskeleton (Hoboken, N.J.) · 2025Review
- TRIMming centrosomal assemblies.Nature structural & molecular biology · 2025Article
- TRIM37 prevents ectopic spindle pole assembly by peptide motif recognition and substrate-dependent oligomerization.Nature structural & molecular biology · 2025Article
- Mesoscale regulation of microtubule-organizing centers by the E3 ligase TRIM37.Nature structural & molecular biology · 2025Article
- The crosstalk between non-coding RNAs and oxidative stress in cancer progression.Genes & diseases · 2025Review
- Skeletal Phenotype in Mulibrey Nanism, A Monogenic Skeletal Dysplasia With Fibrous Dysplasia.Clinical genetics · 2025Article
- CRISPR screens reveal convergent targeting strategies against evolutionarily distinct chemoresistance in cancer.Nature communications · 2024Article
- Centriole elimination during Caenorhabditis elegans oogenesis initiates with loss of the central tube protein SAS-1.The EMBO journal · 2023Article
- Towards understanding centriole elimination.Open biology · 2023Review
- The TRIM37 variants in Mulibrey nanism patients paralyze follicular helper T cell differentiation.Cell discovery · 2023Article
- Article
- Global cellular response to chemical perturbation of PLK4 activity and abnormal centrosome number.eLife · 2022Article
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Authors and funding
10 authors at 3 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
TRIM37 is an E3 ubiquitin ligase mutated in Mulibrey nanism, a disease with impaired organ growth and increased tumor formation. TRIM37 depletion from tissue culture cells results in supernumerary foci bearing the centriolar protein Centrin. Here, we characterize these centriolar protein assemblies (Cenpas) to uncover the mechanism of action of TRIM37. We find that an atypical de novo assembly pathway can generate Cenpas that act as microtubule-organizing centers (MTOCs), including in Mulibrey patient cells. Correlative light electron microscopy reveals that Cenpas are centriole-related or electron-dense structures with stripes. TRIM37 regulates the stability and solubility of Centrobin, which accumulates in elongated entities resembling the striped electron dense structures upon TRIM37 depletion. Furthermore, Cenpas formation upon TRIM37 depletion requires PLK4, as well as two parallel pathways relying respectively on Centrobin and PLK1. Overall, our work uncovers how TRIM37 prevents Cenpas formation, which would otherwise threaten genome integrity.
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