ArticleCell death and differentiation2020
Trim32 suppresses cerebellar development and tumorigenesis by degrading Gli1/sonic hedgehog signaling.
Article in Cell death and differentiation, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 17 citations in OpenAlex.
- TRIM32 drives head and neck squamous cell carcinoma progression via TP53 suppression and lysosomal/autophagy dysregulation.Translational cancer research · 2026Article
- Emerging roles for E3 ubiquitin ligases in neural development and disease.Frontiers in cell and developmental biology · 2025Review
- Article
- CDK2-activated TRIM32 phosphorylation and nuclear translocation promotes radioresistance in triple-negative breast cancer.Journal of advanced research · 2024Article
- Review
- It's a TRIM-endous view from the top: the varied roles of TRIpartite Motif proteins in brain development and disease.Frontiers in molecular neuroscience · 2023Review
- TRIM32 Inhibition Attenuates Apoptosis, Oxidative Stress, and Inflammatory Injury in Podocytes Induced by High Glucose by Modulating the Akt/GSK-3β/Nrf2 Pathway.Inflammation · 2022Article
- TRIM32 promotes radioresistance by disrupting TC45-STAT3 interaction in triple-negative breast cancer.Oncogene · 2022Article
- Up-Regulation of TRIM32 Associated With the Poor Prognosis of Acute Myeloid Leukemia by Integrated Bioinformatics Analysis With External Validation.Frontiers in oncology · 2022Article
- Deficiency of TRIM32 Impairs Motor Function and Purkinje Cells in Mid-Aged Mice.Frontiers in aging neuroscience · 2021Article
- Generation of the short TRIM32 isoform is regulated by Lys 247 acetylation and a PEST sequence.PloS one · 2021Article
- Common germline-somatic variant interactions in advanced urothelial cancer.Nature communications · 2020Article
- Emerging Strategies Targeting Catabolic Muscle Stress Relief.International journal of molecular sciences · 2020Review
- E3 Ubiquitin Ligases in Neurological Diseases: Focus on Gigaxonin and Autophagy.Frontiers in physiology · 2020Review
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Sonic hedgehog (SHH) signaling is crucial for the maintenance of the physiological self-renewal of granule neuron progenitor cells (GNPs) during cerebellar development, and its dysregulation leads to oncogenesis. However, how SHH signaling is controlled during cerebellar development is poorly understood. Here, we show that Trim32, a cell fate determinant, is distributed asymmetrically in the cytoplasm of mitotic GNPs, and that genetic knockout of Trim32 keeps GNPs at a proliferating and undifferentiated state. In addition, Trim32 knockout enhances the incidence of medulloblastoma (MB) formation in the Ptch1 mutant mice. Mechanistically, Trim32 binds to Gli1, an effector of SHH signaling, via its NHL domain and degrades the latter through its RING domain to antagonize the SHH pathway. These findings provide a novel mechanism that Trim32 may be a vital cell fate regulator by antagonizing the SHH signaling to promote GNPs differentiation and a tumor suppressor in MB formation.
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Registered trials
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