ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2024
Tight Junction Component Occludin Binds to FIP5 to Regulate Endosome Trafficking and Mitotic Spindle Function.
Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- Leptomeningeal metastatic cancer cells induce a permissive choroid plexus vasculature through extracellular-vesicle-derived 5-HIAA signaling.Nature cancer · 2026Article
- TRIM68 regulates ubiquitinated degradation of Rabex-5 and plays a role in progression of breast cancer through Rab5-Rac1.American journal of cancer research · 2026Article
- Occludin acts as a dynein adaptor regulating permeability and collateral angiogenesis.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Tight junction proteins in glial tumors development and progression.Frontiers in cellular neuroscience · 2025Review
- Tight Junction Component Occludin Binds to FIP5 to Regulate Endosome Trafficking and Mitotic Spindle Function.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
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Authors and funding
8 authors.
Funding
Abstract
The genetic basis of vertebrate emergence during metazoan evolution has remained largely unknown. Understanding vertebrate-specific genes, such as the tight junction protein Occludin (Ocln), may help answer this question. Here, it is shown that mammary glands lacking Ocln exhibit retarded epithelial branching, owing to reduced cell proliferation and surface expansion. Interestingly, Ocln regulates mitotic spindle orientation and function, and its loss leads to a range of defects, including prolonged prophase and failed nuclear and/or cytoplasmic division. Mechanistically, Ocln binds to the RabGTPase-11 adaptor FIP5 and recruits recycling endosomes to the centrosome to participate in spindle assembly and function. FIP5 loss recapitulates Ocln null, leading to prolonged prophase, reduced cell proliferation, and retarded epithelial branching. These results identify a novel role in OCLN-mediated endosomal trafficking and potentially highlight its involvement in mediating membranous vesicle trafficking and function, which is evolutionarily conserved and essential.
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Registered trials
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