ArticleThe Journal of cell biology2024
Sec23IP recruits VPS13B/COH1 to ER exit site-Golgi interface for tubular ERGIC formation.
Article in The Journal of cell biology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed.
- Remaking an exit: dynamic regulation of ER exit sites by post-translational modifications.Trends in cell biology · 2026Review
- The ER-Golgi intermediate compartment: a central hub integrating membrane trafficking and stress responses.EMBO reports · 2026Review
- Article
- An ER-IMC bridge protein TgVPS13A and an IMC-resident scramblase TgDAT1 drive daughter budding in Toxoplasma gondii.PLoS pathogens · 2026Article
- Cohen syndrome with novel VPS13B variants presenting as early-onset diabetes: a case report.Acta diabetologica · 2026Article
- VPS13B, gene responsible for Cohen syndrome, regulates gingival epithelial barrier function via intracellular trafficking of coxsackievirus and adenovirus receptor.Scientific reports · 2026Article
- Beyond Vesicular Traffic: The ERES as the Gateway for Biosynthetic Secretion.Sub-cellular biochemistry · 2026Review
- Dynamic O-GlcNAcylation of Sec23-interacting protein regulates COPII function.bioRxiv : the preprint server for biology · 2025Article
- Sec14L6 is a phosphoinositide transporter that regulates phosphoinositide homeostasis and biogenesis of lipid droplets.Nature communications · 2025Article
- Effects of Freeze-Dried Sake Lees and Rice Koji Extract on Osteoporosis in a Postmenopausal Mouse Model.Nutrients · 2025Article
- VPS13 and bridge-like lipid transporters, mechanisms, and mysteries.Frontiers in neuroscience · 2025Review
- VPS13B is localized at the interface between Golgi cisternae and is a functional partner of FAM177A1.The Journal of cell biology · 2024Article
- Small GTPase ActIvitY ANalyzing (SAIYAN) system: A method to detect GTPase activation in living cells.The Journal of cell biology · 2024Article
Corrections and comments
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Authors and funding
7 authors.
Funding
Abstract
VPS13B/COH1 is the only known causative factor for Cohen syndrome, an early-onset autosomal recessive developmental disorder with intellectual inability, developmental delay, joint hypermobility, myopia, and facial dysmorphism as common features, but the molecular basis of VPS13B/COH1 in pathogenesis remains largely unclear. Here, we identify Sec23 interacting protein (Sec23IP) at the ER exit site (ERES) as a VPS13B adaptor that recruits VPS13B to ERES-Golgi interfaces. VPS13B interacts directly with Sec23IP via the VPS13 adaptor binding domain (VAB), and the interaction promotes the association between ERES and the Golgi. Disease-associated missense mutations of VPS13B-VAB impair the interaction with Sec23IP. Knockout of VPS13B or Sec23IP blocks the formation of tubular ERGIC, an unconventional cargo carrier that expedites ER-to-Golgi transport. In addition, depletion of VPS13B or Sec23IP delays ER export of procollagen, suggesting a link between procollagen secretion and joint laxity in patients with Cohen disease. Together, our study reveals a crucial role of VPS13B-Sec23IP interaction at the ERES-Golgi interface in the pathogenesis of Cohen syndrome.
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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 Socratic graph.