ArticleeLife2020
Structure and activation mechanism of the BBSome membrane protein trafficking complex.
Article in eLife, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers.
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Who cites it
51 citing papers in PubMed, 88 citations in OpenAlex.
- Primary cilia: master conductors of cellular communication in development and disease.Nature reviews. Nephrology · 2026Review
- BBS5 as a robust prognostic biomarker in esophageal squamous cell carcinoma: validation in two independent cohorts.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2026Article
- Primary Cilia as Integrative Hubs of Metabolic Signaling in Type 2 Diabetes: Inter-Organ Evidence From Central, Peripheral, and Pancreatic Islet Tissues.Journal of cellular physiology · 2026Review
- Bardet-Biedl syndrome 1 mutations differentially impact BBSome integrity and ciliary trafficking.Cell communication and signaling : CCS · 2026Article
- BBSome: An essential component of hypothalamic regulation of energy homeostasis.Reviews in endocrine & metabolic disorders · 2026Review
- Proteome-widebioRxiv : the preprint server for biology · 2025Article
- Phosphoproteomic profiling highlights CDC42 and CDK2 as key players in the regulation of the TGF-β pathway in ALMS1 and BBS1 knockout models.Scientific reports · 2025Article
- Homology search confirms widespread presence of BBSome proteins in Hexapoda with implications for potential non-ciliary BBS protein functions in honey bees.Scientific reports · 2025Article
- Computational Evidence for Digenic Contribution ofInternational journal of molecular sciences · 2025Article
- FGFR2 residence in primary cilia is necessary for epithelial cell signaling.The Journal of cell biology · 2025Article
- The intraflagellar transport cycle.Nature reviews. Molecular cell biology · 2025Review
- Article
- BBSome deficiency in Lotmaria passim reveals divergent functions in trypanosomatid parasites.Parasites & vectors · 2025Article
- N-Acetylcysteine Ameliorates Loss of the Electroretinogram b-wave in a Bardet-Biedl Syndrome Type 10 Mouse Model.Journal of experimental neurology · 2025Article
- Ccrk-Mak/Ick signaling is a ciliary transport regulator essential for retinal photoreceptor survival.Life science alliance · 2024Article
- Protein subcellular relocalization and function of duplicated flagellar calcium binding protein genes in honey bee trypanosomatid parasite.PLoS genetics · 2024Article
- The exocyst complex and intracellular vesicles mediate soluble protein trafficking to the primary cilium.Communications biology · 2024Article
- Review
- Primary cilia in Parkinson's disease: summative roles in signaling pathways, genes, defective mitochondrial function, and substantia nigra dopaminergic neurons.Frontiers in aging neuroscience · 2024Review
- Article
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Bardet-Biedl syndrome (BBS) is a currently incurable ciliopathy caused by the failure to correctly establish or maintain cilia-dependent signaling pathways. Eight proteins associated with BBS assemble into the BBSome, a key regulator of the ciliary membrane proteome. We report the electron cryomicroscopy (cryo-EM) structures of the native bovine BBSome in inactive and active states at 3.1 and 3.5 Å resolution, respectively. In the active state, the BBSome is bound to an Arf-family GTPase (ARL6/BBS3) that recruits the BBSome to ciliary membranes. ARL6 recognizes a composite binding site formed by BBS1 and BBS7 that is occluded in the inactive state. Activation requires an unexpected swiveling of the β-propeller domain of BBS1, the subunit most frequently implicated in substrate recognition, which widens a central cavity of the BBSome. Structural mapping of disease-causing mutations suggests that pathogenesis results from folding defects and the disruption of autoinhibition and activation.
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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.