ArticleThe Journal of biological chemistry2010
Bardet-Biedl syndrome-associated small GTPase ARL6 (BBS3) functions at or near the ciliary gate and modulates Wnt signaling.
Article in The Journal of biological chemistry, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 69 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
69 citing papers in PubMed, 111 citations in OpenAlex.
- Structure Makes a Difference: IFT Complex in Ciliary Function and Ciliopathy.Cytoskeleton (Hoboken, N.J.) · 2026Review
- Delivery of intraflagellar transport proteins to the ciliary base and assembly into trains.Science advances · 2025Article
- Genetic Contributions to Lower Urinary Tract Dysfunction.American journal of medical genetics. Part A · 2025Article
- The Arf family GTPases: Regulation of vesicle biogenesis and beyond.BioEssays : news and reviews in molecular, cellular and developmental biology · 2023Review
- Targeting small GTPases: emerging grasps on previously untamable targets, pioneered by KRAS.Signal transduction and targeted therapy · 2023Review
- Recent advances in the understanding of cilia mechanisms and their applications as therapeutic targets.Frontiers in molecular biosciences · 2023Review
- The complex relationship of Wnt-signaling pathways and cilia.Current topics in developmental biology · 2023Article
- ARL3 mediates BBSome ciliary turnover by promoting its outward movement across the transition zone.The Journal of cell biology · 2022Article
- Specialization of the photoreceptor transcriptome byProceedings of the National Academy of Sciences of the United States of America · 2022Article
- Phylogenetic profiling and cellular analyses of ARL16 reveal roles in traffic of IFT140 and INPP5E.Molecular biology of the cell · 2022Article
- Primary Cilia in Pancreatic β- and α-Cells: Time to Revisit the Role of Insulin-Degrading Enzyme.Frontiers in endocrinology · 2022Review
- Review
- ARL3, a small GTPase with a functionally conserved role in primary cilia and immune synapses.Small GTPases · 2021Review
- Article
- Primary Cilia Formation Does Not Rely on WNT/β-Catenin Signaling.Frontiers in cell and developmental biology · 2021Article
- Review
- The ins and outs of the Arf4-based ciliary membrane-targeting complex.Small GTPases · 2021Review
- Arl4D-EB1 interaction promotes centrosomal recruitment of EB1 and microtubule growth.Molecular biology of the cell · 2020Article
- Exploring Key Challenges of Understanding the Pathogenesis of Kidney Disease in Bardet-Biedl Syndrome.Kidney international reports · 2020Review
- ARF family GTPases with links to cilia.American journal of physiology. Cell physiology · 2020Review
9 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
11 authors at 5 institutions in 2 countries.
Funding
Abstract
The expansive family of metazoan ADP-ribosylation factor and ADP-ribosylation factor-like small GTPases is known to play essential roles in modulating membrane trafficking and cytoskeletal functions. Here, we present the crystal structure of ARL6, mutations in which cause Bardet-Biedl syndrome (BBS3), and reveal its unique ring-like localization at the distal end of basal bodies, in proximity to the so-called ciliary gate where vesicles carrying ciliary cargo fuse with the membrane. Overproduction of GDP- or GTP-locked variants of ARL6/BBS3 in vivo influences primary cilium length and abundance. ARL6/BBS3 also modulates Wnt signaling, a signal transduction pathway whose association with cilia in vertebrates is just emerging. Importantly, this signaling function is lost in ARL6 variants containing BBS-associated point mutations. By determining the structure of GTP-bound ARL6/BBS3, coupled with functional assays, we provide a mechanistic explanation for such pathogenic alterations, namely altered nucleotide binding. Our findings therefore establish a previously unknown role for ARL6/BBS3 in mammalian ciliary (dis)assembly and Wnt signaling and provide the first structural information for a BBS protein.
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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 OpenQuestion graph.