ArticleEMBO reports2023
Ubiquitylation of BBSome is required for ciliary assembly and signaling.
Article in EMBO reports, 2023. 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, 21 citations in OpenAlex.
- Research Progress on the Pathogenesis and Diagnostic and Therapeutic Potential of Ciliopathies Regulated by IFT172.Clinical genetics · 2026Review
- Structure Makes a Difference: IFT Complex in Ciliary Function and Ciliopathy.Cytoskeleton (Hoboken, N.J.) · 2026Review
- Article
- Network-based framework for studying etiology and phenotypic diversity in primary ciliopathies.Genome biology · 2026Article
- The intraflagellar transport cycle.Nature reviews. Molecular cell biology · 2025Review
- Genetic context modulates aging and degeneration in the murine retina.Molecular neurodegeneration · 2025Article
- Clinical features of a novel compound heterozygous genotype of theThe Journal of international medical research · 2024Article
- Genetic context modulates aging and degeneration in the murine retina.bioRxiv : the preprint server for biology · 2024Article
- Functional Divergence and Origin of the Vertebrate Praja Family.Journal of molecular evolution · 2024Article
- Primary cilia as dynamic and diverse signalling hubs in development and disease.Nature reviews. Genetics · 2023Review
- EHD1 promotes CP110 ubiquitination by centriolar satellite delivery of HERC2 to the mother centriole.EMBO reports · 2023Article
- Ubiquitylation of BBSome is required for ciliary assembly and signaling.EMBO reports · 2023Article
- Recent advances in the understanding of cilia mechanisms and their applications as therapeutic targets.Frontiers in molecular biosciences · 2023Review
- Editorial: Regulation of proteostasis and cellular energy homeostasis at the primary cilium.Frontiers in cell and developmental biology · 2023Article
Corrections and comments
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Authors and funding
15 authors at 5 institutions in 3 countries.
Funding
Abstract
Bardet-Biedl syndrome (BBS) is a ciliopathy characterized by retinal degeneration, obesity, renal abnormalities, postaxial polydactyly, and developmental defects. Genes mutated in BBS encode for components and regulators of the BBSome, an octameric complex that controls the trafficking of cargos and receptors within the primary cilium. Although both structure and function of the BBSome have been extensively studied, the impact of ubiquitin signaling on BBSome is largely unknown. We identify the E3 ubiquitin ligase PJA2 as a novel resident of the ciliary compartment and regulator of the BBSome. Upon GPCR-cAMP stimulation, PJA2 ubiquitylates BBSome subunits. We demonstrate that ubiquitylation of BBS1 at lysine 143 increases the stability of the BBSome and promotes its binding to BBS3, an Arf-like GTPase protein controlling the targeting of the BBSome to the ciliary membrane. Downregulation of PJA2 or expression of a ubiquitylation-defective BBS1 mutant (BBS1
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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.