ArticleJournal of cell science2014
Basal body proteins regulate Notch signaling through endosomal trafficking.
Article in Journal of cell science, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 62 papers.
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Who cites it
62 citing papers in PubMed, 98 citations in OpenAlex.
- BBSome: An essential component of hypothalamic regulation of energy homeostasis.Reviews in endocrine & metabolic disorders · 2026Review
- 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
- FGFR2 residence in primary cilia is necessary for epithelial cell signaling.The Journal of cell biology · 2025Article
- Cilia at the crossroad: convergence of regulatory mechanisms to govern cilia dynamics during cell signaling and the cell cycle.Cell & bioscience · 2025Review
- Adherent junctions: Physiology, role in hydrocephalus and potential therapeutic targets.IBRO neuroscience reports · 2025Review
- BBSome deficiency in Lotmaria passim reveals divergent functions in trypanosomatid parasites.Parasites & vectors · 2025Article
- Primary cilia and their role in preeclampsia.International journal of medical sciences · 2025Review
- The implication of ciliary signaling pathways for epithelial-mesenchymal transition.Molecular and cellular biochemistry · 2024Review
- The relationship between intraflagellar transport and upstream protein trafficking pathways and macrocyclic lactone resistance in Caenorhabditis elegans.G3 (Bethesda, Md.) · 2024Article
- 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
- Loss of the centrosomal protein ALMS1 alters lipid metabolism and the regulation of extracellular matrix-related processes.Biology direct · 2023Article
- Organization, functions, and mechanisms of the BBSome in development, ciliopathies, and beyond.eLife · 2023Review
- HOPS-dependent lysosomal fusion controls Rab19 availability for ciliogenesis in polarized epithelial cells.bioRxiv : the preprint server for biology · 2023Article
- BBSome: a New Player in Hypertension and Other Cardiovascular Risks.Hypertension (Dallas, Tex. : 1979) · 2022Review
- Depletion ofFrontiers in molecular biosciences · 2022Article
- Bardet-Biedl syndrome proteins modulate the release of bioactive extracellular vesicles.Nature communications · 2021Article
- The Role of Intracellular Trafficking of Notch Receptors in Ligand-Independent Notch Activation.Biomolecules · 2021Review
- Ciliopathy genes are required for apical secretion of Cochlin, an otolith crystallization factor.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- Epigenetically Mediated Ciliogenesis and Cell Cycle Regulation, and Their Translational Potential.Cells · 2021Review
- Exocrine pancreas proteases regulate β-cell proliferation in zebrafish ciliopathy models and in murine systems.Biology open · 2021Article
2 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
5 authors at 2 institutions in 2 countries.
Funding
Abstract
Proteins associated with primary cilia and basal bodies mediate numerous signaling pathways, but little is known about their role in Notch signaling. Here, we report that loss of the Bardet-Biedl syndrome proteins BBS1 or BBS4 produces increased Notch-directed transcription in a zebrafish reporter line and in human cell lines. Pathway overactivation is accompanied by reduced localization of Notch receptor at both the plasma membrane and the cilium. In Drosophila mutants, overactivation of Notch can result from receptor accumulation in endosomes, and recent studies implicate ciliary proteins in endosomal trafficking, suggesting a possible mechanism by which overactivation occurs in BBS mutants. Consistent with this, we observe genetic interaction of BBS1 and BBS4 with the endosomal sorting complexes required for transport (ESCRT) gene TSG101 and accumulation of receptor in late endosomes, reduced endosomal recycling and reduced receptor degradation in lysosomes. We observe similar defects with disruption of BBS3. Loss of another basal body protein, ALMS1, also enhances Notch activation and the accumulation of receptor in late endosomes, but does not disrupt recycling. These findings suggest a role for these proteins in the regulation of Notch through endosomal trafficking of the receptor.
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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.