ArticleProceedings of the National Academy of Sciences of the United States of America2007
Unc-51-like kinase 1/2-mediated endocytic processes regulate filopodia extension and branching of sensory axons.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 75 papers, 3 of them syntheses that pooled it.
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Who cites it
75 citing papers in PubMed, 3 syntheses or guidelines pooled it, 123 citations in OpenAlex.
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- Autophagy and Its Lineage-Specific Roles in the Hematopoietic System.Oxidative medicine and cellular longevity · 2023Review
- Autophagy and beyond: Unraveling the complexity of UNC-51-like kinase 1 (ULK1) from biological functions to therapeutic implications.Acta pharmaceutica Sinica. B · 2022Review
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- Autophagy-related Proteins in Genome Stability: Autophagy-Dependent and Independent Actions.International journal of biological sciences · 2022Review
- ULK4 in Neurodevelopmental and Neuropsychiatric Disorders.Frontiers in cell and developmental biology · 2022Review
- Crosstalk between autophagy inhibitors and endosome-related secretory pathways: a challenge for autophagy-based treatment of solid cancers.Molecular cancer · 2021Review
- Remodeling without destruction: non-proteolytic ubiquitin chains in neural function and brain disorders.Molecular psychiatry · 2021Review
- Cytoskeleton and Membrane Organization at Axon Branches.Frontiers in cell and developmental biology · 2021Review
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- Axonal autophagosome maturation defect through failure of ATG9A sorting underpins pathology in AP-4 deficiency syndrome.Autophagy · 2020Article
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- Autophagy in the mammalian nervous system: a primer for neuroscientists.Neuronal signaling · 2019Review
15 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
10 authors at 5 institutions in 2 countries.
Funding
Abstract
The molecular mechanism and significance of endocytic processes involved in directional axon elongation are not well understood. The Unc-51 family of serine/threonine kinases was shown to be important for axon growth and was also linked to endocytosis, providing an entry point to study this problem. We found that mouse Unc-51-like kinase 1/2 (Ulk1/2) proteins are localized to vesicular structures in growth cones of mouse spinal sensory neurons. RNAi-mediated knockdown of Ulk1 and/or Ulk2 resulted in impaired endocytosis of nerve growth factor (NGF), excessive axon arborization, and severely stunted axon elongation. The evidence also indicates that Ulk1/2 mediates a non-clathrin-coated endocytosis in sensory growth cones. Interestingly, NGF can induce the interaction of Ulk1 with TrkA receptor complexes through promoting K63-polyubiquitination of Ulk1 and binding of Ulk1 to the scaffolding protein p62. These results and additional studies suggest that Ulk1/2 proteins regulate filopodia extension and neurite branching during sensory axon outgrowth, probably through regulating TrkA receptor trafficking and signaling.
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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.