ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2016
Rab35 Functions in Axon Elongation Are Regulated by P53-Related Protein Kinase in a Mechanism That Involves Rab35 Protein Degradation and the Microtubule-Associated Protein 1B.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 42 citations in OpenAlex.
- TDP-43 Regulates Rab4 Levels to Support Synaptic Vesicle Recycling and Neuromuscular Connectivity inInternational journal of molecular sciences · 2025Article
- The effect of ubiquitination and deubiquitination to imatinib resistance in gastrointestinal stromal tumors.Frontiers in oncology · 2025Review
- Epigenetic characterization of adult rhesus monkey spermatogonial stem cells identifies key regulators of stem cell homeostasis.Nucleic acids research · 2024Article
- A neurodevelopmental disorder associated with a loss-of-function missense mutation in RAB35.The Journal of biological chemistry · 2024Article
- RAB35 is required for murine hippocampal development and functions by regulating neuronal cell distribution.Communications biology · 2023Article
- A Role for Second Messengers in Axodendritic Neuronal Polarity.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2023Review
- Article
- Ubiquitin and its relatives as wizards of the endolysosomal system.Journal of cell science · 2023Article
- Mutation in protein disulfide isomerase A3 causes neurodevelopmental defects by disturbing endoplasmic reticulum proteostasis.The EMBO journal · 2022Article
- p53 Related Protein Kinase is Required for Arp2/3-Dependent Actin Dynamics of Hemocytes inFrontiers in cell and developmental biology · 2022Article
- Microtubule-associated proteins (MAPs) in microtubule cytoskeletal dynamics and spermatogenesis.Histology and histopathology · 2021Review
- Tuba Activates Cdc42 during Neuronal Polarization Downstream of the Small GTPase Rab8a.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2021Article
- Axonal Organelles as Molecular Platforms for Axon Growth and Regeneration after Injury.International journal of molecular sciences · 2021Review
- Ubiquitination-Dependent Regulation of Small GTPases in Membrane Trafficking: From Cell Biology to Human Diseases.Frontiers in cell and developmental biology · 2021Review
- The role of the oncogenic Rab35 in cancer invasion, metastasis, and immune evasion, especially in leukemia.Small GTPases · 2020Review
- The Recycling Endosome in Nerve Cell Development: One Rab to Rule Them All?Frontiers in cell and developmental biology · 2020Review
- [A differential peptidomics analysis of hippocampal tissue in a rat model of premature white matter injury].Zhongguo dang dai er ke za zhi = Chinese journal of contemporary pediatrics · 2019Article
- Cell Clearing Systems Bridging Neuro-Immunity and Synaptic Plasticity.International journal of molecular sciences · 2019Review
- Rabs set the stage for polarity.Small GTPases · 2018Review
- Critical importance of RAB proteins for synaptic function.Small GTPases · 2018Review
Corrections and comments
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Authors and funding
7 authors at 4 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
unlabelledRab35 is a key protein for cargo loading in the recycling endosome. In neuronal immortalized cells, Rab35 promotes neurite differentiation. Here we describe that Rab35 favors axon elongation in rat primary neurons in an activity-dependent manner. In addition, we show that the p53-related protein kinase (PRPK) negatively regulates axonal elongation by reducing Rab35 protein levels through the ubiquitin-proteasome degradation pathway. PRPK-induced Rab35 degradation is regulated by its interaction with microtubule-associated protein 1B (MAP1B), a microtubule stabilizing binding protein essential for axon elongation. Consistently, axon defects found in MAP1B knock-out neurons were reversed by Rab35 overexpression or PRPK inactivation suggesting an epistatic relationship among these proteins. These results define a novel mechanism to support axonal elongation, by which MAP1B prevents PRPK-induced Rab35 degradation. Such a mechanism allows Rab35-mediated axonal elongation and connects the regulation of actin dynamics with membrane trafficking. In addition, our study reveals for the first time that the ubiquitin-proteasome degradation pathway regulates a Rab GTPase. SIGNIFICANCE STATEMENT: Rab35 is required for axonal outgrowth. We define that its protein levels are negatively regulated by p53-related protein kinase (PRPK). We show that microtubule-associated protein 1B (MAP1B) interacts with PRPK, preventing PRPK-dependent Rab35 proteasome degradation. We demonstrate that Rab35 regulates Cdc42 activity in neurons. This is the first evidence showing that a Rab protein is regulated by degradation dependent on the ubiquitin-proteasome system.
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