ArticleNature communications2015
The intellectual disability protein RAB39B selectively regulates GluA2 trafficking to determine synaptic AMPAR composition.
Article in Nature communications, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers.
What it found
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Who cites it
56 citing papers in PubMed, 87 citations in OpenAlex.
- Prolonged visual experience accelerates developmental synaptic downscaling via epigenetic regulation and Rab5c mediated AMPA receptor trafficking.Communications biology · 2026Article
- The Functions of RAB GTPases at the Golgi Complex.Sub-cellular biochemistry · 2026Review
- A novelFrontiers in neuroscience · 2026Article
- Article
- The Role of Rab GTPases in the development of genetic and malignant diseases.Molecular and cellular biochemistry · 2024Review
- Molecular Mechanisms of AMPA Receptor Trafficking in the Nervous System.International journal of molecular sciences · 2023Review
- Increased level of RAB39B leads to neuronal dysfunction and behavioural changes in mice.Journal of cellular and molecular medicine · 2023Article
- PTPA variants and impaired PP2A activity in early-onset parkinsonism with intellectual disability.Brain : a journal of neurology · 2023Article
- Genetic Evidence for Endolysosomal Dysfunction in Parkinson's Disease: A Critical Overview.International journal of molecular sciences · 2023Review
- Pediatric-Onset Epilepsy and Developmental Epileptic Encephalopathies Followed by Early-Onset Parkinsonism.International journal of molecular sciences · 2023Review
- The Role of Rab Proteins in Parkinson's Disease Synaptopathy.Biomedicines · 2022Review
- Therapeutic Targeting of Rab GTPases: Relevance for Alzheimer's Disease.Biomedicines · 2022Review
- Clinical characterization of a novel RAB39B nonstop mutation in a family with ASD and severe ID causing RAB39B downregulation and study of a Rab39b knock down mouse model.Human molecular genetics · 2022Article
- Rab GTPases in Parkinson's disease: a primer.Essays in biochemistry · 2021Article
- RAB39B-mediated trafficking of the GluA2-AMPAR subunit controls dendritic spine maturation and intellectual disability-related behaviour.Molecular psychiatry · 2021Article
- TheGenes · 2021Review
- Pharmacological modulation of AMPA receptors rescues specific impairments in social behavior associated with the A350V Iqsec2 mutation.Translational psychiatry · 2021Article
- RAB39B is redistributed in dementia with Lewy bodies and is sequestered within aβ plaques and Lewy bodies.Brain pathology (Zurich, Switzerland) · 2021Article
- Molecular Characterization of AMPA-Receptor-Containing Vesicles.Frontiers in molecular neuroscience · 2021Article
- C9ORF72: What It Is, What It Does, and Why It Matters.Frontiers in cellular neuroscience · 2021Review
Corrections and comments
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Authors and funding
15 authors at 7 institutions in 4 countries.
Funding
Abstract
RAB39B is a member of the RAB family of small GTPases that controls intracellular vesicular trafficking in a compartment-specific manner. Mutations in the RAB39B gene cause intellectual disability comorbid with autism spectrum disorder and epilepsy, but the impact of RAB39B loss of function on synaptic activity is largely unexplained. Here we show that protein interacting with C-kinase 1 (PICK1) is a downstream effector of GTP-bound RAB39B and that RAB39B-PICK1 controls trafficking from the endoplasmic reticulum to the Golgi and, hence, surface expression of GluA2, a subunit of alpha-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid receptors (AMPARs). The role of AMPARs in synaptic transmission varies depending on the combination of subunits (GluA1, GluA2 and GluA3) they incorporate. RAB39B downregulation in mouse hippocampal neurons skews AMPAR composition towards non GluA2-containing Ca(2+)-permeable forms and thereby alters synaptic activity, specifically in hippocampal neurons. We posit that the resulting alteration in synaptic function underlies cognitive dysfunction in RAB39B-related disorders.
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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.