ArticleThe Journal of biological chemistry2013
Increased expression of reticulon 3 in neurons leads to reduced axonal transport of β site amyloid precursor protein-cleaving enzyme 1.
Article in The Journal of biological chemistry, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
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Who cites it
34 citing papers in PubMed, 46 citations in OpenAlex.
- Tubular ER dysfunction in neurodegenerative diseases.Neurobiology of disease · 2025Review
- RTN3 regulates collagen biosynthesis and profibrotic macrophage differentiation to promote pulmonary fibrosis via interacting with CRTH2.Molecular medicine (Cambridge, Mass.) · 2025Article
- ER-phagy: mechanisms, regulation, and diseases connected to the lysosomal clearance of the endoplasmic reticulum.Physiological reviews · 2022Review
- Loss of RTN3 phenocopies chronic kidney disease and results in activation of the IGF2-JAK2 pathway in proximal tubular epithelial cells.Experimental & molecular medicine · 2022Article
- The Implication of Reticulons (RTNs) in Neurodegenerative Diseases: From Molecular Mechanisms to Potential Diagnostic and Therapeutic Approaches.International journal of molecular sciences · 2021Review
- Is It the Twilight of BACE1 Inhibitors?Current neuropharmacology · 2021Article
- Emerging Trends in the Use of Therapeutic Hypothermia as a Method for Neuroprotection in Brain Damage (Review).Sovremennye tekhnologii v meditsine · 2021Review
- PINK1 phosphorylates Drp1EMBO reports · 2020Article
- RTN4B-mediated suppression of Sirtuin 2 activity ameliorates β-amyloid pathology and cognitive impairment in Alzheimer's disease mouse model.Aging cell · 2020Article
- Axonal Endoplasmic Reticulum Dynamics and Its Roles in Neurodegeneration.Frontiers in neuroscience · 2020Review
- Tau deletion reduces plaque-associated BACE1 accumulation and decelerates plaque formation in a mouse model of Alzheimer's disease.The EMBO journal · 2019Article
- Palmitic Acid-Induced NADNeurochemical research · 2019Article
- A New Vision for Therapeutic Hypothermia in the Era of Targeted Temperature Management: A Speculative Synthesis.Therapeutic hypothermia and temperature management · 2019Review
- The Beta Amyloid Dysfunction (BAD) Hypothesis for Alzheimer's Disease.Frontiers in neuroscience · 2019Article
- Plasma protein profiling reveals candidate biomarkers for multiple sclerosis treatment.PloS one · 2019Article
- BACE1 inhibition more effectively suppresses initiation than progression of β-amyloid pathology.Acta neuropathologica · 2018Article
- BACE1 SUMOylation increases its stability and escalates the protease activity in Alzheimer's disease.Proceedings of the National Academy of Sciences of the United States of America · 2018Article
- Identification of rare RTN3 variants in Alzheimer's disease in Han Chinese.Human genetics · 2018Article
- Amyloid, tau, pathogen infection and antimicrobial protection in Alzheimer's disease -conformist, nonconformist, and realistic prospects for AD pathogenesis.Translational neurodegeneration · 2018Review
- Extended Synaptotagmin Localizes to Presynaptic ER and Promotes Neurotransmission and Synaptic Growth inGenetics · 2017Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 2 countries.
Funding
Abstract
BACE1 is the sole enzyme responsible for cleaving amyloid precursor protein at the β-secretase site, and this cleavage initiates the generation of β-amyloid peptide (Aβ). Because amyloid precursor protein is predominantly expressed by neurons and deposition of Aβ aggregates in the human brain is highly correlated with the Aβ released at axonal terminals, we focused our investigation of BACE1 localization on the neuritic region. We show that BACE1 was not only enriched in the late Golgi, trans-Golgi network, and early endosomes but also in both axons and dendrites. BACE1 was colocalized with the presynaptic vesicle marker synaptophysin, indicating the presence of BACE1 in synapses. Because the excessive release of Aβ from synapses is attributable to an increase in amyloid deposition, we further explored whether the presence of BACE1 in synapses was regulated by reticulon 3 (RTN3), a protein identified previously as a negative regulator of BACE1. We found that RTN3 is not only localized in the endoplasmic reticulum but also in neuritic regions where no endoplasmic reticulum-shaping proteins are detected, implicating additional functions of RTN3 in neurons. Coexpression of RTN3 with BACE1 in cultured neurons was sufficient to reduce colocalization of BACE1 with synaptophysin. This reduction correlated with decreased anterograde transport of BACE1 in axons in response to overexpressed RTN3. Our results in this study suggest that altered RTN3 levels can impact the axonal transport of BACE1 and demonstrate that reducing axonal transport of BACE1 in axons is a viable strategy for decreasing BACE1 in axonal terminals and, perhaps, reducing amyloid deposition.
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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.