ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2013
Protein sorting motifs in the cytoplasmic tail of SorCS1 control generation of Alzheimer's amyloid-β peptide.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers, 1 of them a synthesis that pooled it.
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Who cites it
26 citing papers in PubMed, 1 synthesis or guideline pooled it, 42 citations in OpenAlex.
- Finding memo: versatile interactions of the VPS10p-Domain receptors in Alzheimer's disease.Molecular neurodegeneration · 2022Pooled it
- Golgi dysfunction in Alzheimer disease: from human multiomic signatures to therapeutic targets.Experimental & molecular medicine · 2026Review
- TREM2 in the pathogenesis of AD: a lipid metabolism regulator and potential metabolic therapeutic target.Molecular neurodegeneration · 2022Review
- Genome-wide association study identifies quantitative trait loci affecting cattle temperament.Zoological research · 2022Article
- Typical response of CD14Frontiers in medicine · 2022Article
- Beware of Misdelivery: Multifaceted Role of Retromer Transport in Neurodegenerative Diseases.Frontiers in aging neuroscience · 2022Review
- Impact of Genetic Risk Factors for Alzheimer's Disease on Brain Glucose Metabolism.Molecular neurobiology · 2021Review
- SorCS2 is required for social memory and trafficking of the NMDA receptor.Molecular psychiatry · 2021Article
- APOE ε4 genotype-dependent cerebrospinal fluid proteomic signatures in Alzheimer's disease.Alzheimer's research & therapy · 2020Article
- Type 2 diabetes-associated single nucleotide polymorphism in Sorcs1 gene results in alternative processing of the Sorcs1 protein in INS1 β-cells.Scientific reports · 2019Article
- Autophagic and endo-lysosomal dysfunction in neurodegenerative disease.Molecular brain · 2019Review
- Structural insights into SorCS2-Nerve Growth Factor complex formation.Nature communications · 2018Article
- Retromer Dysfunction and Neurodegenerative Disease.Current genomics · 2018Review
- Article
- Article
- The Role of Retromer in Alzheimer's Disease.Molecular neurobiology · 2016Review
- Complex mechanisms linking neurocognitive dysfunction to insulin resistance and other metabolic dysfunction.F1000Research · 2016Review
- Role of the Retromer Complex in Neurodegenerative Diseases.Frontiers in aging neuroscience · 2016Review
- Candidate genes for Alzheimer's disease are associated with individual differences in plasma levels of beta amyloid peptides in adults with Down syndrome.Neurobiology of aging · 2015Article
- Article
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Authors and funding
6 authors at 4 institutions in 1 country.
Funding
Abstract
Endosomal sorting of the Alzheimer amyloid precursor protein (APP) plays a key role in the biogenesis of the amyloid-β (Aβ) peptide. Genetic lesions underlying Alzheimer's disease (AD) can act by interfering with this physiological process. Specifically, proteins involved in trafficking between endosomal compartments and the trans-Golgi network (TGN) [including the retromer complex (Vps35, Vps26) and its putative receptors (sortilin, SorL1, SorCS1)] have been implicated in the molecular pathology of late-onset AD. Previously, we demonstrated a role for SorCS1 in APP metabolism and Aβ production and, while we implicated a role for the retromer in this regulation, the underlying mechanism remained poorly understood. Here, we provide evidence for a motif within the SorCS1c cytoplasmic tail that, when manipulated, results in perturbed sorting of APP and/or its fragments to endosomal compartments, decreased retrograde TGN trafficking, and increased Aβ production in H4 neuroglioma cells. These perturbations apparently do not involve turnover of the cell surface APP pool, but rather they involve intracellular APP and/or its fragments, downstream of APP endocytosis.
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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.