ArticleThe Journal of biological chemistry2009
Novel role of RanBP9 in BACE1 processing of amyloid precursor protein and amyloid beta peptide generation.
Article in The Journal of biological chemistry, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 60 papers.
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Who cites it
60 citing papers in PubMed, 79 citations in OpenAlex.
- YAP1 Upregulates Cytoskeleton Regulator ARHGEF1 and Tissue Regeneration Factor NEDD9 in a Multiplex Proteomic Study.Neurology international · 2026Article
- APP E590D mutation increases generation of Aβ and Aη peptides and exacerbates tauopathy.NPJ dementia · 2026Article
- Robust Increase in IQCK Protein Expression in Mouse Models of Alzheimer's Disease and iPSC-Derived Neurons.Journal of cellular and molecular medicine · 2025Article
- The interactome of tau phosphorylated at T217 in Alzheimer's disease human brain tissue.Acta neuropathologica · 2025Article
- LRRC25 expression during physiological aging and in mouse models of Alzheimer's disease and iPSC-derived neurons.Frontiers in molecular neuroscience · 2024Article
- Regulatory mechanisms and therapeutic potential of JAB1 in neurological development and disorders.Molecular medicine (Cambridge, Mass.) · 2023Review
- Structural and Functional Insights into GID/CTLH E3 Ligase Complexes.International journal of molecular sciences · 2022Review
- Novel Alzheimer risk factor IQ motif containing protein K is abundantly expressed in the brain and is markedly increased in patients with Alzheimer's disease.Frontiers in cellular neuroscience · 2022Article
- Proteomic analysis of ubiquitination substrates reveals a CTLH E3 ligase complex-dependent regulation of glycolysis.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2021Article
- Molecular Pathogenesis and Interventional Strategies for Alzheimer's Disease: Promises and Pitfalls.ACS pharmacology & translational science · 2020Review
- Review
- Role of Cofilin in Alzheimer's Disease.Frontiers in cell and developmental biology · 2020Review
- Dual role of cofilin in APP trafficking and amyloid-β clearance.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2019Article
- The mammalian CTLH complex is an E3 ubiquitin ligase that targets its subunit muskelin for degradation.Scientific reports · 2019Article
- Cofilin, a Master Node Regulating Cytoskeletal Pathogenesis in Alzheimer's Disease.Journal of Alzheimer's disease : JAD · 2019Review
- Tau Protein Squired by Molecular Chaperones During Alzheimer's Disease.Journal of molecular neuroscience : MN · 2018Review
- Enhanced tau pathology via RanBP9 and Hsp90/Hsc70 chaperone complexes.Human molecular genetics · 2017Article
- Cofilin-mediated Neuronal Apoptosis via p53 Translocation and PLD1 Regulation.Scientific reports · 2017Article
- Cell signalling pathway regulation by RanBPM: molecular insights and disease implications.Open biology · 2017Review
- RanBPM (RanBP9) regulates mouse c-Kit receptor level and is essential for normal development of bone marrow progenitor cells.Oncotarget · 2016Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 4 countries.
Funding
Abstract
Accumulation of the amyloid beta (Abeta) peptide derived from the proteolytic processing of amyloid precursor protein (APP) is the defining pathological hallmark of Alzheimer disease. We previously demonstrated that the C-terminal 37 amino acids of lipoprotein receptor-related protein (LRP) robustly promoted Abeta generation independent of FE65 and specifically interacted with Ran-binding protein 9 (RanBP9). In this study we found that RanBP9 strongly increased BACE1 cleavage of APP and Abeta generation. This pro-amyloidogenic activity of RanBP9 did not depend on the KPI domain or the Swedish APP mutation. In cells expressing wild type APP, RanBP9 reduced cell surface APP and accelerated APP internalization, consistent with enhanced beta-secretase processing in the endocytic pathway. The N-terminal half of RanBP9 containing SPRY-LisH domains not only interacted with LRP but also with APP and BACE1. Overexpression of RanBP9 resulted in the enhancement of APP interactions with LRP and BACE1 and increased lipid raft association of APP. Importantly, knockdown of endogenous RanBP9 significantly reduced Abeta generation in Chinese hamster ovary cells and in primary neurons, demonstrating its physiological role in BACE1 cleavage of APP. These findings not only implicate RanBP9 as a novel and potent regulator of APP processing but also as a potential therapeutic target for Alzheimer disease.
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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.