ArticleFASEB journal : official publication of the Federation of American Societies for Experimental Biology2010
A fragment of the scaffolding protein RanBP9 is increased in Alzheimer's disease brains and strongly potentiates amyloid-beta peptide generation.
Article in FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.
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Who cites it
41 citing papers in PubMed, 58 citations in OpenAlex.
- Robust Increase in IQCK Protein Expression in Mouse Models of Alzheimer's Disease and iPSC-Derived Neurons.Journal of cellular and molecular medicine · 2025Article
- Hyperactivity of Purkinje cell and motor deficits in C9orf72 knockout mice.Molecular and cellular neurosciences · 2022Article
- Neuromechanobiology: An Expanding Field Driven by the Force of Greater Focus.Advanced healthcare materials · 2021Review
- Cloning, expression and purification of the low-complexity region of RanBP9 protein.Protein expression and purification · 2020Article
- Molecular Pathogenesis and Interventional Strategies for Alzheimer's Disease: Promises and Pitfalls.ACS pharmacology & translational science · 2020Review
- Dendritic Spines in Alzheimer's Disease: How the Actin Cytoskeleton Contributes to Synaptic Failure.International journal of molecular sciences · 2020Review
- Review
- Role of Cofilin in Alzheimer's Disease.Frontiers in cell and developmental biology · 2020Review
- Reduced RANBP9 expression is associated with poor prognosis in colorectal cancer patients.Translational cancer research · 2019Article
- The mammalian CTLH complex is an E3 ubiquitin ligase that targets its subunit muskelin for degradation.Scientific reports · 2019Article
- RANBP9 suppresses tumor proliferation in colorectal cancer.Oncology letters · 2019Article
- Regulation of c-Raf Stability through the CTLH Complex.International journal of molecular sciences · 2019Article
- Cofilin, a Master Node Regulating Cytoskeletal Pathogenesis in Alzheimer's Disease.Journal of Alzheimer's disease : JAD · 2019Review
- Early Life Stress and Epigenetics in Late-onset Alzheimer's Dementia: A Systematic Review.Current genomics · 2018Review
- Enhanced tau pathology via RanBP9 and Hsp90/Hsc70 chaperone complexes.Human molecular genetics · 2017Article
- Cell signalling pathway regulation by RanBPM: molecular insights and disease implications.Open biology · 2017Review
- Transcription Factor EB Is Selectively Reduced in the Nuclear Fractions of Alzheimer's and Amyotrophic Lateral Sclerosis Brains.Neuroscience journal · 2016Article
- Aβ Influences Cytoskeletal Signaling Cascades with Consequences to Alzheimer's Disease.Molecular neurobiology · 2015Review
- COPS5 protein overexpression increases amyloid plaque burden, decreases spinophilin-immunoreactive puncta, and exacerbates learning and memory deficits in the mouse brain.The Journal of biological chemistry · 2015Article
- Characterization of RanBPM molecular determinants that control its subcellular localization.PloS one · 2015Article
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 5 countries.
Funding
Abstract
Increasing biochemical and genetic evidence indicates that the amyloid-beta (Abeta) peptide derived from amyloid precursor protein (APP) plays a central role in Alzheimer's disease (AD) pathogenesis. We previously reported that RanBP9 promotes Abeta generation by scaffolding APP/BACE1/LRP complexes together. Interestingly, the RanBP9-Delta1/N60 (residues 1-392) deletion mutant interacted much more strongly with APP/BACE1/LRP than full-length RanBP9. In this study, we found that RanBP9-N60, a processed form of RanBP9 virtually identical to the RanBP9-Delta1/N60 mutant, was strongly increased in AD brains compared with controls. To evaluate the potential pathogenic consequences of this phenotype, we studied the differential biological properties of full-length RanBP9 vs. RanBP9-Delta1/N60 in HEK293T and Neuro-2A cells. The RanBP9-Delta1/N60 fragment, which lacks a nuclear localization signal, displayed enhanced cytoplasmic vs. nuclear localization and >3-fold enhanced stability than full-length RanBP9. Importantly, RanBP9-Delta1/N60, which contains the LisH dimerization domain, retained the capacity to form self-interacting multimeric complexes and increased Abeta generation by approximately 5-fold over vector controls, more potent than the approximately 3-fold increase seen by full-length RanBP9. Taken together, these data indicate that RanBP9-N60 may further drive the amyloid cascade in AD and that the proteolytic processing of RanBP9 may be an attractive therapeutic target.
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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.