ArticleFASEB journal : official publication of the Federation of American Societies for Experimental Biology2012
Role of RanBP9 on amyloidogenic processing of APP and synaptic protein levels in the mouse brain.
Article in FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 23 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
23 citing papers in PubMed, 33 citations in OpenAlex.
- The interactome of tau phosphorylated at T217 in Alzheimer's disease human brain tissue.Acta neuropathologica · 2025Article
- 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
- Molecular Pathogenesis and Interventional Strategies for Alzheimer's Disease: Promises and Pitfalls.ACS pharmacology & translational science · 2020Review
- The mammalian CTLH complex is an E3 ubiquitin ligase that targets its subunit muskelin for degradation.Scientific reports · 2019Article
- 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
- 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
- RanBP9 at the intersection between cofilin and Aβ pathologies: rescue of neurodegenerative changes by RanBP9 reduction.Cell death & disease · 2015Article
- RanBP9 overexpression accelerates loss of dendritic spines in a mouse model of Alzheimer's disease.Neurobiology of disease · 2014Article
- RanBP9 overexpression reduces dendritic arbor and spine density.Neuroscience · 2014Article
- Fragile X mental retardation protein controls synaptic vesicle exocytosis by modulating N-type calcium channel density.Nature communications · 2014Article
- An AXL/LRP-1/RANBP9 complex mediates DC efferocytosis and antigen cross-presentation in vivo.The Journal of clinical investigation · 2014Article
- RanBP9 overexpression accelerates loss of pre and postsynaptic proteins in the APΔE9 transgenic mouse brain.PloS one · 2014Article
- A lentiviral sponge for miR-101 regulates RanBP9 expression and amyloid precursor protein metabolism in hippocampal neurons.Frontiers in cellular neuroscience · 2014Article
- Mitochondrial dysfunction and calcium deregulation by the RanBP9-cofilin pathway.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2013Article
- COPS5 (Jab1) protein increases β site processing of amyloid precursor protein and amyloid β peptide generation by stabilizing RanBP9 protein levels.The Journal of biological chemistry · 2013Article
- RanBP9 aggravates synaptic damage in the mouse brain and is inversely correlated to spinophilin levels in Alzheimer's brain synaptosomes.Cell death & disease · 2013Article
- Protein phosphatase 1γ isoforms linked interactions in the brain.Journal of molecular neuroscience : MN · 2013Article
Corrections and comments
- Erratum issuedErratum.2015
Authors and funding
7 authors at 4 institutions in 5 countries.
Funding
Abstract
We previously reported that RanBP9 binds low-density lipoprotein receptor-related protein (LRP), amyloid precursor protein (APP), and BACE1 and robustly increased Aβ generation in a variety of cell lines and primary neuronal cultures. To confirm the physiological/ pathological significance of this phenotype in vivo, we successfully generated transgenic mice overexpressing RanBP9 as well as RanBP9-null mice. Here we show that RanBP9 overexpression resulted in >2-fold increase in Aβ40 levels as early as 4 mo of age. A sustained increase in Aβ40 levels was seen at 12 mo of age in both CHAPS-soluble and formic acid (FA)-soluble brain fractions. In addition, Aβ42 levels were also significantly increased in FA-soluble fractions at 12 mo of age. More important, increased Aβ levels were translated to increased deposition of amyloid plaques. In addition, RanBP9 overexpression significantly decreased the levels of synaptophysin and PSD-95 proteins. Conversely, RanBP9-null mice showed increased levels of synaptophysin, PSD-95, and drebrin A protein levels. Given that loss of synapses is the best pathological correlate of cognitive deficits in Alzheimer's disease (AD), increased Aβ levels by RanBP9 observed in the present study provides compelling evidence that RanBP9 may indeed play a key role in the etiology of AD. If so, RanBP9 provides a great opportunity to develop novel therapy for AD.
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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.