ArticleCell death & disease2013
RanBP9 aggravates synaptic damage in the mouse brain and is inversely correlated to spinophilin levels in Alzheimer's brain synaptosomes.
Article in Cell death & disease, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 27 citations in OpenAlex.
- Single-microglia transcriptomic transition network-based prediction and real-world patient data validation identifies ketorolac as a repurposable drug for Alzheimer's disease.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025Article
- Differential splicing of neuronal genes in a Trem2*R47H mouse model mimics alterations associated with Alzheimer's disease.BMC genomics · 2023Article
- The reduction of astrocytic tau prevents amyloid-β-induced synaptotoxicity.Brain communications · 2022Article
- Autophagy-Dependent Increased ADAM10 Mature Protein Induced by TFEB Overexpression Is Mediated Through PPARα.Molecular neurobiology · 2021Article
- Alterations of the Endoplasmic Reticulum (ER) Calcium Signaling Molecular Components in Alzheimer's Disease.Cells · 2020Review
- RANBP9 as potential therapeutic target in non-small cell lung cancer.Journal of cancer metastasis and treatment · 2020Article
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- Tau Protein Squired by Molecular Chaperones During Alzheimer's Disease.Journal of molecular neuroscience : MN · 2018Review
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- SPARC and GluA1-Containing AMPA Receptors Promote Neuronal Health Following CNS Injury.Frontiers in cellular neuroscience · 2018Article
- Amyloid β production is regulated by β2-adrenergic signaling-mediated post-translational modifications of the ryanodine receptor.The Journal of biological chemistry · 2017Article
- Cell signalling pathway regulation by RanBPM: molecular insights and disease implications.Open biology · 2017Review
- How Does p73 Cause Neuronal Defects?Molecular neurobiology · 2016Review
- Oridonin Attenuates Synaptic Loss and Cognitive Deficits in an Aβ1-42-Induced Mouse Model of Alzheimer's Disease.PloS one · 2016Article
- 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 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
- RanBP9 overexpression accelerates loss of pre and postsynaptic proteins in the APΔE9 transgenic mouse brain.PloS one · 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
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7 authors at 5 institutions in 2 countries.
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Abstract
We previously demonstrated that overexpression of RanBP9 led to enhanced Aβ generation in a variety of cell lines and primary neuronal cultures, and subsequently, we confirmed increased amyloid plaque burden in a mouse model of Alzheimer's disease (AD). In the present study, we found striking reduction of spinophilin protein levels when RanBP9 is overexpressed. At 12 months of age, we found spinophilin levels reduced by 70% (P<0.001) in the cortex of APΔE9/RanBP9 mice compared with that in wild-type (WT) controls. In the hippocampus, the spinophilin levels were reduced by 45% (P<0.01) in the APΔE9/RanBP9 mice. Spinophilin immunoreactivity was also reduced by 22% (P<0.01) and 12% (P<0.05) in the cortex of APΔE9/RanBP9 and APΔE9 mice, respectively. In the hippocampus, the reductions were 27% (P<0.001) and 14% (P<0.001) in the APΔE9/RanBP9 and APΔE9 mice, respectively. However, in the cerebellum, spinophilin levels were not altered in either APΔE9 or APΔE9/RanBP9 mice. Additionally, synaptosomal functional integrity was reduced under basal conditions by 39% (P<0.001) in the APΔE9/RanBP9 mice and ~23% (P<0.001) in the APΔE9 mice compared with that in WT controls. Under ATP- and KCl-stimulated conditions, we observed higher mitochondrial activity in the WT and APΔE9 mice, but lower in the APΔE9/RanBP9 mice. Significantly, we confirmed the inverse relationship between RanBP9-N60 and spinophilin in the synaptosomes of Alzheimer's brains. More importantly, both APΔE9 and APΔE9/RanBP9 mice showed impaired learning and memory skills compared to WT controls. These data suggest that RanBP9 might play a crucial role in the loss of spines and synapses in AD.
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