ArticleFASEB journal : official publication of the Federation of American Societies for Experimental Biology2013
Mitochondrial dysfunction and calcium deregulation by the RanBP9-cofilin pathway.
Article in FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 34 citations in OpenAlex.
- Molecular Signatures of Early-Onset Bipolar Disorder and Schizophrenia: Transcriptomic and Machine-Learning Insights into Calcium and cAMP Signaling, Including Sex-Specific Patterns.International journal of molecular sciences · 2025Article
- N-terminal α-amino SUMOylation promotes phosphorylation-independent cofilin-1 translocation to the mitochondrial matrix and induces apoptosis.Nature communications · 2025Article
- Cofilin(s) and Mitochondria: Function Beyond Actin Dynamics.International journal of molecular sciences · 2025Review
- Mechanism of HDAC1 Regulating Iron Overload-Induced Neuronal Oxidative Damage After Cerebral Hemorrhage.Molecular neurobiology · 2024Article
- SSH1 impedes SQSTM1/p62 flux and MAPT/Tau clearance independent of CFL (cofilin) activation.Autophagy · 2021Article
- Regulation of Mitochondrial Function by the Actin Cytoskeleton.Frontiers in cell and developmental biology · 2021Review
- Lipopolysaccharide-Induced Acute Lung Injury Is Associated with Increased Ran-Binding Protein in Microtubule-Organizing Center (RanBPM) Molecule Expression and Mitochondria-Mediated Apoptosis Signaling Pathway in a Mouse Model.Medical science monitor : international medical journal of experimental and clinical research · 2020Article
- Dendritic Spines in Alzheimer's Disease: How the Actin Cytoskeleton Contributes to Synaptic Failure.International journal of molecular sciences · 2020Review
- The CTLH Complex in Cancer Cell Plasticity.Journal of oncology · 2019Review
- Activated cofilin exacerbates tau pathology by impairing tau-mediated microtubule dynamics.Communications biology · 2019Article
- The Delivery Challenge in Neurodegenerative Disorders: The Nanoparticles Role in Alzheimer's Disease Therapeutics and Diagnostics.Pharmaceutics · 2018Review
- Scorpins in the DNA Damage Response.International journal of molecular sciences · 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
- Actin dynamics and cofilin-actin rods in alzheimer disease.Cytoskeleton (Hoboken, N.J.) · 2016Review
- Slingshot-Cofilin activation mediates mitochondrial and synaptic dysfunction via Aβ ligation to β1-integrin conformers.Cell death and differentiation · 2015Article
- RanBP9 at the intersection between cofilin and Aβ pathologies: rescue of neurodegenerative changes by RanBP9 reduction.Cell death & disease · 2015Article
- Mitochondrial translocation and interaction of cofilin and Drp1 are required for erucin-induced mitochondrial fission and apoptosis.Oncotarget · 2015Article
- Axonal transport defects in Alzheimer's disease.Molecular neurobiology · 2015Review
Corrections and comments
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Authors and funding
11 authors at 6 institutions in 4 countries.
Funding
Abstract
Mitochondrial dysfunction and synaptic damage are important features of Alzheimer's disease (AD) associated with amyloid β (Aβ) and tau. We reported previously that the scaffolding protein RanBP9, which is overall increased in brains of patients with AD and in mutant APP transgenic mice, simultaneously promotes Aβ generation and focal adhesion disruption by accelerating the endocytosis of APP and β1-integrin, respectively. Moreover, RanBP9 induces neurodegeneration in vitro and in vivo and mediates Aβ-induced neurotoxicity. Here we show in primary hippocampal neurons that RanBP9 potentiates Aβ-induced reactive oxygen species (ROS) overproduction, apoptosis, and calcium deregulation. Analyses of calcium-handling measures demonstrate that RanBP9 selectively delays the clearance of cytosolic Ca(2+) mediated by the mitochondrial calcium uniporter through a process involving the translocation of cofilin into mitochondria and oxidative mechanisms. Further, RanBP9 retards the anterograde axonal transport of mitochondria in primary neurons and decreases synaptic mitochondrial activity in brain. These data indicate that RanBP9, cofilin, and Aβ mimic and potentiate each other to produce mitochondrial dysfunction, ROS overproduction, and calcium deregulation, which leads to neurodegenerative changes reminiscent of those seen in AD.
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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.