ArticleBioarchitecture
The role of the cofilin-actin rod stress response in neurodegenerative diseases uncovers potential new drug targets.
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28 citing papers in PubMed, 50 citations in OpenAlex.
- Characterization of a cofilin mutant with high actin bundling activity in living cells.bioRxiv : the preprint server for biology · 2026Article
- Mitochondria and the Actin Cytoskeleton in Neurodegeneration.Cytoskeleton (Hoboken, N.J.) · 2026Review
- Coincident Fluorescence-Burst Analysis of Actin Cargo Molecules in Secreted Single Diffusing Extracellular Vesicles From Human Induced Pluripotent Stem Cells.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Neuronal Actin Remodeling and Its Role in Higher Nervous Activity.International journal of molecular sciences · 2025Review
- The Central Role of Actin in Creutzfeldt-Jakob Disease: Unlocking Therapeutic Pathways.Molecular neurobiology · 2025Review
- A revised model of nuclear actin import: Importin 9 competes with cofilin, profilin, and RanGTP for actin binding.bioRxiv : the preprint server for biology · 2025Article
- OptoProfilin: A Single Component Biosensor of Applied Cellular Stress.Chembiochem : a European journal of chemical biology · 2024Article
- OptoProfilin: A Single Component Biosensor of Applied Cellular Stress.bioRxiv : the preprint server for biology · 2023Article
- Article
- Insights into early pathogenesis of sporadic Alzheimer's disease: role of oxidative stress and loss of synaptic proteins.Frontiers in neuroscience · 2023Article
- An Update on the Critical Role of α-Synuclein in Parkinson's Disease and Other Synucleinopathies: from Tissue to Cellular and Molecular Levels.Molecular neurobiology · 2022Review
- Cofilin1 oxidation links oxidative distress to mitochondrial demise and neuronal cell death.Cell death & disease · 2021Article
- Synaptic tau: A pathological or physiological phenomenon?Acta neuropathologica communications · 2021Review
- New Insights into Cellular Functions of Nuclear Actin.Biology · 2021Review
- Linking Alpha-Synuclein to the Actin Cytoskeleton: Consequences to Neuronal Function.Frontiers in cell and developmental biology · 2020Review
- GAP-43 and BASP1 in Axon Regeneration: Implications for the Treatment of Neurodegenerative Diseases.Frontiers in cell and developmental biology · 2020Review
- Clinically Precedented Protein Kinases: Rationale for Their Use in Neurodegenerative Disease.Frontiers in aging neuroscience · 2020Review
- Indirect visualization of endogenous nuclear actin by correlative light and electron microscopy (CLEM) using an actin-directed chromobody.Histochemistry and cell biology · 2019Article
- Binucleate germ cells in Caenorhabditis elegans are removed by physiological apoptosis.PLoS genetics · 2018Article
- Cofilin-mediated Neuronal Apoptosis via p53 Translocation and PLD1 Regulation.Scientific reports · 2017Article
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2 authors at 1 institution in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
The cofilin-actin rod stress response is an actin cytoskeletal dynamic arrest that occurs in cells under a variety of stress conditions. Upon stress, the rapidly activated cofilin saturates actin filaments causing them to bundle into rod structures in either the nucleus or cytoplasm, halting actin polymerization and thus freeing ATP. Importantly, these rods dissociate quickly following relief of the transient stress. The rods form inappropriately in neurons involved in the progression of Alzheimer disease (AD) and we have linked dysfunctional dynamics of the nuclear rod response to Huntington disease (HD). Cofilin levels are also perturbed in Parkinson disease (PD), and profilin, an actin binding protein with opposite action to cofilin, is mutated in Amyotrophic Lateral Sclerosis (ALS). The persistence of the rods post-stress suggests that critical molecular switches to turn this response both on and off are being affected in neurodegeneration. We have recently shown that the cofilin protein is regulated by highly conserved nuclear import and export signals and that these signals are required to be functional for an appropriate rod formation during stress. The ability of cofilin to form rods is required in a cell culture model for cells to be resistant to apoptosis under stress conditions, indicating that a normal cofilin-actin rod response is likely integral to proper cell health in higher order organisms. Here we hypothesize on the potential physiological function of nuclear cofilin-actin rods and why the dysregulation of this response could lead to the selective vulnerability of the most susceptible populations of cells in HD. We further suggest that learning more about this cytoskeletal cell stress response will open up new avenues for drug target discovery in neurodegenerative disorders.
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