ReviewInternational journal of molecular sciences2021
Cofilin Signaling in the CNS Physiology and Neurodegeneration.
Review in International journal of molecular sciences, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.
What it found
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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
42 citing papers in PubMed, 64 citations in OpenAlex.
- Sex-Dependent Responses in the Retina Proteome to Ocular Hypertension in a Mouse Model of Glaucoma.International journal of molecular sciences · 2026Article
- DYRK1A and Parkinson's disease, facts and hypotheses.Neurobiology of disease · 2026Review
- Taming the "death receptor": translating the first-in-class p75Journal of translational medicine · 2026Review
- TRPM7 kinase: a target for multimodal drug development in neurological disorders.Acta pharmacologica Sinica · 2026Review
- Discovery and Development of a Potent LIMK2 Isoform-Specific Degrader.ACS chemical biology · 2026Article
- Three-dimensional interactive network: Mitochondrial-metabolic-calcium homeostasis driving Alzheimer's disease.Genes & diseases · 2026Review
- Small molecule modulation of the p75 neurotrophin receptor promotes dendritic spine resilience to pathogenic tau species and reduces their accumulation.Acta neuropathologica communications · 2026Article
- Hippocampal Cofilin and CFL1 gene variants are linked to Alcohol Use Disorder phenotypes.Molecular psychiatry · 2026Article
- Stiff matrix drives microglial cell migration through Piezo1/CaRegenerative biomaterials · 2026Article
- Expression of Nischarin increases with postnatal hippocampal maturation and regulates cofilin phosphorylation.Journal of biosciences · 2026Article
- The Central Role of Actin in Creutzfeldt-Jakob Disease: Unlocking Therapeutic Pathways.Molecular neurobiology · 2025Review
- Cellular responses to short-term intraocular pressure elevation in a porcine eye explant model.Experimental eye research · 2025Article
- Transcriptome Analyses Revealed the Genetic Advantages in Polygynous Males ofEcology and evolution · 2025Article
- α-Cyclodextrin/Moringin Impacts Actin Cytoskeleton Dynamics with Potential Implications for Synaptic Organization: A Preliminary Transcriptomic Study in NSC-34 Motor Neurons.International journal of molecular sciences · 2025Article
- Cofilin(s) and Mitochondria: Function Beyond Actin Dynamics.International journal of molecular sciences · 2025Review
- Sesquiterpene Lactones as Promising Anti-Glioblastoma Drug Candidates Exerting Complex Effects on Glioblastoma Cell Viability and Proneural-Mesenchymal Transition.Biomedicines · 2025Review
- Resilience mechanisms underlying Alzheimer's disease.Metabolic brain disease · 2025Review
- Neuronal expression of S100B triggered by oligomeric AFrontiers in molecular neuroscience · 2025Article
- Article
- α-Synuclein triggers cofilin pathology and dendritic spine impairment via a PrPCell death & disease · 2024Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
All eukaryotic cells are composed of the cytoskeleton, which plays crucial roles in coordinating diverse cellular functions such as cell division, morphology, migration, macromolecular stabilization, and protein trafficking. The cytoskeleton consists of microtubules, intermediate filaments, and actin filaments. Cofilin, an actin-depolymerizing protein, is indispensable for regulating actin dynamics in the central nervous system (CNS) development and function. Cofilin activities are spatiotemporally orchestrated by numerous extra- and intra-cellular factors. Phosphorylation at Ser-3 by kinases attenuate cofilin's actin-binding activity. In contrast, dephosphorylation at Ser-3 enhances cofilin-induced actin depolymerization. Cofilin functions are also modulated by various binding partners or reactive oxygen species. Although the mechanism of cofilin-mediated actin dynamics has been known for decades, recent research works are unveiling the profound impacts of cofilin dysregulation in neurodegenerative pathophysiology. For instance, oxidative stress-induced increase in cofilin dephosphorylation is linked to the accumulation of tau tangles and amyloid-beta plaques in Alzheimer's disease. In Parkinson's disease, cofilin activation by silencing its upstream kinases increases α-synuclein-fibril entry into the cell. This review describes the molecular mechanism of cofilin-mediated actin dynamics and provides an overview of cofilin's importance in CNS physiology and pathophysiology.
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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.