ReviewCells2020
Conventional and Non-Conventional Roles of Non-Muscle Myosin II-Actin in Neuronal Development and Degeneration.
Review in Cells, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
What it found
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Who cites it
17 citing papers in PubMed, 24 citations in OpenAlex.
- Neuropeptide F alters expression of feeding, energy metabolism, and reproduction genes in female freshwater prawn, Macrobrachium rosenbergii.Scientific reports · 2026Article
- The Zinc-Finger Protein POGZ Associates with Polycomb Repressive Complex 1 to Regulate Bone Morphogenetic Protein Signaling During Neuronal Differentiation.Stem cell reviews and reports · 2026Article
- Friedreich ataxia transcriptomic dysregulation and identification of cell type-specific biomarkers: A systematic review and meta-analysis.bioRxiv : the preprint server for biology · 2026Article
- Non-transport functions of motor proteins in corticogenesis.Frontiers in cell and developmental biology · 2026Review
- Non-muscle myosin II is a promising therapeutic target.Trends in pharmacological sciences · 2025Article
- Molecular Motors in Blood-Brain Barrier Maintenance by Astrocytes.Brain sciences · 2025Review
- Ionizing radiation leads to exosome secretion in macrophages through MYC-mediated pathways.PloS one · 2025Article
- Article
- The Aryl Hydrocarbon Receptor Regulates Invasiveness and Motility in Acute Myeloid Leukemia Cells through Expressional Regulation of Non-Muscle Myosin Heavy Chain IIA.International journal of molecular sciences · 2024Article
- Endogenous retroviruses are dysregulated in ALS.iScience · 2024Article
- Aberrant gene expression yet undiminished retinal ganglion cell genesis in iPSC-derived models of optic nerve hypoplasia.Ophthalmic genetics · 2024Article
- Proteomic changes in the hippocampus of large mammals after total-body low dose radiation.PloS one · 2024Article
- Article
- INF2-mediated actin filament reorganization confers intrinsic resilience to neuronal ischemic injury.Nature communications · 2022Article
- Quantitative proteomics and in-cell cross-linking reveal cellular reorganisation during early neuronal differentiation of SH-SY5Y cells.Communications biology · 2022Article
- CLN3, at the crossroads of endocytic trafficking.Neuroscience letters · 2021Article
- Functional Role of Non-Muscle Myosin II in Microglia: An Updated Review.International journal of molecular sciences · 2021Review
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Myosins are motor proteins that use chemical energy to produce mechanical forces driving actin cytoskeletal dynamics. In the brain, the conventional non-muscle myosin II (NMII) regulates actin filament cytoskeletal assembly and contractile forces during structural remodeling of axons and dendrites, contributing to morphology, polarization, and migration of neurons during brain development. NMII isoforms also participate in neurotransmission and synaptic plasticity by driving actin cytoskeletal dynamics during synaptic vesicle release and retrieval, and formation, maturation, and remodeling of dendritic spines. NMIIs are expressed differentially in cerebral non-neuronal cells, such as microglia, astrocytes, and endothelial cells, wherein they play key functions in inflammation, myelination, and repair. Besides major efforts to understand the physiological functions and regulatory mechanisms of NMIIs in the nervous system, their contributions to brain pathologies are still largely unclear. Nonetheless, genetic mutations or deregulation of NMII and its regulatory effectors are linked to autism, schizophrenia, intellectual disability, and neurodegeneration, indicating non-conventional roles of NMIIs in cellular mechanisms underlying neurodevelopmental and neurodegenerative disorders. Here, we summarize the emerging biological roles of NMIIs in the brain, and discuss how actomyosin signaling contributes to dysfunction of neurons and glial cells in the context of neurological disorders. This knowledge is relevant for a deep understanding of NMIIs on the pathogenesis and therapeutics of neuropsychiatric and neurodegenerative diseases.
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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.