ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2012
Filamin a regulates neural progenitor proliferation and cortical size through Wee1-dependent Cdk1 phosphorylation.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.
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Who cites it
48 citing papers in PubMed, 73 citations in OpenAlex.
- When the Cytoskeleton Fails: Primary Structural Defects Underlying Disorders with Neurological Involvement.International journal of molecular sciences · 2026Review
- Knockout of filamin A in KGN granulosa tumor cells impairs proliferation, cell cycle progression, migration, and cytoskeletal organization under mechanical stress.Biological research · 2026Article
- The Cytoskeleton in Adrenal Physiology and Tumours: Functional Roles and Emerging Molecular Targets.International journal of molecular sciences · 2025Review
- Filamin A in focus: unravelling the multifaceted roles of filamin A in neurodevelopment and neurological disorders.Brain : a journal of neurology · 2025Review
- Therapeutic potential of targeting the FLNA-regulated Wee1 kinase in adrenocortical carcinomas.International journal of cancer · 2025Article
- Hyperoxia shows duration-dependent effects on the lengths of cell cycle phases in fetal cortical neural stem cells.Frontiers in cell and developmental biology · 2025Article
- Secretome of the Olfactory Ensheathing Cells Influences the Behavior of Neural Stem Cells.International journal of molecular sciences · 2024Article
- Cytomegalovirus infection lengthens the cell cycle of granule cell precursors during postnatal cerebellar development.JCI insight · 2024Article
- Human platelet lysate stimulates neurotrophic properties of human adipose-derived stem cells better than Schwann cell-like cells.Stem cell research & therapy · 2023Article
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- Emerging concepts involving inhibitory and activating RNA functionalization towards the understanding of microcephaly phenotypes and brain diseases in humans.Frontiers in cell and developmental biology · 2023Review
- Article
- Review
- Filamin-A expression in laryngeal squamous cell carcinoma and its clinical significance.Histology and histopathology · 2022Article
- RhoGDI2-Mediated Rac1 Recruitment to Filamin A Enhances Rac1 Activity and Promotes Invasive Abilities of Gastric Cancer Cells.Cancers · 2022Article
- Specificity and Redundancy of Profilin 1 and 2 Function in Brain Development and Neuronal Structure.Cells · 2021Article
- Roots of the Malformations of Cortical Development in the Cell Biology of Neural Progenitor Cells.Frontiers in neuroscience · 2021Review
- Septo-optic dysplasia caused by a novel FLNA splice site mutation: a case report.BMC medical genetics · 2019Article
- Formin 2 Regulates Lysosomal Degradation of Wnt-Associated β-Catenin in Neural Progenitors.Cerebral cortex (New York, N.Y. : 1991) · 2019Article
- Promyelocytic leukemia zinc finger is involved in the formation of deep layer cortical neurons.Journal of biomedical science · 2019Article
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 2 countries.
Funding
Abstract
Cytoskeleton-associated proteins play key roles not only in regulating cell morphology and migration but also in proliferation. Mutations in the cytoskeleton-associated gene filamin A (FlnA) cause the human disorder periventricular heterotopia (PH). PH is a disorder of neural stem cell development that is characterized by disruption of progenitors along the ventricular epithelium and subsequent formation of ectopic neuronal nodules. FlnA-dependent regulation of cytoskeletal dynamics is thought to direct neural progenitor migration and proliferation. Here we show that embryonic FlnA-null mice exhibited a reduction in brain size and decline in neural progenitor numbers over time. The drop in the progenitor population was not attributable to cell death or changes in premature differentiation, but to prolonged cell cycle duration. Suppression of FlnA led to prolongation of the entire cell cycle length, principally in M phase. FlnA loss impaired degradation of cyclin B1-related proteins, thereby delaying the onset and progression through mitosis. We found that the cdk1 kinase Wee1 bound FlnA, demonstrated increased expression levels after loss of FlnA function, and was associated with increased phosphorylation of cdk1. Phosphorylation of cdk1 inhibited activation of the anaphase promoting complex degradation system, which was responsible for cyclin B1 degradation and progression through mitosis. Collectively, our results demonstrate a molecular mechanism whereby FlnA loss impaired G2 to M phase entry, leading to cell cycle prolongation, compromised neural progenitor proliferation, and reduced brain size.
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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.