ArticleNeuron2009
The adenomatous polyposis coli protein is an essential regulator of radial glial polarity and construction of the cerebral cortex.
Article in Neuron, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 87 papers.
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Who cites it
87 citing papers in PubMed, 135 citations in OpenAlex.
- APC in the nervous system.Medical molecular morphology · 2026Review
- The telomeric valine-arginine dipeptide repeat protein changes state to diffuse staining in mitosis and represses in vitro translation.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Critical Role of Rho Guanine Nucleotide Exchange Factor 4 in Brain Function.Molecular neurobiology · 2025Article
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- APC orchestrates microtubule dynamics by acting as a positive regulator of KIF2A and a negative regulator of CLASPs.Cell insight · 2025Article
- Wnt/β-catenin signaling pathway: proteins' roles in osteoporosis and cancer diseases and the regulatory effects of natural compounds on osteoporosis.Molecular medicine (Cambridge, Mass.) · 2024Review
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- Review
- New insights into the role of GSK-3β in the brain: from neurodegenerative disease to tumorigenesis.PeerJ · 2023Review
- Coordinating cerebral cortical construction and connectivity: Unifying influence of radial progenitors.Neuron · 2022Review
- Secondary loss ofScience advances · 2022Article
- Regulation of Cell Delamination During Cortical Neurodevelopment and Implication for Brain Disorders.Frontiers in neuroscience · 2022Review
- CAMSAPs organize an acentrosomal microtubule network from basal varicosities in radial glial cells.The Journal of cell biology · 2021Article
- Article
- NSCs Under Strain-Unraveling the Mechanoprotective Role of Differentiating Astrocytes in a Cyclically Stretched Coculture With Differentiating Neurons.Frontiers in cellular neuroscience · 2021Article
- Ulk4, a Newly Discovered Susceptibility Gene for Schizophrenia, Regulates Corticogenesis in Mice.Frontiers in cell and developmental biology · 2021Article
- With the Permission of Microtubules: An Updated Overview on Microtubule Function During Axon Pathfinding.Frontiers in molecular neuroscience · 2021Review
- Primary Cilia in Glial Cells: An Oasis in the Journey to Overcoming Neurodegenerative Diseases.Frontiers in neuroscience · 2021Review
- Review
- Branched actin networks are assembled on microtubules by adenomatous polyposis coli for targeted membrane protrusion.The Journal of cell biology · 2020Article
27 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
Radial glia are highly polarized cells that serve as neuronal progenitors and as scaffolds for neuronal migration during construction of the cerebral cortex. How radial glial cells establish and maintain their morphological polarity is unknown. Using conditional gene targeting in mice, we demonstrate that adenomatous polyposis coli (APC) serves an essential function in the maintenance of polarized radial glial scaffold during brain development. In the absence of APC, radial glial cells lose their polarity and responsiveness to the extracellular polarity maintenance cues, such as neuregulin-1. Elimination of APC further leads to marked instability of the radial glial microtubule cytoskeleton. The resultant changes in radial glial function and loss of APC in radial glial progeny lead to defective generation and migration of cortical neurons, severely disrupted cortical layer formation, and aberrant axonal tract development. Thus, APC is an essential regulator of radial glial polarity and is critical for the construction of cerebral cortex in mammals.
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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.