Abstract
In the developing brain, the organization of the neuroepithelium is maintained by a critical balance between proliferation and cell-cell adhesion of neural progenitor cells. The molecular mechanisms that underlie this are still largely unknown. Here, through analysis of a conditional knockout mouse for the Kap3 gene, we show that post-Golgi transport of N-cadherin by the KIF3 molecular motor complex is crucial for maintaining this balance. N-cadherin and beta-catenin associate with the KIF3 complex by co-immunoprecipitation, and colocalize with KIF3 in cells. Furthermore, in KAP3-deficient cells, the subcellular localization of N-cadherin was disrupted. Taken together, these results suggest a potential tumour-suppressing activity for this molecular motor.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Adaptor Proteins, Signal Transducing / genetics
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Adaptor Proteins, Signal Transducing / metabolism
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Animals
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Brain / embryology
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Brain / physiology*
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Cadherins / metabolism
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Cell Adhesion / genetics
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Cell Adhesion / physiology
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Cell Differentiation / genetics
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Cell Differentiation / physiology*
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Cell Transformation, Neoplastic / genetics
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Cell Transformation, Neoplastic / pathology*
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Cells, Cultured
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Cytoskeletal Proteins / genetics
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Cytoskeletal Proteins / metabolism
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Golgi Apparatus / metabolism
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Mice
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Molecular Motor Proteins / genetics
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Molecular Motor Proteins / metabolism*
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Morphogenesis / physiology
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Neuroepithelial Cells / cytology
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Neuroepithelial Cells / metabolism*
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Neurons / cytology
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Neurons / physiology
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Trans-Activators / metabolism
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beta Catenin
Substances
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Adaptor Proteins, Signal Transducing
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CTNNB1 protein, mouse
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Cadherins
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Cytoskeletal Proteins
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Molecular Motor Proteins
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Trans-Activators
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beta Catenin
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Kifap3 protein, mouse