Abstract
Neural adhesion molecule NB-3 plays an important role in the apical dendrite development of layerVpyramidal neurons in the visual cortex, and receptor-like protein-tyrosine phosphatase α (PTPα) mediates NB-3 signaling in this process. Here we investigated the role of PTPα in regulating cell surface expression of NB-3. We found that cortical neurons from PTPα knock-out mice exhibited a lower level of NB-3 at the cell surface. When expressed in COS1 cells, NB-3 was enriched in the Golgi apparatus with a low level of cell surface expression. However, co-expression of PTPα increased the cell surface distribution of NB-3. Further analysis showed that PTPα facilitated Golgi exit of NB-3 and stabilized NB-3 protein at the cell surface by preventing its release from the plasma membrane. The extracellular region of PTPα but not its catalytic activity is necessary for its effect on NB-3 expression. Thus, the PTPα-mediated increase of NB-3 level at the cell surface represents a novel function of PTPα in NB-3 signaling in neural development. © 2011 by The American Society for Biochemistry and Molecular Biology, Inc.
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CITATION STYLE
Ye, H., Zhao, T., Tan, Y. L. J., Liu, J., Pallen, C. J., & Xiao, Z. C. (2011). Receptor-like protein-tyrosine phosphatase α enhances cell surface expression of neural adhesion molecule NB-3. Journal of Biological Chemistry, 286(29), 26071–26080. https://doi.org/10.1074/jbc.M110.214080
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