APC and GSK-3β Are Involved in mPar3 Targeting to the Nascent Axon and Establishment of Neuronal Polarity

By S. Shi, T. Cheng, L. Jan, Y. Jan. 2004

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Neuronal polarity: from extracellular signals to intracellular mechanisms (2007, background): “The PAR complex is transported from the cell body to the axon terminal by the plus-end-directed kinesin motor protein kinesin 2 (which comprises kinesin family member 3 (KIF3) and kinesin superfamily-associated protein 3 (KAP3)”
The aPKC–PAR-6–PAR-3 cell polarity complex localizes to the centrosome attracting body, a macroscopic cortical structure responsible for asymmetric divisions in the early ascidian embryo (2006, background): “…of the kinase GSK3 by aPKC leads to a polarized redistribution of the microtubule plus end-binding protein APC (Etienne-Manneville and Hall, 2003; Shi et al., 2004), whereas in epithelial cells it appears that LGN/Pins links the PAR complex to the microtubule-associated protein NuMA (Du and…”
Rho GTPases: biochemistry and biology. (2005, background): “Localized inhibition of GSK3 is required in the presumptive axon, and this promotes the polarized localization of Par3 and two microtubule plus end–binding proteins, APC and CRMP-2 (Jiang et al. 2005, Shi et al. 2004, Yoshimura et al. 2005).”
Kinesin superfamily motor proteins and intracellular transport (2009, background): “The KIF3 motor transports the tumour suppressor protein adenomatous polyposis coli (APC), the cell polarity proteins PAR3 and PAR6, and atypical protein kinase C (aPKC) to the tip of nascent axon”