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MBC in Press, published online ahead of print November 1, 2006
Mol. Biol. Cell 10.1091/mbc.E06-05-0453

A more recent version of this article appeared on January 1, 2007 Originally published as MBC in Press, 10.1091/mbc.E06-05-0453 on November 8, 2006
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Submitted on May 24, 2006
Revised on September 18, 2006
Accepted on October 19, 2006

Kidins220/ARMS Is Transported by a Kinesin-1-based Mechanism Likely to be Involved in Neuronal Differentiation

Aurora Bracale,*{dagger} Fabrizia Cesca,*{dagger} Veronika E. Neubrand,* Timothy P. Newsome,{ddagger} Michael Way,{ddagger} and Giampietro Schiavo*

*Molecular NeuroPathobiology and {ddagger}Cell Motility Laboratories, Cancer Research UK London Research Institute, London, WC2A 3PX, United Kingdom

Monitoring Editor: Erika Holzbaur

Kidins220/ARMS is a conserved membrane protein mainly expressed in brain and neuroendocrine cells, which is a downstream target of the signaling cascades initiated by neurotrophins and ephrins. We identified KLC1 (kinesin light chain 1) as a binding partner for Kidins220/ARMS by a yeast two-hybrid screen. The interaction between Kidins220/ARMS and the kinesin-1 motor complex was confirmed by GST-pull down and coimmunoprecipitation experiments. In addition, Kidins220/ARMS and kinesin-1 were shown to colocalise in NGF differentiated PC12 cells. Using Kidins220/ARMS and KLC1 mutants, we mapped the regions responsible for the binding to a short sequence of Kidins220/ARMS, termed KLC-interacting motif (KIM), which is sufficient for the interaction with KLC1. Optimal binding of KIM requires a region of KLC1 spanning both the tetratricopeptide repeats and the heptad repeats, previously not involved in cargo recognition. Overexpression of KIM in differentiating PC12 cells impairs the formation and transport of EGFP-Kidins220/ARMS carriers to the tips of growing neurites, leaving other kinesin-1 dependent processes unaffected. Furthermore, KIM overexpression interferes with the activation of the MAPK signaling and neurite outgrowth in NGF-treated PC12 cells. Our results suggest that Kidins220/ARMS-positive carriers undergo a kinesin-1 dependent transport possibly involved in neurotrophin action.

{dagger}These authors contributed equally to this work.

Address correspondence to: Giampietro Schiavo (Giampietro.Schiavo{at}cancer.org.uk)




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J. Li, L. A. Chen, C. M. Townsend Jr., and B. M. Evers
PKD1, PKD2, and Their Substrate Kidins220 Regulate Neurotensin Secretion in the BON Human Endocrine Cell Line
J. Biol. Chem., February 1, 2008; 283(5): 2614 - 2621.
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