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Mutation in KIF1B, a kinesin superfamily motor protein, causes a peripheral neuropathy known as Charcot–Marie–Tooth disease type 2A (CMT2A). Little is known, however, about how a defective KIF1B gene leads to CMT2A. Here we report that KIF1Bα, one of the two splice variants of KIF1B, directly interacts through its C-terminal postsynaptic density-95 (PSD-95)/discs large/zona occludens (PDZ) domain-binding motif with PDZ proteins including PSD-95/synapse-associated protein-90 (SAP90), SAP97, and synaptic scaffolding molecule (S-SCAM)-90 (SAP90). KIF1Bα selectively interacts with PSD-95, SAP97, and S-SCAM in yeast two-hybrid, pull-down, and in vivo coimmunoprecipitation experiments. KIF1Bα, SAP97, and S-SCAM are widely distributed to both dendrites and axons of cultured neurons and are enriched in the small membrane fraction of the brain. In the flotation assay, KIF1Bα cofractionates and coimmunoprecipitates with PSD-95, SAP97, and S-SCAM. These results suggest that the PSD-95 family proteins and S-SCAM have a novel function as KIF1Bα receptors, linking KIF1Bα to its specific cargos, and are involved in peripheral neuropathies.

the journal of neuroscience/the journal of neuroscience

Association of the Kinesin Superfamily Motor Protein KIF1Bα with Postsynaptic Density-95 (PSD-95), Synapse-Associated Protein-97, and Synaptic Scaffolding Molecule PSD-95/Discs Large/Zona Occludens-1 Proteins