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Kinesin-1-dependent transport of the モPIX/GIT complex in neuronal cells.
Eung-Gook Kim 1,* (Professor), Eun-Young Shin 1 (Professor), Chan-Soo Lee2 (Research worker), Han-Byeol Kim1 (Graduate student), Jin-Hee Park1 (Graduate student), Kwangseok Oh1 (Graduate student), Gun-Wu Lee1 (Graduate student), Eun-Yul Cho1 (Graduate student), Hyong Kyu Kim3 (Graduate student)
1Department of Biochemistry, College of Medicine, and Medical Research Center, Chungbuk National University,
2Food Standard Division Scientific Office, Ministry of Food and Drug Safety (KFDA),
3Department of Microbiology, College of Medicine, and Medical Research Center, Chungbuk National University
Proper targeting of the モPAK-interacting exchange factor (モPIX)/G protein-coupled receptor kinase-interacting target protein (GIT) complex into distinct cellular compartments is essential for its diverse functions including neurite extension and synaptogenesis. However, the mechanism for translocation of this complex is unknown. Here we report that the conventional kinesin, called kinesin-1, transports the モPIX/GIT complex. モPIX binds KIF5A, a neuronal isoform of kinesin-1 heavy chain, but not KIF1 and KIF3. Mapping analysis revealed that the tail of KIF5s and LZ domain of モPIX were the respective binding domains. Silencing KIF5A or the expression of a variety of mutant forms of KIF5A inhibited モPIX targeting to the neurite tips in PC12 cells. Furthermore, truncated mutants of モPIX without LZ domain did not interact with KIF5A, and were defective in targeting to the neurite tips in PC12 cells. These results define kinesin-1 as a motor protein of モPIX, and may provide new insights into モPIX/GIT complex-dependent neuronal pathophysiologies.
Abstract, Accepted Manuscript(in press) [Submitted on May 10, 2021, Accepted on May 31, 2021]
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