@article{c0fb7e229a264d4bb3073263f0fc6fef,
title = "A new role of anterograde motor Kif5b in facilitating large clathrin-coated vesicle mediated endocytosis via regulating clathrin uncoating",
abstract = "Kif5b-driven anterograde transport and clathrin-mediated endocytosis (CME) are responsible for opposite intracellular trafficking, contributing to plasma membrane homeostasis. However, whether and how the two trafficking processes coordinate remain unclear. Here, we show that Kif5b directly interacts with clathrin heavy chain (CHC) at a region close to that for uncoating catalyst (Hsc70) and preferentially localizes on relatively large clathrin-coated vesicles (CCVs). Uncoating in vitro is decreased for CCVs from the cortex of kif5b conditional knockout (mutant) mouse and facilitated by adding Kif5b fragments containing CHC-binding site, while cell peripheral distribution of CHC or Hsc70 keeps unaffected by Kif5b depletion. Furthermore, cellular entry of vesicular stomatitis virus that internalizes into large CCV is inhibited by Kif5b depletion or introducing a dominant-negative Kif5b fragment. These findings showed a new role of Kif5b in regulating large CCV-mediated CME via affecting CCV uncoating, indicating Kif5b as a molecular knot connecting anterograde transport to CME.",
author = "Ni, {Yan Xiang} and Nan Zhou and Xue, {Wen Qian} and Li Rong and Yung, {Wing Ho} and Lin, {Rao Zhou} and Kao, {Richard Yi Tsun} and Duan, {Zhi Gang} and Sun, {Hai Tao} and Gong, {Hua Rui} and Tang, {Xu Ming} and Liu, {Meng Fei} and Wen Zhang and Shuang Qi and Sookja Chung and Song, {You Qiang} and Huang, {Jian Dong}",
note = "Funding Information: We would like to thank S. Brady and G. Morfini for the pCDNA3.Kif5b plasmid, D. Jin and J. Ng for the modified pLL3.7/U6 promoter vector, J. Garcia and M. Kudelko for the packaging plasmids for VSV pseudoparticles, and G.Niu for supporting in data analysis. We also thank Y. Guan, H. Zhu and S. Xiu for their helpful advice and support. We thank electron microscopy unit, core facility center, and center of genomic sciences at the University of Hong Kong for their technical support. This work was partially supported by Shenzhen Peacock project (KQTD2015033117210153); a National Basic Research Program of China (973 Program, 2014CB745200) from the Ministry of Science and Technology of PRC, and the Shenzhen Science and Technology Innovation Committee Basic Science Research Grant (JCYJ20150629151046896). The project was also supported by grants from the Hong Kong Research Grants Council (HKU 17127015, HKU 768113M) and the University of Hong Kong Small Project Fund to J.H. and Y.N. Publisher Copyright: {\textcopyright} 2018, The Author(s).",
year = "2018",
month = dec,
day = "1",
doi = "10.1038/s41421-018-0067-5",
language = "English (US)",
volume = "4",
journal = "Cell Discovery",
issn = "2056-5968",
publisher = "Nature Publishing Group",
number = "1",
}