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    Please use this identifier to cite or link to this item: http://asiair.asia.edu.tw/ir/handle/310904400/16438


    Title: COPI-mediated retrograde trafficking from the Golgi to the ER regulates EGFR nuclear transpor
    Authors: ;Wang, YN;Wang, H;Yamaguchi, H;Lee, HJ;Lee, HH;洪明奇;Hung, Mien-Chie
    Contributors: 生物科技學系
    Keywords: Nuclear epidermal growth factor receptor;Nuclear transport;Retrograde trafficking;Coat protein complex I;Golgi;Endoplasmic reticulum
    Date: 2010-06
    Issue Date: 2012-11-23 17:13:06 (UTC+8)
    Abstract: Emerging evidence indicates that cell surface receptors, such as the entire epidermal growth factor receptor (EGFR) family, have been shown to localize in the nucleus. A retrograde route from the Golgi to the endoplasmic reticulum (ER) is postulated to be involved in the EGFR trafficking to the nucleus; however, the molecular mechanism in this proposed model remains unexplored. Here, we demonstrate that membrane-embedded vesicular trafficking is involved in the nuclear transport of EGFR. Confocal immunofluorescence reveals that in response to EGF, a portion of EGFR redistributes to the Golgi and the ER, where its NH2-terminus resides within the lumen of Golgi/ER and COOH-terminus is exposed to the cytoplasm. Blockage of the Golgi-to-ER retrograde trafficking by brefeldin A or dominant mutants of the small GTPase ADP-ribosylation factor, which both resulted in the disassembly of the coat protein complex I (COPI) coat to the Golgi, inhibit EGFR transport to the ER and the nucleus. We further find that EGF-dependent nuclear transport of EGFR is regulated by retrograde trafficking from the Golgi to the ER involving an association of EGFR with γ-COP, one of the subunits of the COPI coatomer. Our findings experimentally provide a comprehensive pathway that nuclear transport of EGFR is regulated by COPI-mediated vesicular trafficking from the Golgi to the ER, and may serve as a general mechanism in regulating the nuclear transport of other cell surface receptors.
    Relation: BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, Volume 399(4):498–504.
    Appears in Collections:[生物科技學系] 期刊論文

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