GRP75 upregulates clathrin-independent endocytosis through actin cytoskeleton reorganization mediated by the concurrent activation of Cdc42 and RhoA
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- 作者：Hang Chena ; Zhihui Gaoa ; Changzheng Hea ; Rong Xiangb ; Toin H. van Kuppeveltc ; Mattias Beltingd ; Sihe Zhanga ; b ; sihezhang@nankai.edu.cn" class="auth_mail" title="E-mail the corresponding author
- 关键词：CME ; Clathrin-mediated endocytosis ; CIE ; Clathrin-independent endocytosis ; HSPG ; Heparan sulfate proteoglycan ; ΔS ; Without mitochondrial-targeting signal peptide ; ATPaseD ; ATPase domain ; SBD ; Substrate-binding domain ; MAC ; Membrane attack complex ; GDI ; Guanine nucleotide dissociation inhibitor ; GPI-APs ; GPI-anchored proteins ; Ab ; Antibody ; αHS ; Anti-heparin sulfate (HS) single chain antibody fragment ; Tfn ; Transferrin ; CTxB ; Cholera toxin B subunit ; RBD ; Rho-binding domain
- 刊名：Experimental Cell Research
- 出版年：2016
- 出版时间：1 May 2016
- 年：2016
- 卷：343
- 期：2
- 页码：223-236
- 全文大小：11034 K
文摘
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GRP75 promotes CIE but inhibits CME.
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Mitochondrial localization and ATPaseD in GRP75 regulate endocytosis.
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GRP75 acts upstream of the concurrent activation of Cdc42 and RhoA.
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GRP75 and ATPaseD increase stress fibers and promote filopodia formation.