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本文引用的文献

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The Png1-Rad23 complex regulates glycoprotein turnover.Png1-Rad23复合物调节糖蛋白周转。
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2
Identification of VCP/p97, carboxyl terminus of Hsp70-interacting protein (CHIP), and amphiphysin II interaction partners using membrane-based human proteome arrays.使用基于膜的人类蛋白质组芯片鉴定VCP/p97、热休克蛋白70相互作用蛋白（CHIP）的羧基末端以及发动蛋白II的相互作用伙伴。
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Multiple modes of interaction of the deglycosylation enzyme, mouse peptide N-glycanase, with the proteasome.去糖基化酶小鼠肽N-聚糖酶与蛋白酶体的多种相互作用模式。
Proc Natl Acad Sci U S A. 2005 Nov 1;102(44):15809-14. doi: 10.1073/pnas.0507155102. Epub 2005 Oct 25.
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Endoplasmic reticulum-associated degradation.内质网相关降解
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5
Recruitment of the p97 ATPase and ubiquitin ligases to the site of retrotranslocation at the endoplasmic reticulum membrane.将p97三磷酸腺苷酶和泛素连接酶招募至内质网膜上逆向转运的位点。
Proc Natl Acad Sci U S A. 2005 Oct 4;102(40):14132-8. doi: 10.1073/pnas.0505006102. Epub 2005 Sep 26.
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Multiprotein complexes that link dislocation, ubiquitination, and extraction of misfolded proteins from the endoplasmic reticulum membrane.连接内质网膜上错误折叠蛋白的错位、泛素化和提取过程的多蛋白复合物。
Proc Natl Acad Sci U S A. 2005 Oct 4;102(40):14296-301. doi: 10.1073/pnas.0505014102. Epub 2005 Sep 26.
7
Ubx2 links the Cdc48 complex to ER-associated protein degradation.Ubx2将Cdc48复合体与内质网相关蛋白降解联系起来。
Nat Cell Biol. 2005 Oct;7(10):993-8. doi: 10.1038/ncb1298. Epub 2005 Sep 18.
8
Membrane-bound Ubx2 recruits Cdc48 to ubiquitin ligases and their substrates to ensure efficient ER-associated protein degradation.膜结合的Ubx2将Cdc48招募到泛素连接酶及其底物上，以确保内质网相关蛋白的高效降解。
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9
Misfolding of glycoproteins is a prerequisite for peptide: N-glycanase mediated deglycosylation.糖蛋白错误折叠是肽：N-聚糖酶介导的去糖基化的前提条件。
FEBS Lett. 2005 Jan 31;579(3):823-6. doi: 10.1016/j.febslet.2004.12.060.
10
Using a small molecule inhibitor of peptide: N-glycanase to probe its role in glycoprotein turnover.使用肽：N-聚糖酶的小分子抑制剂来探究其在糖蛋白周转中的作用。
Chem Biol. 2004 Dec;11(12):1677-87. doi: 10.1016/j.chembiol.2004.11.010.

AAA三磷酸腺苷酶p97将肽N-聚糖酶与内质网相关的E3连接酶自分泌运动因子受体相连接。

The AAA ATPase p97 links peptide N-glycanase to the endoplasmic reticulum-associated E3 ligase autocrine motility factor receptor.

作者信息

Li Guangtao, Zhao Gang, Zhou Xiaoke, Schindelin Hermann, Lennarz William J

机构信息

Department of Biochemistry and Cell Biology, 450 Life Sciences Building, Stony Brook University, Stony Brook, NY 11794-5215, USA.

出版信息

Proc Natl Acad Sci U S A. 2006 May 30;103(22):8348-53. doi: 10.1073/pnas.0602747103. Epub 2006 May 18.

DOI:10.1073/pnas.0602747103
PMID:16709668
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC1482497/
Abstract

Mouse peptide N-glycanase (mPNGase) cleaves the N-glycan chain from misfolded glycoproteins and glycopeptides. Previously, several proteins were found to directly interact with mPNGase; among them, both mHR23B and mS4 were found to link mPNGase to the proteasome. In this study, we found that the cytoplasmic protein mp97 participates in the formation of a ternary complex containing mouse autocrine motility factor receptor (mAMFR), mp97, and mPNGase. This assemblage recruits the cytosolic mPNGase close to the endoplasmic reticulum (ER) membrane, where the retrotranslocation of misfolded glycoproteins is thought to occur. In addition to the ER membrane-associated E3 ligase mAMFR, a cytosolic protein mY33K, containing both UBA and UBX domains, was found to also directly interact with mp97. Thus, a complex containing five proteins, mAMFR, mY33K, mp97, mPNGase, and mHR23B, is formed in close proximity to the ER membrane and serves to couple the activities of retrotranslocation, ubiquitination, and deglycosylation and, thereby, route misfolded glycoproteins to the proteasome.

摘要

小鼠肽 N-聚糖酶（mPNGase）可从错误折叠的糖蛋白和糖肽上切割下 N-聚糖链。此前，已发现几种蛋白质可直接与 mPNGase 相互作用；其中，mHR23B 和 mS4 都被发现可将 mPNGase 与蛋白酶体相连。在本研究中，我们发现细胞质蛋白 mp97 参与了由小鼠自分泌运动因子受体（mAMFR）、mp97 和 mPNGase 组成的三元复合物的形成。这种组合将胞质中的 mPNGase 招募至靠近内质网（ER）膜的位置，错误折叠的糖蛋白的逆向转运被认为在此处发生。除了与 ER 膜相关的 E3 连接酶 mAMFR 外，还发现一种同时含有 UBA 和 UBX 结构域的胞质蛋白 mY33K 也可直接与 mp97 相互作用。因此，一种由 mAMFR、mY33K、mp97、mPNGase 和 mHR23B 这五种蛋白质组成的复合物在靠近 ER 膜的位置形成，并用于耦合逆向转运、泛素化和去糖基化的活性，从而将错误折叠的糖蛋白导向蛋白酶体。