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本文引用的文献

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A dual E3 mechanism for Rub1 ligation to Cdc53.Rub1 与 Cdc53 连接的双重 E3 机制。
Mol Cell. 2010 Sep 10;39(5):784-96. doi: 10.1016/j.molcel.2010.08.030.
2
The human Dcn1-like protein DCNL3 promotes Cul3 neddylation at membranes.人类Dcn1样蛋白DCNL3促进膜上Cul3的Neddylation修饰。
Proc Natl Acad Sci U S A. 2009 Jul 28;106(30):12365-70. doi: 10.1073/pnas.0812528106. Epub 2009 Jul 14.
3
RBX1/ROC1 disruption results in early embryonic lethality due to proliferation failure, partially rescued by simultaneous loss of p27.RBX1/ROC1功能破坏会因增殖失败导致早期胚胎致死，而p27的同时缺失可部分挽救这种情况。
Proc Natl Acad Sci U S A. 2009 Apr 14;106(15):6203-8. doi: 10.1073/pnas.0812425106. Epub 2009 Mar 26.
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E2-RING expansion of the NEDD8 cascade confers specificity to cullin modification.NEDD8级联反应的E2-环扩展赋予了cullin修饰特异性。
Mol Cell. 2009 Feb 27;33(4):483-95. doi: 10.1016/j.molcel.2009.01.011.
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Multimodal activation of the ubiquitin ligase SCF by Nedd8 conjugation.通过Nedd8缀合对泛素连接酶SCF进行多模态激活。
Mol Cell. 2008 Oct 10;32(1):21-31. doi: 10.1016/j.molcel.2008.08.021.
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SCCRO (DCUN1D1) is an essential component of the E3 complex for neddylation.SCCRO（DCUN1D1）是泛素化E3复合物的一个重要组成部分。
J Biol Chem. 2008 Nov 28;283(48):33211-20. doi: 10.1074/jbc.M804440200. Epub 2008 Sep 30.
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DCUN1D3, a novel UVC-responsive gene that is involved in cell cycle progression and cell growth.DCUN1D3，一种参与细胞周期进程和细胞生长的新型紫外线C反应基因。
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8
Structural insights into NEDD8 activation of cullin-RING ligases: conformational control of conjugation.NEDD8激活泛素连接酶的结构见解：共轭作用的构象控制
Cell. 2008 Sep 19;134(6):995-1006. doi: 10.1016/j.cell.2008.07.022.
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Regulation of cullin RING ligases.泛素连接酶的调控。
Annu Rev Plant Biol. 2008;59:467-89. doi: 10.1146/annurev.arplant.58.032806.104011.
10
Dcn1 functions as a scaffold-type E3 ligase for cullin neddylation.Dcn1作为一种用于cullin泛素化修饰的支架型E3连接酶发挥作用。
Mol Cell. 2008 Jan 18;29(1):23-35. doi: 10.1016/j.molcel.2007.12.012.

SCCRO（DCUN1D1）促进核转位和 neddylation E3 复合物的组装。

SCCRO (DCUN1D1) promotes nuclear translocation and assembly of the neddylation E3 complex.

机构信息

Department of Surgery, Laboratory of Epithelial Cancer Biology, Memorial Sloan-Kettering Cancer Center, New York, New York 10065, USA.

出版信息

J Biol Chem. 2011 Mar 25;286(12):10297-304. doi: 10.1074/jbc.M110.203729. Epub 2011 Jan 19.

DOI:10.1074/jbc.M110.203729
PMID:21247897
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3060484/
Abstract

SCCRO/DCUN1D1/DCN1 (squamous cell carcinoma-related oncogene/defective in cullin neddylation 1 domain containing 1/defective in cullin neddylation) serves as an accessory E3 in neddylation by binding to cullin and Ubc12 to allow efficient transfer of Nedd8. In this work we show that SCCRO has broader, pleiotropic effects that are essential for cullin neddylation in vivo. Reduced primary nuclear localization of Cul1 accompanying decreased neddylation and proliferation in SCCRO(-/-) mouse embryonic fibroblasts led us to investigate whether compartmentalization plays a regulatory role. Decreased nuclear localization, neddylation, and defective proliferation in SCCRO(-/-) mouse embryonic fibroblasts were rescued by transgenic expression of SCCRO. Expression of reciprocal SCCRO and Cul1-binding mutants confirmed the requirement for SCCRO in nuclear translocation and neddylation of cullins in vivo. Nuclear translocation of Cul1 by tagging with a nuclear localization sequence allowed neddylation independent of SCCRO, but at a lower level. We found that in the nucleus, SCCRO enhances recruitment of Ubc12 to Cul1 to promote neddylation. These findings suggest that SCCRO has an essential role in neddylation in vivo involving nuclear localization of neddylation components and recruitment and proper positioning of Ubc12.

摘要

SCCRO/DCUN1D1/DCN1（鳞状细胞癌相关癌基因/包含 1 个缺陷的 Cullin Neddylation 结构域/包含 1 个缺陷的 Cullin Neddylation）作为一种辅助 E3，通过与 Cullin 和 Ubc12 结合，允许 Nedd8 的有效转移，从而在 Neddylation 中发挥作用。在这项工作中，我们表明 SCCRO 具有更广泛的、多效性的作用，这对于体内 Cullin Neddylation 是必不可少的。SCCRO(-/-) 小鼠胚胎成纤维细胞中 Cul1 的初级核定位减少伴随 Neddylation 和增殖减少，这促使我们研究区室化是否发挥调节作用。SCCRO 的转基因表达挽救了 SCCRO(-/-) 小鼠胚胎成纤维细胞中的核定位减少、Neddylation 和增殖缺陷。SCCRO 和 Cul1 结合突变体的表达证实了 SCCRO 在体内 Cul1 的核易位和 Neddylation 中的必需性。通过标记核定位序列使 Cul1 发生核易位，可在不依赖 SCCRO 的情况下发生 Neddylation，但效率较低。我们发现，在核内，SCCRO 增强了 Ubc12 对 Cul1 的募集，以促进 Neddylation。这些发现表明，SCCRO 在体内 Neddylation 中具有重要作用，涉及 Neddylation 成分的核定位以及 Ubc12 的募集和正确定位。