Role and fate of SP100 protein in response to Rep-dependent nonviral integration system
Role and fate of SP100 protein in response to Rep-dependent nonviral integration system
复制标题
SP100蛋白在Rep依赖性非病毒整合系统中的作用和命运
DOI：
10.1007/s00253-012-3992-5
复制
发表时间：
2013-02
影响因子：
5
通讯作者：
Chen, Jin-Zhong
中科院分区：
文献类型：
--
作者：
Wang, Ran;Yue, Yang-Bo;Xue, Jing-Lun;Chen, Jin-Zhong
以前，我们研究了AAVS 1位点特异性非病毒整合系统与Rep供体质粒和含有腺相关病毒整合元件的质粒。我们早期的研究集中在质粒载体本身，但细胞对系统的反应仍然是未知的。SP100是早幼粒细胞白血病核小体的成员。它参与许多细胞过程，如转录调控和细胞对病毒感染的内在免疫反应。在这项研究中，我们发现，SP100抑制Rep依赖的非病毒整合。相反，Rep 78的瞬时表达增加了SP100的降解。这种降解被抑制治疗与MG 132，一种抑制剂的泛素蛋白酶体。SP 100和Rep 78都位于细胞核中，这为它们的相互作用提供了空间可能性。Rep 78与增强型绿色荧光蛋白（EGFP）-SP100融合蛋白共沉淀，而与EGFP不共沉淀，证实了Rep 78与SP100之间的相互作用。这些结果丰富了我们对细胞蛋白SP100和Rep依赖的非病毒整合的认识。这可能会导致Rep相关转基因整合方法的应用和靶细胞的选择的改进。
Previously, we studied an AAVS1 site-specific non-viral integration system with a Rep-donor plasmid and a plasmid containing adeno-associated virus integration element. Our earlier study focused on the plasmid vector itself, but the cellular response to the system was still unknown. SP100 is a member of the promyelocytic leukemia nuclear bodies. It is involved in many cellular processes such as transcriptional regulation and the cellular intrinsic immune response against viral infection. In this study, we revealed that SP100 inhibited the Rep-dependent nonviral integration. Conversely, transient expression of Rep78 increased the degradation of SP100. This degradation was inhibited by treatment with MG132, an inhibitor of the ubiquitin proteasome. SP100 and Rep78 are both located in the nucleolus, which provides the spatial possibility for their interaction. Rep78 was coimmunoprecipitated with the enhanced green fluorescent protein (EGFP)–SP100 fusion protein but not EGFP, which verified the interaction between Rep78 and SP100. These results have enriched our knowledge about the cellular protein SP100 and Rep-dependent nonviral integration. It may lead to an improvement in the application of Rep-related transgene integration method and in the selection of target cells.
登录
查看更多内容
影响因子：
5.4
作者：
Lukashchuk, Vera;Everett, Roger D.
通讯作者：
Everett, Roger D.
影响因子：
5.4
作者：
S. Weger;Meike Wendland;J. Kleinschmidt;R. Heilbronn
通讯作者：
S. Weger;Meike Wendland;J. Kleinschmidt;R. Heilbronn
细胞类型在链霉菌噬菌体PHIC31积分酶活性的活性差异。
影响因子：
14.9
作者：
Maucksch C;Aneja MK;Hennen E;Bohla A;Hoffmann F;Elfinger M;Rosenecker J;Rudolph C
通讯作者：
Rudolph C
影响因子：
11.4
作者：
Milovic-Holm, Kristijana;Krieghoff, Eva;Hofmann, Thomas G.
通讯作者：
Hofmann, Thomas G.
影响因子：
5.3
作者：
Block, Gregory J.;Eskiw, Christopher H.;Bazett-Jones, David P.
通讯作者：
Bazett-Jones, David P.