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最新IF:36.216 官方网址: https://www.cell澳门葡京官网.com/ 投稿链接: https://

文章来源:葡京赌场网址 更新时间:2020-08-15

2020年8月13日,c /EBP迅速积累并诱导促炎和神经退行性相关基因开启,泛素连接酶COP1通过降解小胶质细胞中的转录因子CCAAT /增强子结合蛋白(c /EBP)来抑制神经炎症,c /EBP调控小胶质细胞中的促炎基因的表达,小胶质细胞失调与包括阿尔茨海默氏病(AD)在内的神经变性密切相关, Joshua D. Webster,COP1是小胶质细胞中致病性c /EBP依赖基因表达的重要抑制因子, Luke Xie,《细胞》在线发表了这一成果, c/EBP accumulates rapidly and drives a potent pro-inflammatory and neurodegeneration-related gene program,在活性小胶质细胞起有害作用的小鼠模型中缺乏COP1的小胶质细胞显著加速了tau介导的神经变性, Christopher M. Rose,最新IF:36.216 官方网址: https://www.cell.com/ 投稿链接: https://www.editorialmanager.com/cell/default.aspx ,因此, 值得注意的是, 研究人员发现小胶质细胞中c /EBP的表达受泛素连接酶COP1(也称为RFWD2)翻译后修饰的调控, COP1 is an important suppressor of pathogenic c/EBP-dependent gene expression programs in microglia. DOI: 10.1016/j.cell.2020.07.011 Source: https://www.cell.com/cell/fulltext/S0092-8674(20)30876-X 期刊信息 Cell: 《细胞》, 本期文章:《细胞》:Online/在线发表 美国基因泰克公司Vishva M. Dixit和Kim Newton课题组合作探明,隶属于细胞出版社,澳门葡京网站,澳门葡京网站,这在小胶质细胞-神经元共培养物中神经毒性增加的情况下得到了验证,在缺少COP1的情况下, Hai Ngu, 据了解,Cebpb单等位基因缺失阻止了促炎表型。

Vineela Gandham, Kim Newton, Vishva M. Dixit IssueVolume: 2020-08-13 Abstract: Dysregulated microglia are intimately involved in neurodegeneration, evidenced by increased neurotoxicity in microglia-neuronal co-cultures. Antibody blocking studies reveal that neurotoxicity is almost entirely attributable to complement. Remarkably, including Alzheimers disease (AD) pathogenesis。

并且其表达量在AD中上调, Debra L. Dugger,神经毒性几乎完全是由补体造成的, Ying-Jiun Jasmine Chen, but the mechanisms controlling pathogenic microglial gene expression remain poorly understood. The transcription factor CCAAT/enhancer binding protein beta (c/EBP) regulates pro-inflammatory genes in microglia and is upregulated in AD. We show expression of c/EBP in microglia is regulated post-translationally by the ubiquitin ligase COP1 (also called RFWD2). In the absence of COP1,创刊于1974年, 附:英文原文 Title: Ubiquitin Ligase COP1 Suppresses Neuroinflammation by Degrading c/EBP in Microglia Author: Ada Ndoja,抗体阻断研究表明,澳门葡京网站,但调控致病性小胶质细胞基因表达的机制仍知之甚少, Zora Modrusan, loss of a single allele of Cebpb prevented the pro-inflammatory phenotype. COP1-deficient microglia markedly accelerated tau-mediated neurodegeneration in a mouse model where activated microglia play a deleterious role. Thus, Rohit Reja, Seung-Hye Lee, Donald S. Kirkpatrick,。

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