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77篇 您的检索式:作者名="HARHAJ"
    题名 作者 年代 出处 被引量
1Regulation of NF-κB signaling by the A20 deubiquitinase显示文摘NF-κ B 抄写因素是煽动性、天生的有免疫力的发信号小径的一个中央调停人。NF-κ 的激活; B 被哪个的关键发信号的分子的连接 K63 的 polyubiquitination 完成接着激活 Iκ 的成员 kinase 建筑群; B kinase (IKK ) 。Ubiquitination 是一个高度有活力的过程并且被 deubiquitinases 平衡劈开 polyubiquitin 链并且终止下游地发信号的事件。A20 deubiquitinase 是 NF-κ 的一个批评否定管理者; B 和发炎,后来 A20 缺乏的老鼠开发不受管束、自发的多器官发炎。而且,在 A20 genomic 地点的特定的多型性预先安排人到自体免疫的疾病。最近的研究也显示 A20 是在 B 房间淋巴瘤被使失去活性的重要肿瘤 suppressor。因此,指向 A20 可以为自体免疫的疾病和淋巴瘤形成新奇治疗的基础。Noula Shembade Edward W Harhaj 2012Cellular & Molecular Immunology2012,9,2:22
2Regnase-1, a rapid response ribonuclease regulating nflammation and stress responses显示文摘Renfang Mao Riyun Yang Xia Chen Edward W Harhaj Xiaoying Wang Yihui Fan 2017Cellular & Molecular Immunology2017,14,5:3
3Functional implications of mitochondrial reactive oxygen species generated by oncogenic viruses显示文摘被 oncogenic 病毒与感染在 15% 人的癌症和 20% 之间联系。包括 HPV, HBV, HCV 和 HTLV-1, Oncogenic 病毒指向线粒体影响房间增长和幸存。Oncogenic 病毒的基因产品也触发能得到氧化 DNA 损坏并且加强的反应的氧种类的生产 oncogenic 主人发信号小径。病毒的 oncogenes 可以也破坏象 mitophagy 和新陈代谢的改编小径那样的线粒体质量控制机制支持病毒复制。这里,我们将在病毒的 oncogenesis 在 mitophagy 和新陈代谢的改编和他们的角色的病毒的规定上考察最近的进步。Young Bong CHOI Edward William HARHAJ 2014Frontiers in Biology2014,9,6:2
4The NLRP4-DTX4 axis: a key suppressor of TBK1 and innate antiviral signaling显示文摘Soratree Charoenthongtrakul Linlin Gao Edward W Harhaj 2012Cellular & Molecular Immunology2012,9,6:2
5VEGF activation of protein kinase C stimu- lates occludin phosphorylation and contributes to endothelial permeability显示文摘Harhaj NS Felinski EA Wolpert EB Stmdstrom JM Gardner TW Antonetti DA 2006Invest Ophthalmol Vis Sci2006,47,11:1
6Regulation of tight junctions and loss of barrier function in pathophysiology显示文摘Harhaj NS Antonetti DA 2004Int J Biochem Cell Biol2004,36,7:1
7Regulation of NF-κB by deuhiquiti-nases显示文摘Harhaj EW Dixit VM 2012Immunol Rev2012,246,1:1
8Role of post-translational modifications of HTLV-1 Tax in NF-κB activation显示文摘Human T-cell leukemia virus type 1(HTLV-1),the first human retrovirus discovered,is the etiological agent of adult-T-cell leukemia/lymphoma.The HTLV-1 encoded Tax protein is a potent oncoprotein that deregulates gene expression by constitutively activating nuclear factor-κB(NF-κB).Tax activation of NF-κB is critical for the immortalization and survival of HTLV-1-infected T cells.In this review,we summarize the present knowledge on mechanisms underlying Tax-mediated NF-κB activation,with an emphasis on post-translational modifications of Tax.Noula Shembade Edward W Harhaj 2010World Journal of Biological Chemistry2010,1,1:1
9Regulation of tight junctions and loss of barrier function in pathophysiology显示文摘Nicole S Harhaj David A Antonetti 2003International Journal of Biochemistry and Cell Biology2003,,7:1
10VEGF activation of protein kinase C stimulates occludin phosphorylation and contributes to endothelial permeability显示文摘Harhaj NS Felinski EA Wolpert EB 2006Invest Ophthalmol Vis Sci2006,47,11:1
11Human T cell leukemia virus type 1 - induce disease: pathway to cancer and neurodegeneration 显示文摘Barmark K Harhaj E Grant C 2003Virology2003,308,1:1
12Inhibition of NF-kappaBsignaling by A20 through disruption of ubiquitin enzymecomplexes 显示文摘Shembade N Ma A Harhaj EW 2010Science2010,327,:1
13Regulation of tight junctions and loss of barrier function in pathophysiology 显示文摘Harhaj NS Antonetti DA 2004Int J Biochem Cell Biol2004,36,7:1
14Regulation of tight junctions and loss of barrier function in pathophysiology显示文摘HARHAJ N S ANTONETTI D A 2004The International Journal of Biochemistry & Cell Biology2004,36,:1
15Human T cell leukemia virus type I Tax activates CD40 gene expression via the NF-kappa B pathway显示文摘Harhaj EW Harhaj NS Grant C 2005Virology2005,333,1:1
16Regulation of tight junctions and loss of barrier function in pathophysiology 显示文摘Harhaj NS Antonetti DA 2004Inter- national Journal of Biochemistry & Cell Biology2004,36,7:1
17Regulation of tight junctions and loss of barrier function in pathophysiology 显示文摘Harhaj NS Antonetti DA 2004Int J Biochem Cell Biol2004,36,7:1
18Regulation of tight junctions and loss of barrier function in pathophysiology显示文摘Harhaj N S Antonetti D A 2004Int J Biochem Cell Biol2004,36,7:1
19A20 inhibition of NFKB and inflammation 显示文摘Shembade N Harhaj E 2010Cell Cycle2010,9,13:1
20Mechanisms of persistent NF-kappaB activation by HTLV-Ⅰ tax显示文摘Harhaj E W Harhaj N S 2005IU BMB Life2005,57,2:1
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