人巨细胞病毒刺激细胞IKK2活性，且病毒有效复制需要该酶。
Human cytomegalovirus stimulates cellular IKK2 activity and requires the enzyme for productive replication.
作者信息
Caposio Patrizia, Dreano Michel, Garotta Gianni, Gribaudo Giorgio, Landolfo Santo
机构信息
Department of Public Health and Microbiology, University of Torino, Turin, Italy.
出版信息
J Virol. 2004 Mar;78(6):3190-5. doi: 10.1128/jvi.78.6.3190-3195.2004.
Abstract
Human cytomegalovirus (HCMV) exploits the host transcription factor NF-kappaB to enhance its own replication, dissemination, and reactivation from latency. Here we report that HCMV infection activates the upstream IkappaB kinase (IKK) complex and that its catalytic IKK2 subunit is required for HCMV-induced NF-kappaB activation, as well as the replication of different HCMV strains. These results indicate that IKK2 is essential for HCMV replication and emphasize the feasibility of blocking NF-kappaB activation as a way of inhibiting infection.
摘要
人类巨细胞病毒（HCMV）利用宿主转录因子NF-κB来增强其自身的复制、传播以及从潜伏状态的重新激活。在此我们报告，HCMV感染可激活上游的IκB激酶（IKK）复合物，并且其催化性IKK2亚基是HCMV诱导的NF-κB激活以及不同HCMV毒株复制所必需的。这些结果表明IKK2对于HCMV复制至关重要，并强调了阻断NF-κB激活作为一种抑制感染方式的可行性。
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本文引用的文献
1
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Oncogene. 2003 Nov 6;22(50):8187-94. doi: 10.1038/sj.onc.1206963.
2
Models of HCMV latency and reactivation.人巨细胞病毒潜伏和再激活模型。
Trends Microbiol. 2003 Jul;11(7):293-5. doi: 10.1016/s0966-842x(03)00149-5.
3
The human cytomegalovirus.人类巨细胞病毒
Pharmacol Ther. 2003 Jun;98(3):269-97. doi: 10.1016/s0163-7258(03)00034-2.
4
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Cell. 2002 Nov 27;111(5):615-9. doi: 10.1016/s0092-8674(02)01166-2.
5
NF-kappaB--a potential therapeutic target for inhibition of human cytomegalovirus (re)activation?核因子-κB——抑制人巨细胞病毒（再）激活的潜在治疗靶点？
Biol Chem. 2002 Oct;383(10):1601-9. doi: 10.1515/BC.2002.181.
6
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J Clin Virol. 2002 Aug;25 Suppl 2:S123-36. doi: 10.1016/s1386-6532(02)00088-4.
7
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8
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Cell. 2002 Apr;109 Suppl:S81-96. doi: 10.1016/s0092-8674(02)00703-1.
9
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10
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J Clin Invest. 2001 Jan;107(2):143-51. doi: 10.1172/JCI11918.
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