HIV-1 Vpr protein activates the NF-κB pathway to promote G2/M cell cycle arrest
HIV-1 Vpr protein activates the NF-κB pathway to promote G2/M cell cycle arrest
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HIV-1 Vpr蛋白激活NF-κB通路促进G2/M细胞周期阻滞
DOI：
10.1007/s12250-015-3654-8
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发表时间：
2015-12-01
影响因子：
5.5
通讯作者：
Qiao, Wentao
中科院分区：
文献类型：
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作者：
Liang, Zhibin;Liu, Ruikang;Qiao, Wentao
病毒蛋白R（Vpr）在人类免疫缺陷病毒1型（HIV-1）的复制和致病过程中起着重要作用。Vpr的一些功能，包括诱导G2/M期细胞周期阻滞、激活NF-κ B通路和促进病毒逆转录，可能是相互关联的。为了检验这一假设，研究了一组Vpr突变体诱导G2/M期阻滞和激活NF-κ B途径的能力。结果表明，不能激活NF-κ B的Vpr突变体也失去了诱导G2/M期阻滞的活性，这表明通过Vpr诱导G2/M期阻滞至少部分依赖于NF-κ B的激活。后一种可能性得到了数据的支持，这些数据显示敲低NF-κ B通路中的关键因子-p65、RelB、IKK α或IKK β-部分挽救了Vpr诱导的G2/M期阻滞。我们的研究结果表明，NF-κ B B通路可能参与了Vpr诱导的G2/M期细胞阻滞。
Viral protein R (Vpr) plays an important role in the replication and pathogenesis of Human immunodeficiency virus type 1 (HIV-1). Some of the various functions attributed to Vpr, including the induction of G2/M cell cycle arrest, activating the NF-kappa B pathway, and promoting viral reverse transcription, might be interrelated. To test this hypothesis, a panel of Vpr mutants were investigated for their ability to induce G2/M arrest and to activate the NF-kappa B pathway. The results showed that the Vpr mutants that failed to activate NF-kappa B also lost the activity to induce G2/M arrest, which suggests that inducing G2/M arrest via Vpr depends at least partially on the activation of NF-kappa B. This latter possibility is supported by data showing that knocking down the key factors in the NF-kappa B pathway-p65, RelB, IKK alpha, or IKK beta-partially rescued the G2/M arrest induced by Vpr. Our results suggest that the NF-kappa B pathway is probably involved in Vpr-induced G2/M cell cycle arrest.