Human cytomegalovirus infection results in altered Cdk2 subcellular localization
Human cytomegalovirus infection results in altered Cdk2 subcellular localization
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DOI：
10.1099/0022-1317-78-8-1993
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发表时间：
1997-08-01
影响因子：
3.8
通讯作者：
Albrecht, T
中科院分区：
文献类型：
--
作者：
Bresnahan, WA;Thompson, EA;Albrecht, T
人巨细胞病毒（HCMV）感染后刺激许多细胞途径。这些途径之一涉及细胞周期蛋白E/Cdk 2的激活。最近的报道表明，Cdk 2被保留在细胞质中的细胞停滞在GO的血清剥夺，隔离其调节亚基细胞周期蛋白E，这是位于细胞核内。cdk 2迅速进入细胞核，并在用血清生长因子刺激这些细胞时变得活跃。HCMV激活细胞周期蛋白E/Cdk 2的能力，在这两个血清停滞细胞和接触抑制细胞表明，HCMV感染也可能导致Cdk 2易位到细胞核。在这份报告中，我们表明，Cdk 2被隔离在细胞质中的接触抑制，以及那些被血清剥夺逮捕在GO逮捕。HCMV感染导致Cdk 2在感染后24小时内从细胞质易位到细胞核中，无论是在血清抑制和接触抑制细胞中。
Human cytomegalovirus (HCMV) stimulates numerous cellular pathways upon infection. One of these pathways involves activation of cyclin E/Cdk2. Recent reports have demonstrated that Cdk2 is retained in the cytoplasm of cells arrested in GO by serum deprivation, sequestered from its regulatory subunit cyclin E which is located within the nucleus. Cdk2 rapidly enters the nucleus and becomes active upon stimulation of these cells with serum growth factors. The ability of HCMV to activate cyclin E/Cdk2 in both serum-arrested cells and contact-inhibited cells suggests that HCMV infection may also result in the translocation of Cdk2 into the nucleus. In this report, we demonstrate that Cdk2 is sequestered in the cytoplasm of cells arrested in GO by contact inhibition, as well as those arrested by serum deprivation. HCMV infection results in translocation of Cdk2 from the cytoplasm into the nucleus within 24 h of infection, both in serum-arrested and contact-inhibited cells.