人细胞周期蛋白T1可促进Tat与TAR之间的相互作用以及人类免疫缺陷病毒的复制，而细胞周期蛋白T2a或T2b则不能。

Interactions between Tat and TAR and human immunodeficiency virus replication are facilitated by human cyclin T1 but not cyclins T2a or T2b.

作者信息

Wimmer J, Fujinaga K, Taube R, Cujec T P, Zhu Y, Peng J, Price D H, Peterlin B M

机构信息

Department of Medicine, University of California at San Francisco, San Francisco, California 94143-0703, USA.

出版信息

Virology. 1999 Mar 1;255(1):182-9. doi: 10.1006/viro.1998.9589.

DOI:10.1006/viro.1998.9589

PMID:10049833

Abstract

The transcriptional transactivator (Tat) from the human immunodeficiency virus (HIV) does not function efficiently in Chinese hamster ovary (CHO) cells. Only somatic cell hybrids between CHO and human cells and CHO cells containing human chromosome 12 (CHO12) support high levels of Tat transactivation. This restriction was mapped to interactions between Tat and TAR. Recently, human cyclin T1 was found to increase the binding of Tat to TAR and levels of Tat transactivation in rodent cells. By combining individually with CDK9, cyclin T1 or related cyclins T2a and T2b form distinct positive transcription elongation factor b (P-TEFb) complexes. In this report, we found that of these three cyclins, only cyclin T1 is encoded on human chromosome 12 and is responsible for its effects in CHO cells. Moreover, only human cyclin T1, not mouse cyclin T1 or human cyclins T2a or T2b, supported interactions between Tat and TAR in vitro. Finally, after introducing appropriate receptors and human cyclin T1 into CHO cells, they became permissive for infection by and replication of HIV.

摘要

来自人类免疫缺陷病毒（HIV）的转录反式激活因子（Tat）在中国仓鼠卵巢（CHO）细胞中不能有效地发挥作用。只有CHO细胞与人类细胞之间的体细胞杂种以及含有人类12号染色体的CHO细胞（CHO12）能支持高水平的Tat反式激活。这种限制被定位到Tat与TAR之间的相互作用上。最近，发现人类细胞周期蛋白T1能增强Tat与TAR的结合以及在啮齿动物细胞中的Tat反式激活水平。通过分别与CDK9结合，细胞周期蛋白T1或相关的细胞周期蛋白T2a和T2b形成不同的正转录延伸因子b（P-TEFb）复合物。在本报告中，我们发现这三种细胞周期蛋白中，只有细胞周期蛋白T1在人类12号染色体上编码，并对其在CHO细胞中的作用负责。此外，只有人类细胞周期蛋白T1，而不是小鼠细胞周期蛋白T1或人类细胞周期蛋白T2a或T2b，在体外支持Tat与TAR之间的相互作用。最后，在将适当的受体和人类细胞周期蛋白T1导入CHO细胞后，它们变得允许HIV感染和复制。