显性负性Hck对1型人类免疫缺陷病毒病毒体进入的抑制作用。
Inhibition of human immunodeficiency virus type 1 virion entry by dominant-negative Hck.
作者信息
Tokunaga K, Kiyokawa E, Nakaya M, Otsuka N, Kojima A, Kurata T, Matsuda M
机构信息
Department of Pathology, National Institute of Infectious Diseases, Toyama, Shinjuku-ku, Tokyo 162-8640, Japan.
出版信息
J Virol. 1998 Jul;72(7):6257-9. doi: 10.1128/JVI.72.7.6257-6259.1998.
Abstract
To study the role of Src family tyrosine kinases in infection with human immunodeficiency virus type 1 (HIV-1), we constructed an Hck mutant, HckN, that hinders signaling from wild-type Hck. HIV-1 produced in HckN-expressing cells was significantly less infectious to HeLa-CD4-LTR-beta-gal (MAGI) cells than HIV-1 produced in mock-transfected cells. The inhibitory effect of HckN was compensated for by the expression of vesicular stomatitis virus G protein. Finally, we found that the HIV-1 produced in the HckN-expressing cells entered into the cells less efficiently than did the control HIV-1. These results suggest that the Src family tyrosine kinases regulate entry of HIV-1 into target cells.
摘要
为研究Src家族酪氨酸激酶在1型人类免疫缺陷病毒（HIV-1）感染中的作用，我们构建了一种Hck突变体HckN，它可阻断野生型Hck的信号传导。与在mock转染细胞中产生的HIV-1相比，在表达HckN的细胞中产生的HIV-1对HeLa-CD4-LTR-β-半乳糖苷酶（MAGI）细胞的感染性显著降低。水泡性口炎病毒G蛋白的表达可补偿HckN的抑制作用。最后，我们发现表达HckN的细胞中产生的HIV-1进入细胞的效率低于对照HIV-1。这些结果表明，Src家族酪氨酸激酶调节HIV-1进入靶细胞的过程。
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