在猿猴病毒40转化细胞中，信号介导的核转运受大T抗原调控。

Feldherr C M, Lanford R E, Akin D

Department of Anatomy and Cell Biology, University of Florida, College of Medicine, Gainesville 32610.

Proc Natl Acad Sci U S A. 1992 Nov 15;89(22):11002-5. doi: 10.1073/pnas.89.22.11002.

Transformation of cultured cells with simian virus 40 (SV40), or transfection with the early region of the SV40 genome, causes a significant increase in both the rate of signal-mediated nuclear transport and the functional size of the transport channels (located in the pore complexes). By microinjecting purified large tumor (T) antigen into the cytoplasm of murine BALB/c 3T3 cells, we have demonstrated that this protein alone can account for the increase in transport capacity. The T antigen-dependent changes can be partially inhibited by cycloheximide and require a functional nuclear localization sequence. Although necessary, the nuclear localization sequence by itself cannot produce the observed variations in nuclear permeability and presumably function in a "helper" capacity, in association with another, as yet unidentified domain.

用猿猴病毒40（SV40）对培养细胞进行转化，或用SV40基因组的早期区域进行转染，会导致信号介导的核运输速率和运输通道（位于孔复合体中）的功能大小都显著增加。通过将纯化的大T抗原显微注射到小鼠BALB/c 3T3细胞的细胞质中，我们已经证明仅这种蛋白质就能解释运输能力的增加。T抗原依赖性变化可被环己酰亚胺部分抑制，且需要一个功能性核定位序列。尽管核定位序列是必需的，但它本身并不能产生所观察到的核通透性变化，推测其与另一个尚未鉴定的结构域结合，以“辅助”能力发挥作用。