一个突变的SV40大T抗原干扰了异质蛋白的核定位
J Schneider1, C Schindewolf, K van Zee
1Institute for Biochemistry, Munich, Federal Republic of Germany.
Cell
|July 1, 1988
概括
一种类似病毒40 (SV40) 大T抗原变异突变破坏了核蛋白进口,影响了DNA复制和细胞转化. 恢复核定位信号逆转了这些效应,表明T抗原在蛋白质进口机制中的新角色.
科学领域:
- 分子生物学分子生物学
- 病毒学 病毒学
- 细胞生物学 细胞生物学
背景情况:
- SV40大T抗原 (LT) 对于病毒DNA复制和细胞转化至关重要.
- 众所周知,LT的特定区域对于复制和转化是不可或缺的.
- 病毒蛋白的核定位对于它们的功能至关重要.
研究的目的:
- 为了研究SV40大T抗原的特定区域的功能.
- 确定大T抗原在核蛋白定位中的作用.
- 阐明SV40介导的DNA复制和细胞转化背后的机制.
主要方法:
- 在大T抗原中产生突变SV40基因组,具有移突变.
- 对病毒DNA复制和细胞转化能力的分析.
- 免疫光显微镜用于评估宿主细胞内的蛋白质定位.
主要成果:
- 框架转移突变大T抗原未能复制SV40DNA并转化细胞.
- 突变的T抗原表现出异常的核定位,并干扰了腺病毒纤维蛋白核进口.
- 一个双重突变的破坏核定位信号定位到细胞质,但恢复了转变,并没有影响纤维蛋白定位.
结论:
- 大T抗原SV40的炭基末端在核蛋白进口中起着至关重要的,以前未被认可的作用.
- 这一区域的干扰通过干扰核运输而损害病毒复制和细胞转化.
- 这些发现表明了一种新的机制,即通过蛋白质局部化,大T抗原通过蛋白质局部化影响细胞过程.
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