Sompayrac L, Danna K J
Virology. 1986 Sep;153(2):297-309. doi: 10.1016/0042-6822(86)90033-4.
F8dl is an SV40 deletion mutant that lacks over 60% of the coding sequences for large T antigen and yet is able to immortalize early passage rat cells, to transform established cell lines, and to cause tumors in animals. We report here on the further characterization of this mutant and show that (a) transformation by F8dl is protein mediated but does not require the action of the SV40 small t antigen; (b) the F8dl T antigens have, or are associated with, an ATPase activity; (c) the 34-kDa mutant T antigen of F8dl is localized in nuclei and cell membranes of F8dl transformants and binds to double-stranded DNA; (d) the 20-25 kDa forms of the mutant T antigen are cytoplasmic; and (e) the F8dl T antigens do not bind with high affinity to the SV40 origin of viral DNA replication.
F8dl是一种SV40缺失突变体,其大T抗原的编码序列缺失超过60%,但仍能够使原代大鼠细胞永生化,转化已建立的细胞系,并在动物体内引发肿瘤。我们在此报告该突变体的进一步特征,并表明:(a) F8dl介导的转化是由蛋白质介导的,但不需要SV40小t抗原的作用;(b) F8dl T抗原具有或与ATPase活性相关;(c) F8dl的34 kDa突变体T抗原定位于F8dl转化体的细胞核和细胞膜中,并与双链DNA结合;(d) 20 - 25 kDa形式的突变体T抗原位于细胞质中;(e) F8dl T抗原不会与病毒DNA复制的SV40起始位点高亲和力结合。