Rutila J E, Christensen J B, Imperiale M J
Department of Microbiology and Immunology, University of Michigan Medical School, Ann Arbor 48109-0620.
Oncogene Res. 1989;4(4):303-10.
The viability, p53 binding, and SV40 origin binding of a series of SV40 large T antigen point mutants, which map to the amino terminal one-third of the molecule, were examined. Two mutants which yield small plaques were found to have altered kinetics of replication upon infection of permissive cells. Mutants which did not bind to the origin of replication were not able to replicate, but the reverse was not always true. Replication defective mutants which bound the SV40 origin were found; these map both inside and outside of the origin binding domain. All the transformation defective mutants bound the cellular protein, p53.
对一系列SV40大T抗原点突变体进行了活力、p53结合及SV40起始点结合的检测，这些突变体定位于该分子氨基末端的三分之一处。发现两个产生小噬菌斑的突变体在感染允许细胞后复制动力学发生了改变。不与复制起始点结合的突变体无法复制，但反之则不一定成立。发现了与SV40起始点结合的复制缺陷型突变体；这些突变体定位于起始点结合域的内部和外部。所有转化缺陷型突变体都能结合细胞蛋白p53。
