Munroe D G, Rovinski B, Bernstein A, Benchimol S
Ontario Cancer Institute, Toronto, Canada.
Oncogene. 1988 Jun;2(6):621-4.
We have investigated a mutation in the p53 gene leading to expression of a truncated 46,000-dalton protein in a Friend virus-induced erythroleukemia cell line. cDNA sequence analysis revealed a deletion of nucleotide sequences in exon 7 and part of exon 8; 17 additional nucleotides, derived from intron 6, were present in the cDNA and served to maintain the reading frame of the encoded protein. Comparison with p53 protein from other species indicated that the region of the molecule missing in p46 included a highly conserved region. In addition, p46 failed to bind SV40 large T antigen in vitro under conditions which promoted binding of p53 to large T. It seems likely, therefore, that an important functional property of p53 may be affected by the mutation.
我们研究了p53基因中的一个突变，该突变导致在Friend病毒诱导的红白血病细胞系中表达一种截短的46000道尔顿蛋白。cDNA序列分析显示外显子7和部分外显子8中的核苷酸序列缺失；cDNA中存在另外17个来自内含子6的核苷酸，用于维持编码蛋白的阅读框。与其他物种的p53蛋白比较表明，p46分子中缺失的区域包括一个高度保守的区域。此外，在促进p53与大T抗原结合的条件下，p46在体外未能结合SV40大T抗原。因此，p53的一个重要功能特性似乎可能受到该突变的影响。
