LOSS OF THE NORMAL N-RAS ALLELE IN A MOUSE THYMIC LYMPHOMA INDUCED BY A CHEMICAL CARCINOGEN

LOSS OF THE NORMAL N-RAS ALLELE IN A MOUSE THYMIC LYMPHOMA INDUCED BY A CHEMICAL CARCINOGEN
复制标题

DOI:
10.1073/pnas.82.23.7810
复制
发表时间:
1985-01-01
影响因子:
11.1
通讯作者:
PELLICER, A
PELLICER, A
中科院分区:
综合性期刊1区
文献类型:
--
作者:
GUERRERO, I;VILLASANTE, A;PELLICER, A

文献摘要

被引文献

相似文献

注射致癌物N-亚硝基-N-甲基脲的幼鼠在2-4个月后发生胸腺淋巴瘤。我们以前已经表明,这些肿瘤经常包含一个激活的N-ras基因,可以转化啮齿动物成纤维细胞在体内。我们在这里报告这样一个激活的N-ras基因的内含子/外显子结构和它的四个编码外显子的序列。一个单核苷酸变化负责转化改变,即C → C密码子61第一个碱基的颠换。通过使用合成的寡核苷酸作为杂交探针,我们表明,这种肿瘤缺乏正常的等位基因的N-ras基因。这一发现的影响,癌基因的优势进行了讨论。
Young mice injected with the carcinogen N-nitroso-N-methylurea develop thymic lymphomas 2-4 months later. We previously have shown that these tumors frequently contain an activated N-ras gene that can transform rodent fibroblasts in vivo. We report here the intron/exon structure of such an activated N-ras gene and the sequence of its four coding exons. A single nucleotide change is responsible for the transforming alteration, a C .fwdarw. A transversion in the first base of codon 61. Through the use of synthetic oligonucleotides as hybridization probes, we show that this tumor lacks the normal allele of the N-ras gene. The implications of this finding for oncogene dominance are discussed.