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[癌基因在牛3型腺病毒诱变活性中的作用]

[Role of the oncogene in the mutagenic activity of bovine adenovirus type 3].

作者信息

Lukash L L, Varshaver N B, Buzhievskaia T I, Shapiro N I

出版信息

Nauchnye Doki Vyss Shkoly Biol Nauki. 1985(5):80-4.

PMID:4040773
Abstract

The mutagenic and carcinogenic effect of two EcoRI-fragments of bovine adenovirus type 3 (BAV-3) DNA inserted into pBR325 has been studied. The C fragment (located between 3,6 and 19,7 map units) contains the viral oncogene, the C fragment (between 44,3 and 63,7 map units) displays no transforming activity. It has been established that oncogene BAV-3 statistically true increases the yield of mutants resistant to 6-mercaptopurine (6MP) in Chinese hamster cells. The C fragment, pBR325 without viral sequences and DNA fragments of different molecular weights from normal Syrian hamster cells have no mutagenic effect. The control over tumor formation in syngenic mice after injection of C3H10T 1/2 and D. C fragments and pBR325 treatment exposed a parallelism between the mutagenic and transforming effect. The study of the combined effect of viral DNA fragments and the tumor promoter 12-O-tetradecanoylphorbol-13-acetate (TPA) which increases the transforming activity of different carcinogens, shows that the promoter increases the frequency of mutants after viral oncogene treatment and does not induce mutagenic activity of those types of DNA which are unable to transform the cells.

摘要

对插入到pBR325中的牛腺病毒3型(BAV - 3)DNA的两个EcoRI片段的诱变和致癌作用进行了研究。C片段(位于3.6和19.7图谱单位之间)含有病毒癌基因,C片段(在44.3和63.7图谱单位之间)无转化活性。已经确定,BAV - 3癌基因在统计学上确实增加了中国仓鼠细胞中对6 - 巯基嘌呤(6MP)耐药的突变体产量。C片段、不含病毒序列的pBR325以及来自正常叙利亚仓鼠细胞的不同分子量的DNA片段均无诱变作用。在注射C3H10T 1/2和D.C片段以及pBR325处理后,对同基因小鼠肿瘤形成的控制揭示了诱变作用和转化作用之间的平行关系。对病毒DNA片段与肿瘤启动子12 - O - 十四烷酰佛波醇 - 13 - 乙酸酯(TPA)的联合作用的研究表明,该启动子在病毒癌基因处理后增加了突变体频率,并且不会诱导那些无法转化细胞的DNA类型的诱变活性,TPA可增加不同致癌物的转化活性。

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