Suppr超能文献

一种致癌激活的新机制:E26逆转录病毒v-ets癌基因使转录因子c-ets-1的C末端发生了倒置。

A new mechanism of oncogenic activation: E26 retroviral v-ets oncogene has inverted the C-terminal end of the transcription factor c-ets-1.

作者信息

Leprince D, Crepieux P, Laudet V, Flourens A, Stehelin D

机构信息

CNRS URA 1160, Institut Pasteur de Lille, France.

出版信息

Virology. 1993 Jun;194(2):855-7. doi: 10.1006/viro.1993.1330.

Abstract

The v-ets-encoded domain in the P135gag-myb-ets transforming protein of the E26 retrovirus differs mainly from its cellular progenitor, p68c-ets-1 by two point mutations and by the replacement of the 13 last C-terminal amino acids present in c-ets-1 by 16 unrelated residues of previously unknown origin in v-ets. Here, we demonstrate that these v-ets C-terminal specific residues are in fact encoded by the opposite strand of the c-ets-1 C-terminus.

摘要

E26逆转录病毒的P135gag-myb-ets转化蛋白中由v-ets编码的结构域,与其细胞起源蛋白p68c-ets-1主要有两点不同:一是有两个点突变,二是v-ets中16个来源不明的不相关残基取代了c-ets-1中C末端最后13个氨基酸。在此,我们证明这些v-ets C末端特异性残基实际上由c-ets-1 C末端的反义链编码。

文献AI研究员

20分钟写一篇综述,助力文献阅读效率提升50倍。

立即体验

用中文搜PubMed

大模型驱动的PubMed中文搜索引擎

马上搜索

文档翻译

学术文献翻译模型,支持多种主流文档格式。

立即体验