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羧基末端区域的修饰是禽肉瘤病毒S2中src基因激活的原因。

Modification of carboxyl-terminal region is the cause of activation of the src gene in avian sarcoma virus S2.

作者信息

Ikawa S, Yamamoto T, Toyoshima K

出版信息

Jpn J Cancer Res. 1986 Jul;77(7):611-4.

PMID:3017908
Abstract

Viral oncogene product of avian sarcoma virus S2 was reported to have two alterations from proto-src product; a substitution of its extreme carboxyl terminus with a peptide of helper viral protein and a point mutation which altered the 501st amino acid from arginine to lysine. However, the following data suggest that lysine501 is more common in proto-src product than arginine501. Proto-src from two independent embryos which we analyzed encoded lysine for the 501st amino acid. Rous sarcoma virus and S1, another isolate which had transduced proto-src, also coded for lysine at the same position. Thus, in the case of S2, the oncogenic activation of the src gene appeared to be achieved with only an alteration at its carboxyl terminus and enhanced expression by long terminal repeats.

摘要

据报道,禽肉瘤病毒S2的病毒癌基因产物与原癌基因src产物相比有两处改变;其极端羧基末端被辅助病毒蛋白的一个肽段所取代,以及一个点突变,该突变将第501位氨基酸从精氨酸改变为赖氨酸。然而,以下数据表明,原癌基因src产物中赖氨酸501比精氨酸501更常见。我们分析的来自两个独立胚胎的原癌基因src在第501位氨基酸编码的是赖氨酸。劳氏肉瘤病毒和另一个转导了原癌基因src的分离株S1在相同位置也编码赖氨酸。因此,就S2而言,src基因的致癌激活似乎仅通过其羧基末端的改变以及长末端重复序列的增强表达来实现。

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