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原癌基因dbl的N端区域下调其转化活性。

The N-terminal region of proto-dbl down regulates its transforming activity.

作者信息

Ron D, Graziani G, Aaronson S A, Eva A

机构信息

Laboratory of Cellular and Molecular Biology, National Cancer Institute, Bethesda, Maryland 20892.

出版信息

Oncogene. 1989 Sep;4(9):1067-72.

PMID:2674851
Abstract

The dbl proto-oncogene can transform NIH3T3 cells when overexpressed, but its transforming activity is about 50 to 70 fold lower than that of the dbl oncogene. The dbl oncogene encodes a protein of 478 amino-acids while proto-dbl encodes a protein of 925 amino-acids. The genesis of dbl involved the loss of the first 497 amino-acids of proto-dbl and the acquisition of a new N-terminus from another human locus. The last 428 amino-acids of proto-dbl and dbl product are identical with the exception of a single conservative amino-acid change. Any of these alterations could be responsible for the greater transforming activity of dbl. In order to define the role of these alterations more precisely, we constructed two deletion mutants, one derived from proto-dbl and the second from dbl in which only their last 428 amino-acids were retained. Under the control elements of the same promoter, the transforming activity of each of these mutants was similar to that of the dbl oncogene, i.e. 60-80 fold greater than that of proto-dbl. This finding suggests that the loss of the first 497 amino-acid of proto-dbl, rather than the acquisition of a new N-terminus, is crucial to the enhanced transforming activity of the dbl oncogene. Both mutant proteins were equally distributed between the membrane and cytosolic fractions, a pattern similar to that of their corresponding parental proteins. These results suggest that the subcellular distribution of proto-dbl is determined by its C-terminal 428 amino-acids. Unlike their parental proteins, neither mutant was phosphorylated, indicating that phosphorylation is not required for dbl transforming activity. In addition to the lack of phosphorylation, each mutant protein had a half-life of 5-6 h while the half-life of proto-dbl was about 1 h. Thus, our data suggest that the N-terminal half of proto-dbl can down regulate its transforming activity and that sequences within this region are responsible for rapid turnover of the protein.

摘要

原癌基因dbl在过表达时可转化NIH3T3细胞,但其转化活性比dbl癌基因低约50至70倍。dbl癌基因编码一种478个氨基酸的蛋白质,而原dbl编码一种925个氨基酸的蛋白质。dbl的产生涉及原dbl前497个氨基酸的缺失以及从另一个人类基因座获得新的N末端。原dbl和dbl产物的最后428个氨基酸除了一个保守的氨基酸变化外是相同的。这些改变中的任何一个都可能导致dbl更大的转化活性。为了更精确地定义这些改变的作用,我们构建了两个缺失突变体,一个来自原dbl,另一个来自dbl,其中仅保留它们的最后428个氨基酸。在相同启动子的控制元件下,这些突变体中每一个的转化活性与dbl癌基因相似,即比原dbl高60 - 80倍。这一发现表明,原dbl前497个氨基酸的缺失而非新N末端的获得对dbl癌基因增强的转化活性至关重要。两种突变蛋白在膜和胞质部分中均匀分布,这一模式与其相应的亲本蛋白相似。这些结果表明原dbl的亚细胞分布由其C末端的428个氨基酸决定。与它们的亲本蛋白不同,两种突变体都没有被磷酸化,表明磷酸化对于dbl的转化活性不是必需的。除了缺乏磷酸化外,每种突变蛋白的半衰期为5 - 6小时,而原dbl的半衰期约为1小时。因此,我们的数据表明原dbl的N末端一半可以下调其转化活性,并且该区域内的序列负责该蛋白的快速周转。

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