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细胞质中SV40大T抗原的异常定位并非由与DNA或p53结合失败所致。

The abnormal location of cytoplasmic SV40 large T is not caused by failure to bind to DNA or to p53.

作者信息

Paucha E, Kalderon D, Richardson W D, Harvey R W, Smith A E

出版信息

EMBO J. 1985 Dec 1;4(12):3235-40. doi: 10.1002/j.1460-2075.1985.tb04071.x.

Abstract

We have examined the large T encoded by an SV40 mutant, d10, which fails to localize to the nucleus. The DNA sequence of the mutant predicts the alteration of Lys 128----Thr within the sequence 127 Lys Lys Lys Arg Lys 131 of large T. The results show that d10 large T is capable of binding to SV40 DNA, to cellular DNA and to the cellular phosphoprotein p53 as well as wild-type large T. These data suggest that the cytoplasmic location of d10 large T is not due to an inability of the protein to be retained within the nucleus, but argues instead that the protein fails to reach the nucleus because it contains a defective nuclear location signal.

摘要

我们研究了由SV40突变体d10编码的大T抗原,该突变体无法定位于细胞核。该突变体的DNA序列预测在大T抗原的127位赖氨酸-赖氨酸-赖氨酸-精氨酸-赖氨酸131序列内,第128位赖氨酸发生了由赖氨酸到苏氨酸的改变。结果表明,d10大T抗原能够像野生型大T抗原一样,与SV40 DNA、细胞DNA以及细胞磷蛋白p53结合。这些数据表明,d10大T抗原定位于细胞质并非由于该蛋白质无法保留在细胞核内,而是相反,该蛋白质未能到达细胞核是因为它含有缺陷的核定位信号。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c34d/554648/4d97d040ff70/emboj00277-0190-a.jpg

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