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通过与HTLV-I Tax癌蛋白结合将Int-6排除在PML核体之外。

Exclusion of Int-6 from PML nuclear bodies by binding to the HTLV-I Tax oncoprotein.

作者信息

Desbois C, Rousset R, Bantignies F, Jalinot P

机构信息

Centre National de la Recherche Scientifique UMR49, Ecole Normale Supérieure de Lyon, 69364 Lyon Cedex 07, France.

出版信息

Science. 1996 Aug 16;273(5277):951-3. doi: 10.1126/science.273.5277.951.

Abstract

The Tax transactivator of the human T cell leukemia virus type I (HTLV-I) exhibits oncogenic properties. A screen for proteins interacting with Tax yielded a complementary DNA (cDNA) encoding the human Int-6 protein. In mice, the Int-6 gene can be converted into a putative dominant negative oncogene after retroviral insertion. Here, Int-6 was localized in the cell nucleus to give a speckled staining pattern superposed to that of the promyelocytic leukemia (PML) protein. The binding of Tax to Int-6 caused its redistribution from the nuclear domains to the cytoplasm. Thus, Int-6 is a component of the PML nuclear bodies and Tax disrupts its normal cellular localization by binding to it.

摘要

人类I型T细胞白血病病毒(HTLV-I)的Tax反式激活因子具有致癌特性。一项针对与Tax相互作用蛋白的筛选得到了一个编码人类Int-6蛋白的互补DNA(cDNA)。在小鼠中,逆转录病毒插入后,Int-6基因可转化为一种假定的显性负癌基因。在这里,Int-6定位于细胞核,呈现出与早幼粒细胞白血病(PML)蛋白叠加的斑点状染色模式。Tax与Int-6的结合导致其从核结构域重新分布到细胞质。因此,Int-6是PML核体的一个组成部分,而Tax通过与它结合破坏其正常的细胞定位。

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