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The murine AIDS virus Gag precursor protein binds to the SH3 domain of c-Abl.

机译:鼠艾滋病病毒的Gag前体蛋白与c-Abl的SH3结构域结合。

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摘要

The Pr60gag protein of the murine AIDS (MAIDS) defective virus promotes the proliferation of the infected target B cells and is responsible for inducing a severe immunodeficiency disease. Using the yeast two-hybrid system, we identified the SH3 domain of c-Abl as interacting with the proline-rich p12 domain of Pr60gag. The two proteins were shown to associate in vitro and in vivo in MAIDS virus-infected B cells. Overexpression of Pr60(gag) in these cells led to a detectable increase of the levels of c-Abl protein and to its translocation at the membrane. These results suggest that this viral protein serves as a docking site for signaling molecules and that c-Abl may be involved in the proliferation of infected B cells.
机译:鼠艾滋病(MAIDS)缺陷病毒的Pr60gag蛋白促进了感染的目标B细胞的增殖,并导致了严重的免疫缺陷疾病。使用酵母双杂交系统,我们确定c-Abl的SH3结构域与Pr60gag富含脯氨酸的p12结构域相互作用。已显示这两种蛋白在MAIDS病毒感染的B细胞中在体内和体外缔合。 Pr60(gag)在这些细胞中的过表达导致c-Abl蛋白水平的可检测增加及其在膜上的易位。这些结果表明,该病毒蛋白充当信号分子的停靠位点,而c-Abl可能参与了受感染B细胞的增殖。

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