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1型人类免疫缺陷病毒Nef蛋白在体外与丝氨酸/苏氨酸蛋白激酶的结合及磷酸化作用

In vitro binding and phosphorylation of human immunodeficiency virus type 1 Nef protein by serine/threonine protein kinase.

作者信息

Bodéus M, Marie-Cardine A, Bougeret C, Ramos-Morales F, Benarous R

机构信息

INSERM U332, Institut Cochin de Génétique Moléculaire, Université Paris V-René Descartes, France.

出版信息

J Gen Virol. 1995 Jun;76 ( Pt 6):1337-44. doi: 10.1099/0022-1317-76-6-1337.

Abstract

Although the human immunodeficiency virus type 1 (HIV-1) nef gene still has no precisely defined function, in vivo studies have demonstrated that Nef is an important pathogenic determinant of HIV. In order to identify cellular proteins capable of binding to Nef, the HIV-1LAI nef gene product was expressed in the bacterial vector pGEX-2T as a glutathione S-transferase (GST)-Nef fusion protein. Deletion mutants corresponding to 86 and 35 N-terminal residues of the Nef protein were prepared. The GST-Nef constructs were used to identify cellular kinases capable of interacting with Nef. After incubation with a Jurkat cell lysate, the GST-Nef constructs immobilized on glutathione-agarose beads bound to cellular kinase(s) and were phosphorylated at three sites in vitro: one on threonine at position 15, one on serine between residues 1 and 35, and one on threonine between residues 36 and 86. The Nef-phosphorylating activity was inhibited by protein kinase C (PKC)-selective inhibitors. Cell fractionation showed that this Nef-binding kinase was mainly in the membrane-associated fraction. These results suggest that kinase(s) of the PKC family are specifically bound to and phosphorylate Nef in vitro. The interaction of Nef with cellular kinases and its phosphorylation may be important in mediating the effects of Nef in HIV-1 pathogenesis.

摘要

尽管人类免疫缺陷病毒1型(HIV-1)的nef基因功能仍未完全明确,但体内研究表明Nef是HIV的重要致病决定因素。为了鉴定能够与Nef结合的细胞蛋白,HIV-1LAI nef基因产物在细菌载体pGEX-2T中作为谷胱甘肽S-转移酶(GST)-Nef融合蛋白表达。制备了与Nef蛋白N端86和35个残基对应的缺失突变体。GST-Nef构建体用于鉴定能够与Nef相互作用的细胞激酶。与Jurkat细胞裂解物孵育后,固定在谷胱甘肽琼脂糖珠上的GST-Nef构建体与细胞激酶结合,并在体外三个位点被磷酸化:一个在第15位的苏氨酸上,一个在第1至35位残基之间的丝氨酸上,一个在第36至86位残基之间的苏氨酸上。Nef磷酸化活性被蛋白激酶C(PKC)选择性抑制剂抑制。细胞分级分离显示这种Nef结合激酶主要存在于膜相关部分。这些结果表明PKC家族的激酶在体外与Nef特异性结合并使其磷酸化。Nef与细胞激酶的相互作用及其磷酸化可能在介导Nef在HIV-1发病机制中的作用方面很重要。

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