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首页> 外文期刊>African Journal of Biotechnology >Human immunodeficiency virus (HIV)-1 Tat downregulates the phosphorylation of recepteur dorigine nantais (RON) receptor tyrosine kinase induced by macrophage-stimulating protein
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Human immunodeficiency virus (HIV)-1 Tat downregulates the phosphorylation of recepteur dorigine nantais (RON) receptor tyrosine kinase induced by macrophage-stimulating protein

机译：人类免疫缺陷病毒（HIV）-1 Tat下调巨噬细胞刺激蛋白诱导的受体多吉因南泰（RON）受体酪氨酸激酶的磷酸化

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The aim of this study is?to examine the effects of the human immunodeficiency virus (HIV)-1 Tat protein on the expression and phosphorylation of recepteur d'origine nantais (RON) receptor tyrosine kinase and the mechanisms involved. We first determined the expression levels of RON and macrophage-stimulating protein (MSP) were determined in the peripheral blood of HIV-positive patients and control subjects. The 293T cells were transfected with the pDR2-RON plasmid to establish the 293T-RON cell line. The pcDNA3.1 (+)-Tat-His plasmid was constructed to obtain recombinant Tat protein. The 293T-RON cells pretreated with MSP were co-cultured with the H9/HTLV-IIIB cells or were stimulated with the Tat protein; then, the change of RON expression was determined. This study revealed higher expression of RON and relatively lower expression of MSP in HIV-infected patients than in the uninfected patients. We demonstrated that HIV-1 Tat down-regulated the expression and phosphorylation of RON in 293T-RON cells. Flow cytometry analysis of 293T-RON cells revealed that RON was expressed in 293T-RON cells. The 293T-RON cells co-cultured with the H9/HTLV-IIIB cells RON expression did not change significantly, while stimulation with 500 ng/ml Tat considerably decreased RON expression in 293T-RON cells.?These findings imply that?Tat may play a role in modulating the function of RON, which is activated by MSP; this may provide a permissive environment for both HIV and other opportunistic microbes.
机译：这项研究的目的是研究人类免疫缺陷病毒（HIV）-1 Tat蛋白对d'origine nantais（RON）受体酪氨酸激酶的表达和磷酸化的影响及其机制。我们首先确定了HIV阳性患者和对照组受试者外周血中RON和巨噬细胞刺激蛋白（MSP）的表达水平。用pDR2-RON质粒转染293T细胞以建立293T-RON细胞系。构建pcDNA3.1（+）-Tat-His质粒以获得重组Tat蛋白。用MSP预处理的293T-RON细胞与H9 / HTLV-IIIB细胞共培养或用Tat蛋白刺激。然后，确定RON表达的变化。这项研究表明，与未感染艾滋病毒的患者相比，在HIV感染患者中RON的表达较高，而MSP则相对较低。我们证明了HIV-1 Tat下调了293T-RON细胞中RON的表达和磷酸化。 293T-RON细胞的流式细胞仪分析表明RON在293T-RON细胞中表达。与H9 / HTLV-IIIB细胞共培养的293T-RON细胞的RON表达没有明显变化，而用500 ng / ml Tat刺激显着降低了293T-RON细胞的RON表达。这些发现表明，Tat可能发挥作用由MSP激活的调节RON功能的作用;这可能为艾滋病毒和其他机会性微生物提供宽松的环境。

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