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Downregulation of Lck-mediated signal transduction by tip of herpesvirus saimiri.猴疱疹病毒顶端对Lck介导的信号转导的下调作用
J Virol. 1995 Dec;69(12):7814-22. doi: 10.1128/JVI.69.12.7814-7822.1995.
2
Enhanced downregulation of Lck-mediated signal transduction by a Y114 mutation of herpesvirus Saimiri tip.通过疱疹病毒Saimiri尖端的Y114突变增强Lck介导的信号转导的下调
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3
Growth transformation of human T cells by herpesvirus saimiri requires multiple Tip-Lck interaction motifs.猴疱疹病毒导致人类T细胞的生长转化需要多个Tip-Lck相互作用基序。
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Identification of Lck-binding elements in tip of herpesvirus saimiri.在猴疱疹病毒顶端鉴定Lck结合元件。
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Mutation of the Lck-binding motif of Tip enhances lymphoid cell activation by herpesvirus saimiri.Tip的Lck结合基序的突变增强了赛米利疱疹病毒对淋巴细胞的激活作用。
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Activation of the Lck tyrosine protein kinase by the Herpesvirus saimiri tip protein involves two binding interactions.赛米利疱疹病毒tip蛋白对Lck酪氨酸蛋白激酶的激活涉及两种结合相互作用。
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Lck protein tyrosine kinase is a key regulator of T-cell activation and a target for signal intervention by Herpesvirus saimiri and other viral gene products.Lck蛋白酪氨酸激酶是T细胞活化的关键调节因子，也是赛米利疱疹病毒和其他病毒基因产物进行信号干预的靶点。
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The Lck binding domain of herpesvirus saimiri tip-484 constitutively activates Lck and STAT3 in T cells.猴疱疹病毒saimiri tip-484的Lck结合结构域在T细胞中持续激活Lck和STAT3。
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Tip, an Lck-interacting protein of Herpesvirus saimiri, causes Fas- and Lck-dependent apoptosis of T lymphocytes.Tip是猴疱疹病毒的一种与Lck相互作用的蛋白，可引起T淋巴细胞的Fas和Lck依赖性凋亡。
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Downregulation of p56(lck) tyrosine kinase activity in T cells of squirrel monkeys (Saimiri sciureus) correlates with the nontransforming and apathogenic properties of herpesvirus saimiri in its natural host.松鼠猴（Saimiri sciureus）T细胞中p56(lck)酪氨酸激酶活性的下调与其自然宿主中疱疹病毒Saimiri的非转化和无致病性相关。
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Growth transformation of human T cells by herpesvirus saimiri requires multiple Tip-Lck interaction motifs.猴疱疹病毒导致人类T细胞的生长转化需要多个Tip-Lck相互作用基序。
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7
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Activation of mitogen-activated protein kinase and NF-kappaB pathways by a Kaposi's sarcoma-associated herpesvirus K15 membrane protein.卡波西肉瘤相关疱疹病毒K15膜蛋白对丝裂原活化蛋白激酶和核因子κB信号通路的激活作用
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本文引用的文献

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Tyrosine kinase-stimulated guanine nucleotide exchange activity of Vav in T cell activation.酪氨酸激酶刺激的Vav鸟嘌呤核苷酸交换活性在T细胞活化中的作用
Science. 1993 May 7;260(5109):822-5. doi: 10.1126/science.8484124.
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T cell antigen receptor signal transduction: a tale of tails and cytoplasmic protein-tyrosine kinases.T细胞抗原受体信号转导：尾巴与细胞质蛋白酪氨酸激酶的故事
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Palmitylation of an amino-terminal cysteine motif of protein tyrosine kinases p56lck and p59fyn mediates interaction with glycosyl-phosphatidylinositol-anchored proteins.蛋白酪氨酸激酶p56lck和p59fyn氨基末端半胱氨酸基序的棕榈酰化介导了与糖基磷脂酰肌醇锚定蛋白的相互作用。
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IL-2 independent growth and cytotoxicity of herpesvirus saimiri-infected human CD8 cells and involvement of two open reading frame sequences of the virus.疱疹病毒萨米里感染的人CD8细胞的白细胞介素-2非依赖性生长和细胞毒性以及该病毒两个开放阅读框序列的作用
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猴疱疹病毒顶端对Lck介导的信号转导的下调作用

Downregulation of Lck-mediated signal transduction by tip of herpesvirus saimiri.

作者信息

Jung J U, Lang S M, Jun T, Roberts T M, Veillette A, Desrosiers R C

机构信息

New England Regional Primate Research Center, Department of Microbiology and Molecular Genetics, Harvard Medical School, Southborough, Massachusetts 01772-9102, USA.

出版信息

J Virol. 1995 Dec;69(12):7814-22. doi: 10.1128/JVI.69.12.7814-7822.1995.

DOI:10.1128/JVI.69.12.7814-7822.1995
PMID:7494293
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC189725/
Abstract

A protein, called tip, of herpesvirus saimiri associates with Lck in transformed T cells. To investigate the effects of complex formation on cellular signal transduction, we constructed human Jurkat-T-cell lines expressing tip. The expression of tip in Jurkat-T cells dramatically suppressed cellular tyrosine phosphorylation and surface expression of lymphocyte antigens. The expression of tip also blocked the induction of tyrosine phosphorylation by anti-CD3 stimulation. The expression of tip in fibroblast cells suppressed the transforming activity of oncogenic F505 Lck. Binding assays showed that the SH3 domain of Lck is sufficient to form a stable complex with tip in vitro. These results demonstrate that tip acts at an early stage of the T-cell signal transduction cascade by associating with Lck and downregulating Lck-mediated activation. Inhibition of Lck-mediated signal transduction by tip in T cells appears to be analogous to the inhibition of Lyn/Syk-mediated signal transduction in B cells by LMP2A of the B-cell-tropic Epstein-Barr virus.

摘要

赛氏疱疹病毒的一种名为Tip的蛋白质在转化的T细胞中与Lck相关联。为了研究复合物形成对细胞信号转导的影响，我们构建了表达Tip的人Jurkat - T细胞系。Tip在Jurkat - T细胞中的表达显著抑制了细胞酪氨酸磷酸化以及淋巴细胞抗原的表面表达。Tip的表达还阻断了抗CD3刺激诱导的酪氨酸磷酸化。Tip在成纤维细胞中的表达抑制了致癌性F505 Lck的转化活性。结合试验表明，Lck的SH3结构域在体外足以与Tip形成稳定的复合物。这些结果表明，Tip通过与Lck相关联并下调Lck介导的激活作用于T细胞信号转导级联反应的早期阶段。Tip在T细胞中对Lck介导的信号转导的抑制作用似乎类似于嗜B细胞的爱泼斯坦 - 巴尔病毒的LMP2A对B细胞中Lyn/Syk介导的信号转导的抑制作用。