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Targeting the PI3K and MAPK pathways to treat Kaposi's sarcoma-associated herpes virus infection and pathogenesis.

机译:靶向PI3K和MAPK途径来治疗卡波济氏肉瘤相关疱疹病毒感染和发病机理。

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摘要

Cells require the ability to appropriately respond to signals in their extracellular environment. To initiate, inhibit and control these processes, the cell has developed a complex network of signaling cascades. The phosphatidylinositol 3-kinase (PI3K) and mitogen-activated protein kinase (MAPK) signaling pathways regulate several responses including mitosis, apoptosis, motility, proliferation, differentiation and many others. It is not surprising, therefore, that many viruses target the PI3K and MAPK pathways as a means to manipulate cellular function. Recently, Kaposi's sarcoma-associated herpes virus (KSHV) has been added to the list. KSHV manipulates the PI3K and MAPK pathways to control such divergent processes as cell survival, cellular migration, immune responses, and to control its own reactivation and lytic replication. Manipulation of the PI3K and MAPK pathways also plays a role in malignant transformation. Here, the authors review the potential to target the PI3K and MAPK signaling pathways to inhibit KSHV infection and pathogenesis.
机译:细胞需要在细胞外环境中对信号做出适当反应的能力。为了启动,抑制和控制这些过程,该细胞建立了一个复杂的信号级联网络。磷脂酰肌醇3激酶(PI3K)和有丝分裂原激活的蛋白激酶(MAPK)信号传导途径调节多种反应,包括有丝分裂,细胞凋亡,运动性,增殖,分化等。因此,毫不奇怪的是,许多病毒将PI3K和MAPK路径作为操纵细胞功能的一种手段。最近,卡波西氏肉瘤相关疱疹病毒(KSHV)已添加到列表中。 KSHV操纵PI3K和MAPK途径来控制诸如细胞存活,细胞迁移,免疫反应之类的发散过程,并控制其自身的活化和裂解复制。 PI3K和MAPK途径的操纵在恶性转化中也起作用。在这里,作者回顾了靶向PI3K和MAPK信号通路来抑制KSHV感染和发病机理的潜力。

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