Adenovirus endocytosis via αv integrins requires phosphoinositide-3-OH kinase
Adenovirus endocytosis via αv integrins requires phosphoinositide-3-OH kinase
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DOI：
10.1128/jvi.72.3.2055-2061.1998
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发表时间：
1998-03-01
影响因子：
5.4
通讯作者：
Nemerow, GR
中科院分区：
文献类型：
--
作者：
Li, EG;Stupack, D;Nemerow, GR
整合素介导细胞在细胞外基质上的粘附和运动，但它们也促进病毒附着和/或进入。有证据表明，腺病毒内化α（V）整合素需要激活磷脂酰肌醇-3-OH激酶（PI 3 K），而α（V）整合素介导的细胞运动依赖于ERK 1/ERK 2丝裂原活化蛋白激酶途径。腺病毒与α（v）整合素的相互作用诱导PI 3 K的活化。内源性PI 3 K活性的药理学或遗传破坏阻断了腺病毒内化和病毒介导的基因递送，但对整合素介导的细胞粘附或运动性没有影响。因此，整合素连接参与促进病毒内吞或细胞运动的不同信号传导途径。
Integrins mediate cell adhesion and motility on the extracellular matrix, yet they also promote viral attachment and/or entry. Evidence is presented that adenovirus internalization by alpha(v) integrins requires activation of phosphoinositide-3-OH kinase (PI3K), whereas alpha(v) integrin-mediated cell motility depends on the ERK1/ERK2 mitogen-activated protein kinase pathway. Interaction of adenovirus with alpha(v) integrins induced activation of PI3K. Pharmacologic or genetic disruption of endogenous PI3K activity blocked adenovirus internalization and virus-mediated gene delivery yet had no effect on integrin-mediated cell adhesion or motility, Therefore, integrin ligation engages distinct signaling pathways that promote viral endocytosis or cell movement.