Hijacking GPCRs by viral pathogens and tumor

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• 作者：Junjie Zhang^a ; ^{junjie.zhang@usc.edu" class="auth_mail" title="E-mail the corresponding author} ; Hao Feng^b ; Simin Xu^a ; Pinghui Feng^a ; ^{pinghui.feng@usc.edu" class="auth_mail" title="E-mail the corresponding author}
• 关键词：GPCR ; Signaling ; Hijack ; Herpesvirus ; Pathogens ; Cancer
• 刊名：Biochemical Pharmacology
• 出版年：2016
• 出版时间：15 August 2016
• 年：2016
• 卷：114
• 期：Complete
• 页码：69-81
• 全文大小：1824 K

文摘

G protein-coupled receptors (GPCRs) constitute the largest family of molecules that transduce signals across the plasma membrane. Herpesviruses are successful pathogens that evolved diverse mechanisms to benefit their infection. Several human herpesviruses express GPCRs to exploit cellular signaling cascades during infection. These viral GPCRs demonstrate distinct biochemical and biophysical properties that result in the activation of a broad spectrum of signaling pathways. In immune-deficient individuals, human herpesvirus infection and the expression of their GPCRs are implicated in virus-associated diseases and pathologies. Emerging studies also uncover diverse mutations in components, particularly GPCRs and small G proteins, of GPCR signaling pathways that render the constitutive activation of proliferative and survival signal, which contributes to the oncogenesis of various human cancers. Hijacking GPCR-mediated signaling is a signature shared by diseases associated with constitutively active viral GPCRs and cellular mutations activating GPCR signaling, exposing key molecules that can be targeted for anti-viral and anti-tumor therapy.