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Biochem Pharmacol. 2016 Aug 15;114:69-81. doi: 10.1016/j.bcp.2016.03.021. Epub 2016 Apr 6.

Hijacking GPCRs by viral pathogens and tumor.

Author information

1
Department of Molecular Microbiology and Immunology, Norris Comprehensive Cancer Center, 1441 Eastlake Avenue, Los Angeles, CA 90033, United States. Electronic address: junjie.zhang@usc.edu.
2
Key Laboratory of Protein Chemistry and Fish Developmental Biology of Education Ministry of China, College of Life Sciences, Hunan Normal University, Changsha 410081, Hunan, China.
3
Department of Molecular Microbiology and Immunology, Norris Comprehensive Cancer Center, 1441 Eastlake Avenue, Los Angeles, CA 90033, United States.
4
Department of Molecular Microbiology and Immunology, Norris Comprehensive Cancer Center, 1441 Eastlake Avenue, Los Angeles, CA 90033, United States. Electronic address: pinghui.feng@usc.edu.

Abstract

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.

KEYWORDS:

Cancer; GPCR; Herpesvirus; Hijack; Pathogens; Signaling

PMID:
27060663
PMCID:
PMC4972684
DOI:
10.1016/j.bcp.2016.03.021
[Indexed for MEDLINE]
Free PMC Article

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