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Hijacking GPCRs by viral pathogens and tumor
Junjie Zhang1, Hao Feng2, Simin Xu1
1Department of Molecular Microbiology and Immunology, Norris Comprehensive Cancer Center, 1441 Eastlake Avenue, Los Angeles, CA 90033, United States.
Viral G protein-coupled receptors (GPCRs) hijack cellular pathways for herpesvirus infections and cancer. Targeting these GPCRs offers potential anti-viral and anti-tumor therapies.
Area of Science:
- Molecular biology
- Virology
- Oncology
Background:
- G protein-coupled receptors (GPCRs) are crucial cell signaling molecules.
- Herpesviruses utilize diverse strategies, including expressing viral GPCRs, to manipulate host cells.
- Dysregulated GPCR signaling, via viral or cellular mutations, contributes to diseases and cancer.
Purpose of the Study:
- To explore the role of viral GPCRs in herpesvirus infections.
- To investigate the link between GPCR pathway mutations and human cancers.
- To identify GPCRs as potential therapeutic targets for viral diseases and oncogenesis.
Main Methods:
- Analysis of GPCR structure and function.
- Investigation of signaling pathway activation by viral and mutated cellular GPCRs.
- Review of clinical implications in immune-deficient individuals and cancer patients.
Main Results:
- Viral GPCRs exhibit unique properties activating diverse signaling pathways.
- Constitutive GPCR activation due to mutations drives cancer cell proliferation and survival.
- Herpesvirus infections involving GPCRs are linked to pathologies, especially in immune-deficient individuals.
Conclusions:
- Hijacked GPCR-mediated signaling is a common mechanism in viral infections and cancer.
- Viral and cellular GPCRs represent shared targets for therapeutic intervention.
- Targeting GPCRs holds promise for developing novel anti-viral and anti-cancer treatments.
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