ArticleFrontiers in pharmacology2026
High-affinity ELR+ CXC chemokines display balanced G protein-, GRK- and β-arrestin-associated transducer engagement at the viral G protein-coupled receptor ORF74.
Article in Frontiers in pharmacology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Open reading frame 74 (ORF74) is the single G protein-coupled receptor (GPCR) encoded in the genome of Kaposi's sarcoma-associated herpesvirus (KSHV). Due to its high constitutive activity and broad chemokine binding profile, ORF74 contributes to KSHV-associated diseases through autocrine and paracrine mechanisms that promote cell proliferation, inflammation and angiogenesis. Previous studies showed that ELR+ CXC chemokines (i.e., CXCL1-3 and CXCL5-8), which contain a conserved Glu-Leu-Arg motif, bind ORF74 with high affinity. Among these chemokines, CXCL1-3 and CXCL6-8 act as full or partial agonists in ORF74-mediated G protein signaling and β-arrestin recruitment, whereas CXCL5 behaves as a neutral ligand. However, whether these chemokines preferentially engage specific intracellular transducers remains unclear. We therefore applied a unified NanoLuc Binary Technology (NanoBiT) platform in HEK293A cells to systematically compare how ELR+ CXC chemokines modulate ORF74-transducer proximity across the G protein-GRK-β-arrestin axis. CXCL1-3 and CXCL6-8, but not CXCL5, induced concentration-dependent ORF74-specific responses involving miniG
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