{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Pati S"],"funding":["NCI NIH HHS"],"pagination":["8660-73"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC115111"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["75(18)"],"pubmed_abstract":["Infection with human herpesvirus 8 (HHV-8), also known as Kaposi's sarcoma (KS)-associated herpesvirus, is necessary for the development of KS. The HHV-8 lytic-phase gene ORF74 is related to G protein-coupled receptors, particularly interleukin-8 (IL-8) receptors. ORF74 activates the inositol phosphate/phospholipase C pathway and the downstream mitogen-activated protein kinases, JNK/SAPK and p38. We show here that ORF74 also activates NF-kappaB independent of ligand when expressed in KS-derived HHV-8-negative endothelial cells or primary vascular endothelial cells. NF-kappaB activation was enhanced by the chemokine GROalpha, but not by IL-8. Mutation of Val to Asp in the ORF74 second cytoplasmic loop did not affect ligand-independent signaling activity, but it greatly increased the respons"],"journal":["Journal of virology"],"pubmed_title":["Activation of NF-kappaB by the human herpesvirus 8 chemokine receptor ORF74: evidence for a paracrine model of Kaposi's sarcoma pathogenesis."],"pmcid":["PMC115111"],"funding_grant_id":["R01 CA055293","R01 CA55293","P01 CA78817"],"pubmed_authors":["Foulke JS","Feldman RA","Guo HG","Pati S","Kim J","Cavrois M","Reitz M"],"additional_accession":[]},"is_claimable":false,"name":"Activation of NF-kappaB by the human herpesvirus 8 chemokine receptor ORF74: evidence for a paracrine model of Kaposi's sarcoma pathogenesis.","description":"Infection with human herpesvirus 8 (HHV-8), also known as Kaposi's sarcoma (KS)-associated herpesvirus, is necessary for the development of KS. The HHV-8 lytic-phase gene ORF74 is related to G protein-coupled receptors, particularly interleukin-8 (IL-8) receptors. ORF74 activates the inositol phosphate/phospholipase C pathway and the downstream mitogen-activated protein kinases, JNK/SAPK and p38. We show here that ORF74 also activates NF-kappaB independent of ligand when expressed in KS-derived HHV-8-negative endothelial cells or primary vascular endothelial cells. NF-kappaB activation was enhanced by the chemokine GROalpha, but not by IL-8. Mutation of Val to Asp in the ORF74 second cytoplasmic loop did not affect ligand-independent signaling activity, but it greatly increased the respons","dates":{"release":"2001-01-01T00:00:00Z","publication":"2001 Sep","modification":"2025-05-31T23:22:52.795Z","creation":"2019-03-27T00:17:06Z"},"accession":"S-EPMC115111","cross_references":{"pubmed":["11507211"],"doi":["10.1128/jvi.75.18.8660-8673.2001"]}}