155971-5581

pubmed-article:11141237, pubmed-article:11504923, pubmed-article:15689238, pubmed-article:1832084, pubmed-article:19363595, pubmed-article:1970444, pubmed-article:2139676, pubmed-article:22114277, pubmed-article:3259291, pubmed-article:7642615, pubmed-article:7850771, pubmed-article:8206685, pubmed-article:8599832

A specific interaction between CD4 and HIV-1 gp120 is required for phosphorylation of CD4, which could involve protein kinase C, A synthetic peptide containing residues 581-597 from HIV-1 gp41 inhibits protein kinase C (pkC)-mediated phosphorylation of the CD3 gamma-chain in intact cells and directly inhibits partially purified pkC, A synthetic peptide corresponding to cytoplasmic domain residues 828-848 of HIV-1 gp41 inhibits pKC-catalysed phosphorylation of a protein substrate, Down modulation of the interaction between HIV-1 gp120 and CD4 by TPA is blocked by protein kinase C (PKC) inhibitors, suggesting PKC may play an important role in HIV-1 infection, HIV-1 gp120 activates forward trafficking and surface clustering of NMDA receptors in membrane microdomains by a PKA-dependent phosphorylation of the NR1 C-terminal Ser897, followed by a PKC-dependent phosphorylation of Ser896, HIV-1 gp120 increases the levels of calcium-dependent and -independent PKC isozymes; the most striking change is observed in PKC-zeta isozyme levels, HIV-1 gp160-induced AP-1 complex formation is dependent upon protein tyrosine phosphorylation and is abolished by inhibitors of protein kinase C, but it is unaffected by calcium channel blockers or cyclosporine A, IL-16 induces rapid translocation of PKC from the cytosol to the membrane in CD4+ cells; PKC inhibitors completely block IL-16-induced lymphocyte migration as well as the motile response induced by HIV-1 gp120 and anti-CD4 antibody binding to CD4, Induction of apoptosis in cell cultures through binding of HIV-1 gp120 or gp160 to CXCR4 involves protein kinase C, basic fibroblast growth factor, caspase-3, and the pro-apoptotic molecule Bax, Pre-treatment of endothelial cells with fibroblast growth factor 2 (FGF2) protects cells from HIV-1 gp120 angiotoxicity; this protection is regulated by crosstalk among the ERK, PI3K-AKT and PKC signaling pathways, c-FLIPL inhibits Bax activation via modulating PKC expression at the transcriptional level involving AP-2 during gp120 treatment