Signaling proteins responsible for the DCIR-mediated enhancing effect on HIV-1 binding/entry are also required to achieve a superior virus infection. (A) Raji-CD4 and Raji-CD4-DCIR were either left untreated or preincubated for 10 minutes with the tyrosine phosphatase inhibitor SSG (100μg/mL), Syk inhibitor piceatannol (10μM), Src inhibitor PP2 (10μM), classic PKC inhibitor Gö6976 (1μM), MAPK p38 inhibitor SB203580 (2 μM), or MAP kinase inhibitor PD98059 (20nM). (B) Raji-CD4 and Raji-CD4-DCIR were treated with Oligofectamine and then either left untreated or treated for 5 hours with sense or antisense oligonucleotides specific for the listed signaling proteins. Next, cells were exposed to NL4-3 for 24 hours. Virus infection was determined by real-time PCR of spliced Tat mRNA. Data shown correspond to the means ± SD of triplicate samples from 3 independent experiments. The statistical significance of differences between untreated and treated cells or nontransfected and Raji-CD4-DCIR transfected with antisense oligonucleotides is denoted by asterisks: *P < .05; **P < .01; ***P < .001.