Figure 5
Figure 5. DCIR-mediated enhancing effect on HIV-1 binding/entry involves ERK1/2 and p38. Experimental procedures used here are similar to the ones described for Figure 2 except that the following inhibitors and oligonucleotides were tested: (A) ERK1/2 inhibitor PD98059 (20nM), (B) p38 inhibitor SB203580 (2μM), and oligonucleotides specific for (C) ERK1/2 and (D) p38. Data shown correspond to the means ± SD of triplicate samples from 3 combined 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 < .001. After gene silencing, the diminution of the targeted protein was verified by Western blotting and actin was used as a loading control marker (provided as inserts for each graph). Vertical lines have been inserted to indicate repositioned gel lanes.

DCIR-mediated enhancing effect on HIV-1 binding/entry involves ERK1/2 and p38. Experimental procedures used here are similar to the ones described for Figure 2 except that the following inhibitors and oligonucleotides were tested: (A) ERK1/2 inhibitor PD98059 (20nM), (B) p38 inhibitor SB203580 (2μM), and oligonucleotides specific for (C) ERK1/2 and (D) p38. Data shown correspond to the means ± SD of triplicate samples from 3 combined 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 < .001. After gene silencing, the diminution of the targeted protein was verified by Western blotting and actin was used as a loading control marker (provided as inserts for each graph). Vertical lines have been inserted to indicate repositioned gel lanes.

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