Figure 4
Figure 4. DCIR-mediated enhancing effect on HIV-1 binding/entry involves PKC-α. Experimental procedures used here are similar to those described for Figure 2 except that the following inhibitors and oligonucleotides were tested: (A) classic PKC inhibitor Gö6976 (1μM), (B) oligonucleotides specific for PKC-α, and (C) PKA inhibitor H89 (10μM). 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 PKC-α. Experimental procedures used here are similar to those described for Figure 2 except that the following inhibitors and oligonucleotides were tested: (A) classic PKC inhibitor Gö6976 (1μM), (B) oligonucleotides specific for PKC-α, and (C) PKA inhibitor H89 (10μM). 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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