Skip to main content
. 2014 May 21;9(5):e98304. doi: 10.1371/journal.pone.0098304

Figure 1. Activation of the HIV-1 LTR by Rad51 and NF-κB p65 requires the κB motif.

Figure 1

(A) Primary cultures of human astrocytes were transfected with luciferase reporter plasmids pGL3-LTR encompassing various segments of the LTR (as indicated), either alone or together with plasmids expressing NF-κB p65 and/or Rad51. The total amount of DNA was equalized with relevant plasmid vector DNA. (B) Western blot of protein extracts from the cells shown in Panel A showing NF-κB p65 and Rad51 levels in each sample. α-Tubulin served as a protein loading control. (C) Primary cultures of human astrocytes were transfected with NF-κB p65 siRNA and Rad51 siRNA alone or together. The total amount of siRNA was equalized with non-target siRNA. After 48 hours, cells were lysed and luciferase assays performed. (D) Western blot analysis illustrating the levels of NF-κB p65 and Rad51 in cells treated with various siRNAs as indicated. Transcriptional activity represents fold effect in which controls (NF-κB p65 and Rad51) were set at 1.0.