PKD3 is required for prostratin-activated HIV-1 transcription

Prostratin has been shown to promote transcriptional activation of HIV-1 provirus, however, the underlying mechanism is not fully understood. By using HeLa cells with a stably integrated HIV-LTR-Luciferase gene as a reporter system, we investigated the role of protein kinase D (PKD) in HIV-1 activation by prostratin treatment. Knocking-down of PKD3, but not PKD1 or PKD2, inhibited both the basal and prostratin-induced HIV-LTR-Luciferase expression. Moreover, prostratin triggered PKD3 activation by inducing the phosphorylation of its activation loop. Furthermore, the overexpression of constitutively active form of PKD3, but not the wild type or kinase dead form of PKD3, augmented HIV-LTR-Luciferase expression. These results suggest that activated PKD3 is critical for prostratin stimulating HIV-LTR transcription.