sHBZ suppressed Tax-mediated NF-κB activation but did not interfere with the Tax/IKKγ complex. (A,B) sHBZ repressed Tax-induced NF-κB activation. Jurkat cells were cotransfected with κB-Luc and phRL-TK, with or without 1 μg pCG-Tax, pCG-Tax M47, pCG Tax M22, and with 1 or 3 μg pME18Sneo-sHBZ, usHBZ, or TTG-HBZ. After 48 hours, luciferase activity was measured. (C) Tax overexpression overcame sHBZ-mediated suppression of NF-κB activation. Jurkat cells were cotransfected with κB-Luc and phRL-TK, with or without pCG-Tax and pME18Sneo-sHBZ. The total amount of DNA was equalized by adding empty vectors. (D) sHBZ could not modulate the Tax-driven phosphorylation of IκBα. Jurkat cells were transfected with pCG-Tax and pME18Sneo-sHBZ. Cell lysates were subjected to FunctionELISA IκBα assay. (E) sHBZ did not influence the interaction between Tax and IKKγ. 293FT cells were transfected with the indicated cDNA expression constructs. Cell lysates were subjected to immunoprecipitation (IP) with anti–c-Myc and anti-HA followed by immunoblotting (IB) using anti-Tax or anti-His, respectively. The expression levels of Tax, IKKγ and sHBZ were analyzed. *P < .05; **P < .01.