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AIM:p73,as a novel member of a family of p53-relatedtranscription factors,shares redundant functions with p53,such as the abilities of inducing apoptosis and suppressinggrowth.It is well known that p53 can repress HBV expressionand transcription efficiently.The aim of this paper is toinvestigate the transcriptional effect of p73α and p73β onhepatitis B virus(HBV)and to understand the correlationbetween HBV and p73.METHODS:To construct an x-gene inactivated HBV plasmidwhich was cotransfected with p73α or p73β expressionvectors into HepG2 cells.After transiently transfection,HBVsurface antigen(HBsAg)and HBV e antigen(HBeAg)weredetected by ELISA.Viral transcripts synthesized by HBV wereevaluated by Northern blotting analysis.The activities ofHBV regulatory elements,including enhancer I/X promoter(ENI/Xp)and enhancer Ⅱ/core promoter(ENII/Cp)weremonitored by luciferase assays.RESULTS:Both p73α and p73β could repress HBsAg andHBeAg expression by downregulating the ENI/Xp and ENⅡ/Cp activities.But p73β exerted stronger inhibition on theactivity of ENI/Xp than p73α,resulting in much lower levelof viral transcripts and the antigens expression.CONCLUSION:p73β as a novel member of p53 family canefficiently inhibit HBV transcription mainly throughdownregulating the activities of the HBV ENI/Xp regulatoryelements.
AIM: p73, as a novel member of a family of p53-related transcription factors, shares redundant functions with p53, such as the abilities of inducing apoptosis and suppressing growth. It is well known that p53 can repress HBV expression and transcription efficiently. paper is to investigate the transcriptional effect of p73α and p73β onhepatitis B virus (HBV) and to understand the correlation between HBV and p73. METHODS: To construct an x-gene inactivated HBV plasmidwhich was cotransfected with p73α or p73β expression vectors into HepG2 cells. After transiently transfection , HBVsurface antigen (HBsAg) and HBV e antigen (HBeAg) weredetected by ELISA. Viral transcripts synthesized by HBV wereevaluated by Northern blotting analysis. Activities of HBV regulatory elements, including enhancer I / X promoter (ENI / Xp) and enhancer II / core promoter (ENII / Cp) weremonitored by luciferase assays .RESULTS: Both p73α and p73β could repress HBsAg and HBeAg expression by downregulating the ENI / Xp and ENⅡ / Cp activities. But p73β exerted stronger inhibition on the activity of ENI / Xp than p73α, resulting in much lower level of viral transcripts and the antigens expression. CONCLUSION: p73β as a novel member of p53 family canefficiently inhibit HBV transcription mainly through downregulating the activities of the HBV ENI / Xp regulatoryelements.