HUMAN LIVER CARCINOGENESIS

B肝炎病毒与DNA修复 我们和其他人以前曾报道过p53可以调节核苷酸水平， 切除修复使用宿主再活化试验，我们的初步数据 表明HBx抑制再活化，即，紫外线修复 光（UV-C，254 nm）损伤质粒。这就引出了一个假设， HBx抑制p53与基底细胞中XPB或XPD DNA解旋酶的结合， 转录核苷酸切除修复复合物。我们有 先前证实HBx蛋白抑制体外p53结合， 在XPB。HBx与XPB结合。HBx与p53的羧基端结合 这也是XPB结合的位点。我们目前正在调查 HBx与TFIIH多蛋白的其他成员结合的假设 复杂.我们正试图获得HBVX的晶体和共晶体 用于精细结构分析。

Hepatitis B Virus and DNA Repair We and others have previously reported that p53 can modulate nucleotide excision repair. Using a host reactivation assay, our preliminary data indicate that HBx inhibits reactivation, i.e., repair of the ultraviolet light (UV-C, 254 nm) damage plasmid. This leads to the hypothesis that HBx inhibits p53 binding to XPB or XPD DNA helicases in the basal transcription-nucleotide excision repair complex, TFIIH. We have previously demonstrated that HBx protein inhibits in vitro p53 binding to XPB. HBx binds to XPB. HBx binds to the carboxyl terminus of p53 which also is the site of XPB binding. We are currently investigating the hypothesis that HBx binds to other members of the TFIIH multiprotein complex. We are attempting to obtain crystals of HBVX and co-crystals of its binding partners for fine detail structural analysis.