Wang H, Liu K, Yuan F, Berdichevsky L, Taichman L B, Auborn K
Department of Otolaryngology, Long Island Jewish Medical Center, Long Island Campus of Albert Einstein College of Medicine, New Hyde Park, New York 11040, USA.
J Virol. 1996 Jul;70(7):4839-44. doi: 10.1128/JVI.70.7.4839-4844.1996.
We have evaluated the impact of the CCAAT enhancer-binding protein (C/EBP) transcription factors on human papillomavirus type 11 (HPV11). C/EBPbeta is in nuclei of cultured foreskin keratinocytes and binds its consensus sequence in HPV11 DNA. We have used the novel approach of depleting the availability of C/EBPs in vivo using nuclease-resistant oligomers containing C/EBP DNA binding sites. In cultured foreskin keratinocytes containing replicating HPV11 DNA, levels of both HPV11 transcripts and HPV DNA increase after treatment with oligomers; containing the C/EBPbeta DNA binding motif. These results indicate that C/EBPbeta is a repressor for HPV11 in keratinocytes.
我们评估了CCAAT增强子结合蛋白(C/EBP)转录因子对11型人乳头瘤病毒(HPV11)的影响。C/EBPβ存在于培养的包皮角质形成细胞核中,并与HPV11 DNA中的共有序列结合。我们采用了一种新方法,即使用含有C/EBP DNA结合位点的核酸酶抗性寡聚物在体内减少C/EBPs的可利用性。在含有复制型HPV11 DNA的培养包皮角质形成细胞中,用含有C/EBPβ DNA结合基序的寡聚物处理后,HPV11转录本和HPV DNA的水平均升高。这些结果表明,C/EBPβ是角质形成细胞中HPV11的一种阻遏物。