Smith C D, Baglia L A, Curristin S M, Ruddell A
Department of Microbiology and Immunology, University of Rochester School of Medicine, New York 14642.
J Virol. 1994 Oct;68(10):6232-42. doi: 10.1128/JVI.68.10.6232-6242.1994.
Two long terminal repeat (LTR) enhancer-binding proteins which may regulate high rates of avian leukosis virus (ALV) LTR-enhanced c-myc transcription during bursal lymphomagenesis have been identified (A. Ruddell, M. Linial, and M. Groudine, Mol. Cell. Biol. 9:5660-5668, 1989). The genes encoding the a1/EBP and a3/EBP binding factors were cloned by expression screening of a lambda gt11 cDNA library from chicken bursal lymphoma cells. The a1/EBP cDNA encodes a novel leucine zipper transcription factor (W. Bowers and A. Ruddell, J. Virol. 66:6578-6586, 1992). The partial a3/EBP cDNA clone encodes amino acids 84 to 313 of vitellogenin gene-binding protein (VBP), a leucine zipper factor that binds the avian vitellogenin II gene promoter (S. Iyer, D. Davis, and J. Burch, Mol. Cell. Biol. 11:4863-4875, 1991). Multiple VBP mRNAs are expressed in B cells in a pattern identical to that previously observed for VBP in other cell types. The LTR-binding activities of VBP, a1/EBP, and B-cell nuclear extract protein were compared and mapped by gel shift, DNase I footprinting, and methylation interference assays. The purified VBP and a1/EBP bacterial fusion proteins bind overlapping but distinct subsets of CCAAT/enhancer elements in the closely related ALV and Rous sarcoma virus (RSV) LTR enhancers. Protein binding to these CCAAT/enhancer elements accounts for most of the labile LTR enhancer-binding activity observed in B-cell nuclear extracts. VBP and a1/EBP could mediate the high rates of ALV and RSV LTR-enhanced transcription in bursal lymphoma cells and many other cell types.
已鉴定出两种长末端重复序列（LTR）增强子结合蛋白，它们可能在法氏囊淋巴瘤发生过程中调节禽白血病病毒（ALV）LTR增强的c-myc转录的高发生率（A. Ruddell、M. Linial和M. Groudine，《分子细胞生物学》9:5660 - 5668，1989年）。通过对来自鸡法氏囊淋巴瘤细胞的λgt11 cDNA文库进行表达筛选，克隆了编码α1/EBP和α3/EBP结合因子的基因。α1/EBP cDNA编码一种新型亮氨酸拉链转录因子（W. Bowers和A. Ruddell，《病毒学杂志》66:6578 - 6586，1992年）。α3/EBP cDNA部分克隆编码卵黄生成素基因结合蛋白（VBP）的第84至313个氨基酸，VBP是一种结合禽卵黄生成素II基因启动子的亮氨酸拉链因子（S. Iyer、D. Davis和J. Burch，《分子细胞生物学》11:4863 - 4875，1991年）。多种VBP mRNA在B细胞中的表达模式与先前在其他细胞类型中观察到的VBP表达模式相同。通过凝胶迁移、DNase I足迹分析和甲基化干扰试验，比较并定位了VBP、α1/EBP和B细胞核提取物蛋白的LTR结合活性。纯化的VBP和α1/EBP细菌融合蛋白结合密切相关的ALV和劳斯肉瘤病毒（RSV）LTR增强子中重叠但不同的CCAAT/增强子元件子集。蛋白质与这些CCAAT/增强子元件的结合占B细胞核提取物中观察到的大部分不稳定LTR增强子结合活性。VBP和α1/EBP可介导法氏囊淋巴瘤细胞及许多其他细胞类型中ALV和RSV LTR增强的高转录率。
