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Myb protein binds to human immunodeficiency virus 1 long terminal repeat (LTR) sequences and transactivates LTR-mediated transcription 总被引:11,自引:1,他引:11 下载免费PDF全文
P Dasgupta P Saikumar C D Reddy E P Reddy 《Proceedings of the National Academy of Sciences of the United States of America》1990,87(20):8090-8094
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Repeated B motifs in the human immunodeficiency virus type I long terminal repeat enhancer region do not exhibit cooperative factor binding. 总被引:10,自引:2,他引:8 下载免费PDF全文
R B Gaynor M D Kuwabara F K Wu J A Garcia D Harrich M Briskin R Wall D S Sigman 《Proceedings of the National Academy of Sciences of the United States of America》1988,85(24):9406-9410
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Kawamura T Ono K Morimoto T Akao M Iwai-Kanai E Wada H Sowa N Kita T Hasegawa K 《Circulation research》2004,94(11):1492-1499
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Tumor necrosis factor alpha activates human immunodeficiency virus type 1 through induction of nuclear factor binding to the NF-kappa B sites in the long terminal repeat. 总被引:88,自引:16,他引:72 下载免费PDF全文
E J Duh W J Maury T M Folks A S Fauci A B Rabson 《Proceedings of the National Academy of Sciences of the United States of America》1989,86(15):5974-5978
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Julius Wehrle Thalia S. Seeger Sven Schwemmers Dietmar Pfeifer Alla Bulashevska Heike L. Pahl 《Haematologica》2013,98(7):1073-1080
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Toshihiko Izumi Ryoji Fujii Tomonori Izumi Minako Nakazawa Naoko Yagishita Kaneyuki Tsuchimochi Yoshihisa Yamano Tomoo Sato Hidetoshi Fujita Satoko Aratani Natsumi Araya Kazuko Azakami Daisuke Hasegawa Shunji Kasaoka Ryosuke Tsuruta Masahiro Yokouti Kosei Ijiri Moroe Beppu Ikuro Maruyama Kusuki Nishioka Tsuyoshi Maekawa Setsuro Komiya Toshihiro Nakajima 《Arthritis \u0026amp; Rheumatology》2009,60(1):63-72
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Cyclic amplification and selection of targets for multicomponent complexes: myogenin interacts with factors recognizing binding sites for basic helix-loop-helix, nuclear factor 1, myocyte-specific enhancer-binding factor 2, and COMP1 factor. 下载免费PDF全文
W D Funk W E Wright 《Proceedings of the National Academy of Sciences of the United States of America》1992,89(20):9484-9488
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Site-specific mutations alter in vitro factor binding and change promoter expression pattern in transgenic plants. 总被引:64,自引:6,他引:58 下载免费PDF全文
E Lam P N Benfey P M Gilmartin R X Fang N H Chua 《Proceedings of the National Academy of Sciences of the United States of America》1989,86(20):7890-7894
The 35S promoter of cauliflower mosaic virus (CaMV) is able to confer high-level gene expression in most organs of transgenic plants. A cellular factor from pea and tobacco leaf tissue, which recognizes nucleotides in a tandemly repeated TGACG motif at the -75 region of this promoter, has been detected by DNase I footprinting and gel retardation assays. This factor is named activation sequence factor 1 (ASF-1). A cellular factor binding to the two TGACG motifs can also be detected in tobacco root extracts. Mutations at these motifs inhibit binding of ASF-1 to the 35S promoter in vitro. When examined in transgenic tobacco, these mutations cause a 50% drop in leaf expression of the 35S promoter. In addition, these same mutations attenuate stem and root expression of the 35S promoter about 5- to 10-fold when compared to the level of expression in leaf. In contrast, mutations at two adjacent CCAAT-box-like sequences have no dramatic effect on promoter activity in vivo. A 21-base-pair element containing the two TGACG motifs is sufficient for binding of ASF-1 in vitro when inserted in a green-tissue-specific promoter. In vivo, the insertion of an ASF-1 binding site caused high levels of expression in root. Thus, a single factor binding site that is defined by site-specific mutations is shown to be sufficient to alter the expression pattern of promoters in vivo. 相似文献
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