RETINOBLASTOMA-REPRESSION OF E2F-DEPENDENT TRANSCRIPTION DEPENDS ON THE ABILITY OF THE RETINOBLASTOMA PROTEIN TO INTERACT WITH E2F AND IS ABROGATED BY THE ADENOVIRUS E1A ONCOPROTEIN
RETINOBLASTOMA-REPRESSION OF E2F-DEPENDENT TRANSCRIPTION DEPENDS ON THE ABILITY OF THE RETINOBLASTOMA PROTEIN TO INTERACT WITH E2F AND IS ABROGATED BY THE ADENOVIRUS E1A ONCOPROTEIN
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DOI：
10.1093/nar/20.22.5947
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发表时间：
1992-11-25
影响因子：
14.9
通讯作者：
RAYCHAUDHURI, P
中科院分区：
文献类型：
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作者：
ARROYO, M;RAYCHAUDHURI, P
视网膜母细胞瘤肿瘤抑制基因的产物与转录因子E2 F相互作用。在视网膜母细胞瘤基因产物（Rb）和E2 F之间可以检测到两种不同类型的相互作用。第一种类型涉及Rb结合蛋白RBP 60。在RBP 60存在下形成的Rb/E2 F复合物能够结合DNA，并且在凝胶阻滞测定中以不同的迁移率迁移。第二种类型的Rb/E2 F复合物在不存在RBP 60的情况下可见。第二种类型的Rb/E2 F复合物在凝胶阻滞试验中不形成带移复合物，其形成导致E2 F的DNA结合活性的明显抑制或丧失。使用一系列的Rb突变体，我们表明，这两种类型的Rb/E2 F复合物依赖于共同的结构域的Rb蛋白。Rb蛋白的T/E1 A结合区以及羧基端对于这两种类型的Rb/E2 F相互作用是至关重要的。我们还表明，视网膜母细胞瘤蛋白抑制E2 F依赖的转录，这种Rb抑制E2 F依赖的转录依赖于Rb与E2 F相互作用的能力。此外，结合Rb的腺病毒E1 A基因产物抵消Rb抑制并恢复E2 F依赖性转录。
The product of the retinoblastoma tumor suppressor gene interacts with the transcription factor E2F. Two distinct types of interactions can be detected between the retinoblastoma gene product (Rb) and E2F. The first type involves an Rb-binding protein, RBP60. The Rb/E2F complex formed in the presence of RBP60 is able to bind DNA and migrates with a distinct mobility in gel retardation assays. The second type of Rb/E2F complex is seen in the absence of RBP60. This second type of Rb/E2F complex does not form a band-shift complex in gel retardation assays and its formation results in an apparent inhibition or loss of the DNA binding activity of E2F. Using a series of Rb-mutants we show that these two types of Rb/E2F complexes depend on common domains of the Rb protein. The T/E1A-binding region as well as the carboxyl-terminus of the Rb protein are critical for these two types of Rb/E2F interactions. We also show that the retinoblastoma protein represses the E2F-dependent transcription, and this Rb-repression of the E2F-dependent transcription depends on the ability of Rb to interact with E2F. Moreover, the adenovirus E1A gene product, which binds Rb, counteracts the Rb-repression and restores E2F-dependent transcription.