Arany Z, Newsome D, Oldread E, Livingston D M, Eckner R
Dana Farber Cancer Institute, Boston, Massachusetts.
Nature. 1995 Mar 2;374(6517):81-4. doi: 10.1038/374081a0.
The cellular protein p300 is a target of the adenoviral E1A oncoprotein and is thought to participate in preventing the G0/G1 transition in the cell cycle, activating certain enhancers and stimulating differentiation pathways. CBP is a protein that is associated with and coactivates the transcription factor CREB, mediating the induction by cyclic AMP of certain responsive promoters. The sequences of p300 and CBP are highly related. We show here that p300, like CBP2, can stimulate transcription. This activity is directly and specifically inhibited by E1A. We also find that CBP exists in a DNA-bound complex containing a member of the CREB family and that E1A and CBP interact with one another in vivo. In keeping with the idea that E1A functionally targets CBP, cAMP-dependent transcription is repressed by E1A. Thus, p300 and CBP define a family of transcriptional adaptor proteins that are specifically targeted by the E1A oncoprotein.
细胞蛋白p300是腺病毒E1A癌蛋白的作用靶点，被认为参与阻止细胞周期中的G0/G1期转换、激活某些增强子并刺激分化途径。CBP是一种与转录因子CREB相关并协同激活它的蛋白，介导环磷酸腺苷对某些反应性启动子的诱导作用。p300和CBP的序列高度相关。我们在此表明，p300与CBP一样，能够刺激转录。这种活性受到E1A的直接且特异性抑制。我们还发现，CBP存在于一个与CREB家族成员结合的DNA复合物中，并且E1A与CBP在体内相互作用。与E1A在功能上靶向CBP这一观点一致的是，E1A抑制了环磷酸腺苷依赖性转录。因此，p300和CBP定义了一类转录衔接蛋白家族，它们是E1A癌蛋白的特异性作用靶点。
