Yang X J, Ogryzko V V, Nishikawa J, Howard B H, Nakatani Y
Laboratory of Molecular Growth Regulation, National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, Maryland 20892-2753, USA.
Nature. 1996 Jul 25;382(6589):319-24. doi: 10.1038/382319a0.
The adenoviral oncoprotein E1A induces progression through the cell cycle by binding to the products of the p300/CBP and retinoblastoma gene families. A new cellular p300/CBP-associated factor (P/CAF) having intrinsic histone acetylase activity has been identified that competes with E1A. Exogenous expression of P/CAF in HeLa cells inhibits cell-cycle progression and counteracts the mitogenic activity of E1A. E1A disturbs the normal cellular interaction between p300/CBP and its associated histone acetylase.
腺病毒癌蛋白E1A通过与p300/CBP和视网膜母细胞瘤基因家族的产物结合来诱导细胞周期进程。已鉴定出一种具有内在组蛋白乙酰转移酶活性的新的细胞p300/CBP相关因子(P/CAF),它可与E1A竞争。P/CAF在HeLa细胞中的外源性表达抑制细胞周期进程,并抵消E1A的促有丝分裂活性。E1A扰乱了p300/CBP与其相关组蛋白乙酰转移酶之间的正常细胞相互作用。