MacPartlin Mary, Zeng Shelya, Lee Hunjoo, Stauffer Daniel, Jin Yetao, Thayer Mathew, Lu Hua
Department of Biochemistry and Molecular Biology, Oregon Health and Science University, Portland, Oregon 97239, USA.
J Biol Chem. 2005 Aug 26;280(34):30604-10. doi: 10.1074/jbc.M503352200. Epub 2005 Jun 17.
The transcriptional co-activator p300 has been reported to regulate the tumor suppressor p53 and its ortholog p73. Here we describe a study showing that this coactivator also regulates the transcriptional function of p63. p300 bound to the N-terminal domain of p63gamma, and p63gamma bound to the N terminus of p300 in vitro and in cells. p300, but not its acetylase-defective mutant AT2, stimulated p63gamma-dependent transcription and induction of p21 in cells, consequently leading to G1 arrest. Inversely, the deltaN-p63gamma isoform as well as p300AT2 inhibited the induction of p21 by p63gamma. These results suggest that p300 regulates p63-dependent transcription of p21.
转录共激活因子p300已被报道可调控肿瘤抑制因子p53及其同源物p73。在此，我们描述一项研究，该研究表明这种共激活因子还可调控p63的转录功能。在体外和细胞内，p300与p63γ的N端结构域结合，而p63γ与p300的N端结合。p300而非其乙酰化缺陷型突变体AT2可刺激细胞中p63γ依赖的转录及p21的诱导，从而导致G1期阻滞。相反，ΔN-p63γ异构体以及p300AT2可抑制p63γ对p21的诱导。这些结果表明p300可调控p63依赖的p21转录。
