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p300调节p63的转录活性。

p300 regulates p63 transcriptional activity.

作者信息

MacPartlin Mary, Zeng Shelya, Lee Hunjoo, Stauffer Daniel, Jin Yetao, Thayer Mathew, Lu Hua

机构信息

Department of Biochemistry and Molecular Biology, Oregon Health and Science University, Portland, Oregon 97239, USA.

出版信息

J Biol Chem. 2005 Aug 26;280(34):30604-10. doi: 10.1074/jbc.M503352200. Epub 2005 Jun 17.

Abstract

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.

摘要

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。

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