p300 does not require its acetylase activity to stimulate p73 function

被引:35
作者
Zeng, XY
Lee, HJ
Zhang, QH
Lui, H
机构
[1] Oregon Hlth Sci Univ, Dept Biochem & Mol Biol, Portland, OR 97201 USA
[2] Oregon Hlth Sci Univ, Vollum Inst, Portland, OR 97201 USA
关键词
D O I
10.1074/jbc.C000722200
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
We previously reported that p73, like p53, utilizes p300 or cAMP-response element-binding protein-binding protein as its coactivator. Here, we extended this work by further examining whether the intrinsic acetylase activity of p300 is necessary for stimulating p73 function. Although p300 acetylated the C-terminal fragment of p73 (amino acids 311-636) in vitro, it was unable to efficiently acetylate the full-length p73. Consistently, p300 did not acetylate p73 in vivo when both the proteins were overexpressed in cells. Also, an acetylase-defective mutant p300 named p300AT2 was able to elevate p73-dependent transcription in cells. p300 associated with p73 when forming DNA-protein complexes and stabilized p73 proteins. These results demonstrate that p300 does not need its acetylase activity to be a coactivator of p73.
引用
收藏
页码:48 / 52
页数:5
相关论文
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