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核因子Y(NF-Y)与p53的联系:远不止于抑制作用。

The NF-Y/p53 liaison: well beyond repression.

作者信息

Imbriano Carol, Gnesutta Nerina, Mantovani Roberto

机构信息

Dipartimento di Biologia, Università degli Studi di Modena e Reggio Emilia, Via Campi 213/d, 41100 Modena, Italy.

出版信息

Biochim Biophys Acta. 2012 Apr;1825(2):131-9. doi: 10.1016/j.bbcan.2011.11.001. Epub 2011 Nov 22.

Abstract

NF-Y is a sequence-specific transcription factor - TF - targeting the common CCAAT promoter element. p53 is a master TF controlling the response to stress signals endangering genome integrity, often mutated in human cancers. The NF-Y/p53 - and p63, p73 - interaction results in transcriptional repression of a subset of genes within the vast NF-Y regulome under DNA-damage conditions. Recent data shows that NF-Y is also involved in pro-apoptotic activities, either directly, by mediating p53 transcriptional activation, or indirectly, by being targeted by a non coding RNA, PANDA. The picture is subverted in cells carrying Gain-of-function mutant p53, through interactions with TopBP1, a protein also involved in DNA repair and replication. In summary, the connection between p53 and NF-Y is crucial in determining cell survival or death.

摘要

核因子Y(NF-Y)是一种序列特异性转录因子(TF),靶向常见的CCAAT启动子元件。p53是一种主要的转录因子,控制着对危及基因组完整性的应激信号的反应,在人类癌症中经常发生突变。NF-Y与p53以及p63、p73的相互作用导致在DNA损伤条件下,庞大的NF-Y调控组内一部分基因的转录抑制。最近的数据表明,NF-Y也参与促凋亡活动,要么通过介导p53转录激活直接参与,要么通过被一种非编码RNA即PANDA靶向间接参与。在携带功能获得性突变p53的细胞中,通过与也参与DNA修复和复制的蛋白质TopBP1相互作用,这种情况被颠覆。总之,p53和NF-Y之间的联系在决定细胞存活或死亡方面至关重要。

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