Imbriano Carol, Gnesutta Nerina, Mantovani Roberto
Dipartimento di Biologia, Università degli Studi di Modena e Reggio Emilia, Via Campi 213/d, 41100 Modena, Italy.
Biochim Biophys Acta. 2012 Apr;1825(2):131-9. doi: 10.1016/j.bbcan.2011.11.001. Epub 2011 Nov 22.
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.
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。
