Balint Eva, Phillips Andrew C, Kozlov Serguei, Stewart Colin L, Vousden Karen H
Regulation of Cell Growth Laboratory, Cancer and Developmental Biology Laboratory, National Cancer Institute, Frederick, MD 21702-1201, USA.
Proc Natl Acad Sci U S A. 2002 Mar 19;99(6):3529-34. doi: 10.1073/pnas.062491899. Epub 2002 Mar 12.
The p53-related protein p73 has many functions similar to that of p53 including the ability to induce cell-cycle arrest and apoptosis. Both p53 and p73 function as transcription factors, and p73 activates expression of many genes that also are regulated by p53. Despite their similarities, it is evident that p53 and p73 are not interchangeable functionally, with p73 playing a role in normal growth and development that is not shared by p53. In this paper we describe the ability of p73beta but not p53 to activate expression of the cyclin-dependent kinase inhibitor p57(KIP) and KvLQT1, two genes that are coregulated in an imprinted region of the genome. Our results suggest that p73 may regulate expression of genes through mechanisms that are not shared by p53, potentially explaining the different contributions of p53 and p73 to normal development.
与p53相关的蛋白p73具有许多与p53相似的功能,包括诱导细胞周期停滞和凋亡的能力。p53和p73均作为转录因子发挥作用,并且p73激活许多也受p53调控的基因的表达。尽管它们有相似之处,但很明显p53和p73在功能上不可互换,p73在正常生长和发育中发挥着p53所不具备的作用。在本文中,我们描述了p73β而非p53激活细胞周期蛋白依赖性激酶抑制剂p57(KIP)和KvLQT1表达的能力,这两个基因在基因组的一个印记区域中共同受到调控。我们的结果表明,p73可能通过p53所不具备的机制调控基因表达,这可能解释了p53和p73对正常发育的不同贡献。