Induction of p57KIP2 expression by p73β
Induction of p57KIP2 expression by p73β
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DOI：
10.1073/pnas.062491899
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发表时间：
2002-03-19
影响因子：
11.1
通讯作者：
Vousden, KH
中科院分区：
文献类型：
--
作者：
Bálint, É;Phillips, AC;Vousden, KH
p53相关蛋白p73具有许多与p53相似的功能，包括诱导细胞周期阻滞和凋亡的能力。p53和p73都具有转录因子的功能，p73激活了许多受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在功能上不能互换，p73在正常生长发育中所起的作用是p53所不具有的。在本文中，我们描述了p73beta而不是p53激活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印迹区域中共同调节。我们的研究结果表明，p73可能通过p53不共享的机制调节基因的表达，这可能解释了p53和p73对正常发育的不同贡献。
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.