BMB Rep. 2015; 48(2): 81-90  
Structure and apoptotic function of p73
Mi-Kyung Yoon1, Ji-Hyang Ha1, Min-Sung Lee1,2 & Seung-Wook Chi1,2,*
1Structural Biology & Nanopore Research Laboratory, Functional Genomics Research Center, KRIBB, Daejeon 305-806, 2Department of Bio-Analytical Science, University of Science and Technology, Daejeon 305-350, Korea
Correspondence to: Tel: +82-42-860-4277; Fax: +82-42-879-8596; E-mail: swchi@kribb.re.kr
Received: December 1, 2014; Published online: February 28, 2015.
© Korean Society for Biochemistry and Molecular Biology. All rights reserved.

Abstract
p73 is a structural and functional homologue of the p53 tumor suppressor protein. Like p53, p73 induces apoptosis and cell cycle arrest and transactivates p53-responsive genes, conferring its tumor suppressive activity. In addition, p73 has unique roles in neuronal development and differentiation. The importance of p73-induced apoptosis lies in its capability to substitute the pro-apoptotic activity of p53 in various human cancer cells in which p53 is mutated or inactive. Despite the great importance of p73-induced apoptosis in cancer therapy, little is known about the molecular basis of p73-induced apoptosis. In this review, we discuss the p73 structures reported to date, detailed structural comparisons between p73 and p53, and current understanding of the transcription-dependent and -independent mechanisms of p73-induced apoptosis.
Keywords: Apoptosis, Cancer therapy, p53 protein family, p73, Structure


This Article

e-submission

Archives