Table of Contents
International Journal of Proteomics
Volume 2010, Article ID 283863, 12 pages
Review Article

p73-Binding Partners and Their Functional Significance

1Laboratory of Anti-tumor Research, Chiba Cancer Center Research Institute, Chiba 260-8717, Japan
2Laboratory of Innovative Cancer Therapeutics, Chiba Cancer Center Research Institute, 666-2 Nitona-Cho, Chuo-ku, Chiba 260-8717, Japan

Received 27 September 2010; Accepted 26 October 2010

Academic Editor: Jen-Fu Chiu

Copyright © 2010 Toshinori Ozaki et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


p73 is one of the tumor-suppressor p53 family of nuclear transcription factor. As expected from the structural similarity between p53 and p73, p73 has a tumor-suppressive function. However, p73 was rarely mutated in human primary tumors. Under normal physiological conditions, p73 is kept at an extremely low level to allow cells normal growth. In response to a certain subset of DNA damages, p73 is induced dramatically and transactivates an overlapping set of p53-target genes implicated in the promotion of cell cycle arrest and/or apoptotic cell death. Cells undergo cell cycle arrest and/or apoptotic cell death depending on the type and strength of DNA damages. p73 is regulated largely through the posttranslational modifications such as phosphorylation and acetylation. These chemical modifications are tightly linked to direct protein-protein interactions. In the present paper, the authors describe the functional significance of the protein-protein interactions in the regulation of proapoptotic p73.