z-logo
open-access-imgOpen Access
p73-Binding Partners and Their Functional Significance
Author(s) -
Toshinori Ozaki,
Natsumi Kubo,
Akira Nakagawara
Publication year - 2010
Publication title -
international journal of proteomics
Language(s) - English
Resource type - Journals
eISSN - 2090-2174
pISSN - 2090-2166
DOI - 10.1155/2010/283863
Subject(s) - acetylation , microbiology and biotechnology , transcription factor , dna damage , cell cycle checkpoint , suppressor , apoptosis , cell cycle , dna repair , gene , biology , phosphorylation , transcription (linguistics) , cancer research , dna , genetics , linguistics , philosophy
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.

The content you want is available to Zendy users.

Already have an account? Click here to sign in.
Having issues? You can contact us here
Accelerating Research

Address

John Eccles House
Robert Robinson Avenue,
Oxford Science Park, Oxford
OX4 4GP, United Kingdom