Mutant and wild-type p53 form complexes with p73 upon phosphorylation by the kinase JNK
Author:
Affiliation:
1. Department of Biochemistry and Molecular Biology, Indiana University School of Medicine, Indianapolis, IN 46202, USA.
2. Herman B Wells Center for Pediatric Research, Indiana University School of Medicine, Indianapolis, IN 46202, USA.
Abstract
Funder
National Cancer Institute
Riley Children’s Foundation
Jeff Gordon Children’s Foundation
Publisher
American Association for the Advancement of Science (AAAS)
Subject
Cell Biology,Molecular Biology,Biochemistry
Reference45 articles.
1. p73 Function Is Inhibited by Tumor-Derived p53 Mutants in Mammalian Cells
2. A Subset of Tumor-Derived Mutant Forms of p53 Down-Regulate p63 and p73 through a Direct Interaction with the p53 Core Domain
3. Tumor predisposition in mice mutant for p63 and p73: Evidence for broader tumor suppressor functions for the p53 family
4. p73 and p63 Are Homotetramers Capable of Weak Heterotypic Interactions with Each Other but Not with p53
5. Structural evolution of p53, p63, and p73: Implication for heterotetramer formation
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