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.
Publication types
-
Research Support, Non-U.S. Gov't
-
Review
MeSH terms
-
Apoptosis Regulatory Proteins / chemistry
-
Apoptosis Regulatory Proteins / metabolism
-
Apoptosis*
-
Cell Cycle Checkpoints
-
DNA-Binding Proteins / chemistry
-
DNA-Binding Proteins / genetics
-
DNA-Binding Proteins / metabolism*
-
Humans
-
Mitochondrial Proteins / metabolism
-
Nuclear Proteins / chemistry
-
Nuclear Proteins / genetics
-
Nuclear Proteins / metabolism*
-
Protein Structure, Tertiary
-
TNF-Related Apoptosis-Inducing Ligand / metabolism
-
Transcription, Genetic
-
Tumor Protein p73
-
Tumor Suppressor Protein p53 / metabolism
-
Tumor Suppressor Proteins / chemistry
-
Tumor Suppressor Proteins / genetics
-
Tumor Suppressor Proteins / metabolism*
-
fas Receptor / chemistry
-
fas Receptor / metabolism
Substances
-
Apoptosis Regulatory Proteins
-
DNA-Binding Proteins
-
GRAMD4 protein, human
-
Mitochondrial Proteins
-
Nuclear Proteins
-
TNF-Related Apoptosis-Inducing Ligand
-
TP73 protein, human
-
Tumor Protein p73
-
Tumor Suppressor Protein p53
-
Tumor Suppressor Proteins
-
fas Receptor