Germ-line-derived hinge domain p53 mutants have lost apoptotic but not cell cycle arrest functions

The protein p53 is a critical tumor suppressor, as demonstrated by its frequent mutation in human cancers. Overexpression of the wild-type form of the p53 tumor suppressor gene in human cancer cell lines has been shown to lead to either cell cycle arrest or apoptosis. A study of two Li-Fraumeni synd...

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Bibliographic Details
Published in:Cancer research (Chicago, Ill.) Ill.), 1998-05, Vol.58 (10), p.2190-2195
Main Authors: AURELIO, O. N, CAJOT, J.-F, HUA, M. L.-H, KHWAJA, Z, STANBRIDGE, E. J
Format: Article
Language:English
Subjects:
Adolescent
Adult
Apoptosis - genetics
Biological and medical sciences
Cell Cycle - genetics
Cell physiology
Cell transformation and carcinogenesis. Action of oncogenes and antioncogenes
Fundamental and applied biological sciences. Psychology
Germ-Line Mutation
Humans
Molecular and cellular biology
Neoplasm Proteins - genetics
Protein Conformation
Tumor Cells, Cultured
Tumor Stem Cell Assay
Tumor Suppressor Protein p53 - genetics
Tumor Suppressor Protein p53 - physiology
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Summary:The protein p53 is a critical tumor suppressor, as demonstrated by its frequent mutation in human cancers. Overexpression of the wild-type form of the p53 tumor suppressor gene in human cancer cell lines has been shown to lead to either cell cycle arrest or apoptosis. A study of two Li-Fraumeni syndrome-derived p53 hinge domain mutants shows that both mutants retain the ability to arrest cell growth but are significantly impaired for the induction of apoptosis in human p53-null cell lines. This indicates that the hinge domain may be important in the regulation of p53-dependent apoptosis.
ISSN:0008-5472
1538-7445