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 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.
Aurelio
O N
ON
Department of Microbiology and Molecular Genetics, University of California-Irvine, 92697-4025, USA.
Cajot
J F
JF
Hua
M L
ML
Khwaja
Z
Z
Stanbridge
E J
EJ
D000293:Adolescent; D000328:Adult; D017209:Apoptosis / Q000235:genetics*; D002453:Cell Cycle / Q000235:genetics*; D018095:Germ-Line Mutation; D006801:Humans; D009363:Neoplasm Proteins / Q000235:genetics*; D011487:Protein Conformation; D014407:Tumor Cells, Cultured; D014410:Tumor Stem Cell Assay; D016159:Tumor Suppressor Protein p53 / Q000235:genetics* / Q000502:physiology
D009363:Neoplasm Proteins; D016159:Tumor Suppressor Protein p53