Ontology highlight
ABSTRACT:
SUBMITTER: Foo RS
PROVIDER: S-EPMC2409226 | biostudies-literature | 2007 Dec
REPOSITORIES: biostudies-literature
Foo Roger S-Y RS Nam Young-Jae YJ Ostreicher Marc Jason MJ Metzl Mark D MD Whelan Russell S RS Peng Chang-Fu CF Ashton Anthony W AW Fu Weimin W Mani Kartik K Chin Suet-Feung SF Provenzano Elena E Ellis Ian I Figg Nichola N Pinder Sarah S Bennett Martin R MR Caldas Carlos C Kitsis Richard N RN
Proceedings of the National Academy of Sciences of the United States of America 20071217 52
Inactivation of the transcription factor p53 is central to carcinogenesis. Yet only approximately one-half of cancers have p53 loss-of-function mutations. Here, we demonstrate a mechanism for p53 inactivation by apoptosis repressor with caspase recruitment domain (ARC), a protein induced in multiple cancer cells. The direct binding in the nucleus of ARC to the p53 tetramerization domain inhibits p53 tetramerization. This exposes a nuclear export signal in p53, triggering Crm1-dependent relocatio ...[more]