Switching from life to death: the Miz-ing link between Myc and p53.
Cells can respond to the activation of the tumor suppressor protein p53 by undergoing cell cycle arrest or apoptosis, and Myc has now been shown to help switch the response to apoptosis by repressing the expression of p21(CIP1), a cyclin-dependent kinase inhibitor with antiapoptotic activity.
Vousden
Karen H
KH
Beatson Institute for Cancer Research, Garscube Estate, Switchback Road, Bearsden, Galsgow G61 1BD, UK. k.vousden@beatson.gla.ac.uk
D000818:Animals; D017209:Apoptosis / Q000235:genetics*; D050759:Cyclin-Dependent Kinase Inhibitor p21; D016213:Cyclins / Q000378:metabolism; D004268:DNA-Binding Proteins / Q000378:metabolism*; D006801:Humans; D051741:Kruppel-Like Transcription Factors; D008957:Models, Genetic; D009687:Nuclear Proteins / Q000378:metabolism*; D016271:Proto-Oncogene Proteins c-myc / Q000235:genetics / Q000378:metabolism*; D014157:Transcription Factors; D016159:Tumor Suppressor Protein p53 / Q000235:genetics / Q000378:metabolism*
C493956:CDKN1A protein, human; D050759:Cyclin-Dependent Kinase Inhibitor p21; D016213:Cyclins; D004268:DNA-Binding Proteins; D051741:Kruppel-Like Transcription Factors; D009687:Nuclear Proteins; D016271:Proto-Oncogene Proteins c-myc; D014157:Transcription Factors; D016159:Tumor Suppressor Protein p53; C107961:ZBTB17 protein, human