Antagonism of Myc functions by Arf.
The Arf-Mdm2-p53 tumor suppressor pathway is activated by sustained hyperproliferative signals emanating from oncoproteins such as Myc. A recent study reveals a novel level of feedback control, whereby induced p19(Arf) binds to Myc and blocks cell proliferation by selectively impairing its transactivation functions.
Cleveland
John L
JL
Department of Biochemistry, St. Jude Children's Research Hospital, Memphis, TN 38105, USA.
Sherr
Charles J
CJ
D000818:Animals; D002455:Cell Division; D006801:Humans; D009687:Nuclear Proteins / Q000378:metabolism; D011518:Proto-Oncogene Proteins / Q000378:metabolism; D051736:Proto-Oncogene Proteins c-mdm2; D016271:Proto-Oncogene Proteins c-myc / Q000037:antagonists & inhibitors* / Q000378:metabolism*; D015398:Signal Transduction; D025803:Tumor Suppressor Protein p14ARF / Q000378:metabolism*; D016159:Tumor Suppressor Protein p53 / Q000378:metabolism
D009687:Nuclear Proteins; D011518:Proto-Oncogene Proteins; D016271:Proto-Oncogene Proteins c-myc; D025803:Tumor Suppressor Protein p14ARF; D016159:Tumor Suppressor Protein p53; C497206:MDM2 protein, human; D051736:Proto-Oncogene Proteins c-mdm2