Abstract:
:The ability of DNA damage to stabilize p53 in all cell cycle stages has not been examined in actively growing cells. The chemotherapeutic drug camptothecin is a topoisomerase I poison. Zeocin is a member of the bleomycin/phleomycin family of antibiotics, known to bind DNA. Both increase the level of p53 albeit by different mechanisms. We have utilized centrifugal elutriation to separate exponentially growing ML-1 cells (containing wild-type p53) into cell cycle fractions and have subsequently treated these cells with the two drugs. We provide evidence that both drugs can mediate an increase in p53 protein levels independent of the cell cycle stage. The p53 induced by both drugs was able to bind to DNA; however, only the p53 induced by camptothecin was phosphorylated at serine-392. This is the first demonstration that camptothecin and Zeocin can differentially signal for increased levels of modified p53 during all stages of the cell cycle.
journal_name
Biochem Biophys Res Communjournal_title
Biochemical and biophysical research communicationsauthors
Houser S,Koshlatyi S,Lu T,Gopen T,Bargonetti Jdoi
10.1006/bbrc.2001.6073subject
Has Abstractpub_date
2001-12-21 00:00:00pages
998-1009issue
5eissn
0006-291Xissn
1090-2104pii
S0006-291X(01)96073-5journal_volume
289pub_type
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