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.
Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callMore From: Biochemical and Biophysical Research Communications
Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
