Kaufmann, William K <br/><br/>
Degradation of ATM-independent decatenation checkpoint function in human cells is secondary to inactivation of p53 and correlated with chromosomal destabilization.  [electronic resource] 

 -  Cell cycle (Georgetown, Tex.)   
 - 210-9 p.  digital 
<br/><br/> Publication Type: Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S. 
<br/><br/><label>ISSN: </label>1538-4101 
<br/><br/><label>Subjects--Topical Terms: </label><br/>Ataxia Telangiectasia Mutated Proteins<br/>Caffeine--pharmacology<br/>Cell Cycle--physiology<br/>Cell Cycle Proteins<br/>Cell Line<br/>Chromosomes<br/>DNA Damage<br/>DNA-Binding Proteins<br/>Diketopiperazines<br/>Dose-Response Relationship, Drug<br/>Dose-Response Relationship, Radiation<br/>Fibroblasts--metabolism<br/>G2 Phase<br/>Humans<br/>Mitosis<br/>Models, Biological<br/>Piperazines--pharmacology<br/>Protein Serine-Threonine Kinases--metabolism<br/>Signal Transduction<br/>Telomerase--metabolism<br/>Time Factors<br/>Tumor Cells, Cultured<br/>Tumor Suppressor Protein p53--metabolism<br/>Tumor Suppressor Proteins