Degradation of ATM-independent decatenation checkpoint function in human cells is secondary to inactivation of p53 and correlated with chromosomal destabilization. [electronic resource]
Producer: 20021210Description: 210-9 p. digitalISSN:- 1538-4101
- Ataxia Telangiectasia Mutated Proteins
- Caffeine -- pharmacology
- Cell Cycle -- physiology
- Cell Cycle Proteins
- Cell Line
- Chromosomes
- DNA Damage
- DNA-Binding Proteins
- Diketopiperazines
- Dose-Response Relationship, Drug
- Dose-Response Relationship, Radiation
- Fibroblasts -- metabolism
- G2 Phase
- Humans
- Mitosis
- Models, Biological
- Piperazines -- pharmacology
- Protein Serine-Threonine Kinases -- metabolism
- Signal Transduction
- Telomerase -- metabolism
- Time Factors
- Tumor Cells, Cultured
- Tumor Suppressor Protein p53 -- metabolism
- Tumor Suppressor Proteins
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Publication Type: Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
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