Degradation of ATM-independent decatenation checkpoint function in human cells is secondary to inactivation of p53 and correlated with chromosomal destabilization.

Kaufmann, William K; Campbell, Christine B; Simpson, Dennis A; Deming, Paula B; Filatov, Leonid; Galloway, Denise A; Zhao, Xiu J; Creighton, Andrew M; Downes, C Stephen

Kaufmann, William K; Campbell, Christine B; Simpson, Dennis A; Deming, Paula B; Filatov, Leonid; Galloway, Denise A; Zhao, Xiu J; Creighton, Andrew M; Downes, C Stephen.

Affiliation

Kaufmann WK; CB7295, Rm 31-325, Lineberger Comprehensive Cancer Center, UNC-CH, Chapel Hill, North Carolina 27599-7295, USA. wkarlk@med.unc.edu

Cell Cycle ; 1(3): 210-9, 2002.

Article in En | MEDLINE | ID: mdl-12429935

Subject(s)

Cell Cycle/physiology; Chromosomes; G2 Phase; Protein Serine-Threonine Kinases/metabolism; Tumor Suppressor Protein p53/metabolism; Ataxia Telangiectasia Mutated Proteins; Caffeine/pharmacology; Cell Cycle Proteins; Cell Line; DNA Damage; DNA-Binding Proteins; Diketopiperazines; Dose-Response Relationship, Drug; Dose-Response Relationship, Radiation; Fibroblasts/metabolism; Humans; Mitosis; Models, Biological; Piperazines/pharmacology; Signal Transduction; Telomerase/metabolism; Time Factors; Tumor Cells, Cultured; Tumor Suppressor Protein p53/physiology; Tumor Suppressor Proteins

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Collection: 01-internacional Database: MEDLINE Main subject: Cell Cycle / G2 Phase / Tumor Suppressor Protein p53 / Chromosomes / Protein Serine-Threonine Kinases Type of study: Prognostic_studies Limits: Humans Language: En Journal: Cell Cycle Year: 2002 Document type: Article

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