ATM is required for rapid degradation of cyclin D1 in response to γ-irradiation

Biochemical and Biophysical Research Communications

Volumn 378, Issue 4, 2009, Pages 847-850

  Choo, Dong Wan ^a,b   Baek, Hye Jung ^a   Motoyama, Noboru ^c   Cho, Kwan Ho ^a   Kim, Hye Sun ^b   Kim, Sang Soo ^a  

^a National Cancer Center   (South Korea)

^b Ajou University   (South Korea)

^c NATIONAL CENTER FOR GERIATRICS AND GERONTOLOGY   (Japan)

Author keywords

Irradiation; ATM; Cyclin D1; Degradation; Ubiquitination

Indexed keywords

ATM PROTEIN; CYCLIN D1; GLYCOGEN SYNTHASE KINASE 3BETA; PROTEASOME INHIBITOR; PROTEIN P53; THREONINE;

ANIMAL CELL; ANIMAL EXPERIMENT; ARTICLE; CELL CYCLE ARREST; CONTROLLED STUDY; DNA DAMAGE; EMBRYO; GAMMA IRRADIATION; GENOME; HUMAN; HUMAN CELL; INHIBITION KINETICS; MOUSE; MUTANT; MUTATION; NONHUMAN; PRIORITY JOURNAL; PROTEIN DEGRADATION; PROTEIN EXPRESSION; PROTEIN PHOSPHORYLATION; PROTEIN STABILITY; REDUCTION; REGULATORY MECHANISM; UBIQUITINATION;

ANIMALS; CELL CYCLE; CELL CYCLE PROTEINS; CELL LINE, TUMOR; CYCLIN D1; CYCLOHEXIMIDE; DNA DAMAGE; DNA-BINDING PROTEINS; ENZYME ACTIVATION; GAMMA RAYS; GLYCOGEN SYNTHASE KINASE 3; HUMANS; MICE; PROTEIN SYNTHESIS INHIBITORS; PROTEIN-SERINE-THREONINE KINASES; TUMOR SUPPRESSOR PROTEINS; UBIQUITIN;

EID: 58049218851     PISSN: 0006291X     EISSN: 10902104     Source Type: Journal    
DOI: 10.1016/j.bbrc.2008.11.132     Document Type: Article

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