The ARF/oncogene pathway activates p53 acetylation within the DNA binding domain

Cell Cycle

Volumn 6, Issue 11, 2007, Pages 1304-1306

  Mellert, Hestia ^a   Sykes, Stephen M ^a   Murphy, Maureen E ^b   McMahon, Steven B ^c  

^a UNIVERSITY OF PENNSYLVANIA   (United States)

^b FOX CHASE CANCER CENTER   (United States)

^c THOMAS JEFFERSON UNIVERSITY   (United States)

Author keywords

Acetylation; Apoptosis; CDKN2A; hMOF; K120; p19ARF; p53; TIP60

Indexed keywords

ARF PROTEIN; LYSINE; LYSINE 120; PROTEIN P19ARF; PROTEIN P53; TUMOR SUPPRESSOR PROTEIN; UNCLASSIFIED DRUG; CDKN2A PROTEIN, MOUSE; DNA; DOXYCYCLINE; HISTONE ACETYLTRANSFERASE; HTATIP PROTEIN, HUMAN; HYBRID PROTEIN; MYST1 PROTEIN, HUMAN; PHOSPHATIDYLETHANOLAMINE; PROTEIN P16INK4A; TRANSFECTACE;

ACETYLATION; APOPTOSIS; CARCINOGENESIS; DNA BINDING; DNA DAMAGE; GENE ACTIVATION; GENE MUTATION; GENOTOXICITY; HUMAN; ONCOGENE; PROTEIN STABILITY; REVIEW; ANIMAL; BINDING SITE; CELL LINE; CELL TRANSFORMATION; CHEMISTRY; GENETICS; METABOLISM; MOUSE; PHYSIOLOGY; PROTEIN BINDING; PROTEIN PROCESSING; PROTEIN TERTIARY STRUCTURE; STRESS; TUMOR SUPPRESSOR GENE;

ACETYLATION; ANIMALS; BINDING SITES; CELL LINE; CELL TRANSFORMATION, NEOPLASTIC; CYCLIN-DEPENDENT KINASE INHIBITOR P16; DNA; DNA DAMAGE; DOXYCYCLINE; GENES, P53; HISTONE ACETYLTRANSFERASES; HUMANS; LYSINE; MICE; PHOSPHATIDYLETHANOLAMINES; PROTEIN BINDING; PROTEIN PROCESSING, POST-TRANSLATIONAL; PROTEIN STRUCTURE, TERTIARY; RECOMBINANT FUSION PROTEINS; STRESS; TUMOR SUPPRESSOR PROTEIN P53;

EID: 34547669249     PISSN: 15384101     EISSN: 15514005     Source Type: Journal    
DOI: 10.4161/cc.6.11.4343     Document Type: Review

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