Developmental defects and p53 hyperacetylation in Sir2 homolog (SIRT1)-deficient mice

Proceedings of the National Academy of Sciences of the United States of America

Volumn 100, Issue 19, 2003, Pages 10794-10799

  Cheng, Hwei Ling ^a   Mostoslavsky, Raul ^a   Saito, Shin'ichi ^c   Manis, John P ^a   Gu, Yansong ^a,d   Patel, Parin ^a   Bronson, Roderick ^b   Appella, Ettore ^c   Alt, Frederick W ^a   Chua, Katrin F ^a  

^a HARVARD MEDICAL SCHOOL   (United States)

^b TUFTS UNIVERSITY   (United States)

^c NATIONAL CANCER INSTITUTE   (United States)

^d UNIVERSITY OF WASHINGTON SCHOOL OF MEDICINE   (United States)

Author keywords

[No Author keywords available]

Indexed keywords

GENE PRODUCT; MUTANT PROTEIN; PROTEIN P21; PROTEIN P53; PROTEIN SIRT1; SILENT INFORMATION REGULATOR PROTEIN 2; TUMOR SUPPRESSOR PROTEIN; UNCLASSIFIED DRUG;

ACETYLATION; ANIMAL CELL; ANIMAL EXPERIMENT; ANIMAL MODEL; ANIMAL TISSUE; APOPTOSIS; ARTICLE; CELL AGING; CONGENITAL HEART MALFORMATION; CONTROLLED STUDY; DEVELOPMENTAL DISORDER; DNA DAMAGE; FIBROBLAST; GENE MUTATION; GENE OVEREXPRESSION; IONIZING RADIATION; MOUSE; NONHUMAN; PHENOTYPE; PRIORITY JOURNAL; PROTEIN DOMAIN; PROTEIN INDUCTION; REGULATORY MECHANISM; RETINA MALFORMATION; SACCHAROMYCES CEREVISIAE; SURVIVAL; THYMOCYTE;

ABNORMALITIES; ANIMALS; APOPTOSIS; CELL CYCLE; DNA DAMAGE; INFRARED RAYS; MICE; MICE, KNOCKOUT; SIRTUINS; TUMOR SUPPRESSOR PROTEIN P53;

ANIMALIA; MAMMALIA; SACCHAROMYCES; SACCHAROMYCES CEREVISIAE;

EID: 0141814680     PISSN: 00278424     EISSN: None     Source Type: Journal    
DOI: 10.1073/pnas.1934713100     Document Type: Article

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