Reduced c-Myc signaling triggers telomere-independent senescence by regulating Bmi-1 and p16INK4a

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

Volumn 103, Issue 10, 2006, Pages 3645-3650

  Guney, Isil ^a,b   Wu, Shirley ^a,c   Sedivy, John M ^a  

^a BROWN UNIVERSITY   (United States)

^b DANA FARBER CANCER INSTITUTE   (United States)

^c STANFORD UNIVERSITY SCHOOL OF MEDICINE   (United States)

Author keywords

Aging; Cellular senescence; Epigenetics; Signaling networks; Stress response

Indexed keywords

BMI 1 PROTEIN; CYCLIN DEPENDENT KINASE INHIBITOR; MYC PROTEIN; PROTEIN P16INK4A; RAS PROTEIN; REPRESSOR PROTEIN; UNCLASSIFIED DRUG;

ADULT; AGING; ARTICLE; CANCER INHIBITION; CELL DIVISION; CELL PROLIFERATION; CONTROLLED STUDY; EMBRYO; EPIGENETICS; FEMALE; FIBROBLAST; GENE; GENE EXPRESSION; GENE INACTIVATION; GENETIC TRANSCRIPTION; HOMOLOGOUS RECOMBINATION; HUMAN; HUMAN CELL; MITOGENESIS; NORMAL HUMAN; ONCOGENE C MYC; POLYCOMB GROUP GENE; PRIORITY JOURNAL; SENESCENCE; SIGNAL TRANSDUCTION; STRESS; TELOMERE;

BASE SEQUENCE; CELL AGING; CELLS, CULTURED; CYCLIN-DEPENDENT KINASE INHIBITOR P16; DNA; GENES, MYC; HUMANS; NUCLEAR PROTEINS; PROTO-ONCOGENE PROTEINS; PROTO-ONCOGENE PROTEINS C-MYC; REPRESSOR PROTEINS; RNA INTERFERENCE; RNA, MESSENGER; SIGNAL TRANSDUCTION; TELOMERE;

EID: 33644871338     PISSN: 00278424     EISSN: None     Source Type: Journal    
DOI: 10.1073/pnas.0600069103     Document Type: Article

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