Rb inactivation promotes genomic instability by uncoupling cell cycle progression from mitotic control

Nature

Volumn 430, Issue 7001, 2004, Pages 797-802

  Hernando, Eva ^a   Nahlé, Zaher ^b,c   Juan, Gloria ^a   Diaz Rodriguez, Elena ^a   Alaminos, Miguel ^a,d   Hemann, Michael ^b   Michel, Loren ^a   Mittal, Vivek ^b   Gerald, William ^a   Benezra, Robert ^a   Lowe, Scott W ^b   Cordon Cardo, Carlos ^a  

^a MEMORIAL SLOAN KETTERING CANCER CENTER   (United States)

^b Simons Center for Quantitative Biology   (United States)

^c WASHINGTON UNIVERSITY SCHOOL OF MEDICINE   (United States)

^d UNIVERSITY OF GRANADA   (Spain)

Author keywords

[No Author keywords available]

Indexed keywords

CELL CULTURE; GENES; TUMORS;

MITOSIS; RETINOBLASTOMA (RB);

NATURAL SCIENCES;

PROTEIN MAD2; RETINOBLASTOMA PROTEIN; TRANSCRIPTION FACTOR E2F; CARRIER PROTEIN; CELL CYCLE PROTEIN; DNA BINDING PROTEIN; MAD2L1 PROTEIN, MOUSE; MAD2L2 PROTEIN, MOUSE; MESSENGER RNA; NUCLEAR PROTEIN; TRANSCRIPTION FACTOR;

BIOLOGY;

ACCURACY; ADVANCED CANCER; ANEUPLOIDY; ARTICLE; CANCER GENETICS; CANCER PATIENT; CARCINOGENESIS; CELL CYCLE; CELL TRANSFORMATION; CHROMOSOME; CONTROLLED STUDY; GENE MUTATION; GENOME; HUMAN; HUMAN CELL; MITOSIS; PATHOPHYSIOLOGY; PHENOTYPE; PRIORITY JOURNAL; PROTEIN EXPRESSION; ANIMAL; CELL LINE; ENZYME SPECIFICITY; FLUORESCENCE IN SITU HYBRIDIZATION; GENE EXPRESSION REGULATION; GENETICS; GENOMIC INSTABILITY; HUMAN CHROMOSOME; IMMUNOHISTOCHEMISTRY; KARYOTYPING; METABOLISM; MOUSE; MUTATION; PHYSIOLOGY; SIGNAL TRANSDUCTION; TUMOR CELL LINE;

ANEUPLOIDY; ANIMALS; CARRIER PROTEINS; CELL CYCLE; CELL CYCLE PROTEINS; CELL LINE; CELL LINE, TUMOR; CHROMOSOMES, HUMAN; DNA-BINDING PROTEINS; E2F TRANSCRIPTION FACTORS; GENE EXPRESSION REGULATION, NEOPLASTIC; GENOMIC INSTABILITY; HUMANS; IMMUNOHISTOCHEMISTRY; IN SITU HYBRIDIZATION, FLUORESCENCE; KARYOTYPING; MICE; MITOSIS; MUTATION; NUCLEAR PROTEINS; RETINOBLASTOMA PROTEIN; RNA, MESSENGER; SIGNAL TRANSDUCTION; SUBSTRATE SPECIFICITY; TRANSCRIPTION FACTORS;

EID: 4043093341     PISSN: 00280836     EISSN: None     Source Type: Journal    
DOI: 10.1038/nature02820     Document Type: Article

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