An oncogenic form of p53 confers a dominant, gain-of-function phenotype that disrupts spindle checkpoint control

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

Volumn 95, Issue 9, 1998, Pages 5166-5171

  Gualberto, Antonio ^a,c   Aldape, Kenneth ^b   Kozakiewicz, Krystyna ^b   Tlsty, Thea D ^a,b  

^a LAWRENCE BERKELEY NATIONAL LABORATORY   (United States)

^b UNIVERSITY OF CALIFORNIA   (United States)

^c CASE WESTERN RESERVE UNIVERSITY SCHOOL OF MEDICINE   (United States)

Author keywords

[No Author keywords available]

Indexed keywords

DEMECOLCINE; PROTEIN P53;

ALLELE; ANIMAL CELL; ARTICLE; FAMILIAL CANCER; GENETIC STABILITY; GENETIC TRANSFORMATION; HUMAN; HUMAN CELL; MITOSIS SPINDLE; MOUSE; NONHUMAN; PHENOTYPE; PRIORITY JOURNAL; TRANSCRIPTION REGULATION; TUMOR SUPPRESSOR GENE;

ANIMALS; CELL CYCLE; DEMECOLCINE; DNA REPLICATION; DNA, NEOPLASM; GENE EXPRESSION REGULATION, NEOPLASTIC; GENES, DOMINANT; HETEROZYGOTE; HUMANS; LI-FRAUMENI SYNDROME; MICE; MITOTIC SPINDLE APPARATUS; MUTATION; S PHASE; SPECIES SPECIFICITY; TRANSCRIPTION, GENETIC; TUMOR SUPPRESSOR PROTEIN P53;

ANIMALIA;

EID: 0032574788     PISSN: 00278424     EISSN: None     Source Type: Journal    
DOI: 10.1073/pnas.95.9.5166     Document Type: Article

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