K-ras Asp12 mutant neither interacts with Raf, nor signals through Erk and is less tumorigenic than K-ras Val12

Carcinogenesis

Volumn 27, Issue 11, 2006, Pages 2190-2200

  Céspedes, María Virtudes ^a   Sancho, Francesc Josep ^b   Guerrero, Silvia ^c   Parreño, Matilde ^a   Casanova, Isolda ^a   Pavón, Miguel Angel ^a   Marcuello, Eugenio ^b   Trias, Manuel ^b   Cascante, Marta ^c   Capellà, Gabriel ^d   Mangues, Ramon ^a  

^a HOSPITAL DE LA SANTA CREU I SANT PAU   (Spain)

^b HSCSP   (Spain)

^c UNIVERSITY OF BARCELONA   (Spain)

^d BELLVITGE BIOMEDICAL RESEARCH INSTITUTE IDIBELL   (Spain)

Author keywords

[No Author keywords available]

Indexed keywords

ASPARTIC ACID; CYCLIN B; CYCLINE; CYSTEINE; FOCAL ADHESION KINASE; K RAS PROTEIN; MITOGEN ACTIVATED PROTEIN KINASE; ONCOPROTEIN; PHOSPHATIDYLINOSITOL 3 KINASE; PROTEIN KINASE B; RAF PROTEIN; RAS PROTEIN; RETINOBLASTOMA PROTEIN; STRESS ACTIVATED PROTEIN KINASE; SYNAPTOPHYSIN; VALINE;

APOPTOSIS; ARTICLE; CANCER RECURRENCE; CANCER SURVIVAL; CARCINOGENESIS; CARCINOGENICITY; CELL CYCLE; CELL CYCLE G1 PHASE; CELL CYCLE G2 PHASE; CELL CYCLE M PHASE; CELL CYCLE S PHASE; CELL GROWTH; CELL PROLIFERATION; CELL STRAIN 3T3; CODON; COLORECTAL CANCER; CONTROLLED STUDY; DISEASE MODEL; GENE INTERACTION; GENE MUTATION; GENETIC ANALYSIS; GROWTH RATE; HISTOPATHOLOGY; HUMAN; HUMAN CELL; MALIGNANT TRANSFORMATION; METASTASIS POTENTIAL; MITOSIS; MITOSIS RATE; NUDE MOUSE; PHENOTYPE; PRIORITY JOURNAL; PROTEIN INTERACTION; PROTEIN PHOSPHORYLATION; SIGNAL TRANSDUCTION; TUMOR GROWTH; TUMOR XENOGRAFT; UPREGULATION;

EID: 33750474485     PISSN: 01433334     EISSN: 14602180     Source Type: Journal    
DOI: 10.1093/carcin/bgl063     Document Type: Article

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