Disrupting the pairing between let-7 and Hmga2 enhances oncogenic transformation

Science

Volumn 315, Issue 5818, 2007, Pages 1576-1579

  Mayr, Christine ^a   Hemann, Michael T ^a   Bartel, David P ^a  

^a MASSACHUSETTS INSTITUTE OF TECHNOLOGY   (United States)

Author keywords

[No Author keywords available]

Indexed keywords

MICRORNA; NUCLEOTIDE;

CANCER; CHROMOSOME; GENE EXPRESSION; PHENOTYPE; RNA; TUMOR;

ANCHORAGE INDEPENDENT GROWTH; ANIMAL CELL; ARTICLE; CARCINOGENESIS; CELL STRAIN 3T3; GENE FUNCTION; GENE REPRESSION; HMGA2 GENE; LET7 GENE; MALIGNANT TRANSFORMATION; NONHUMAN; ONCOGENE; PHENOTYPE; PRIORITY JOURNAL; PROTEIN BINDING; PROTEIN EXPRESSION; PROTEIN PROTEIN INTERACTION;

3' UNTRANSLATED REGIONS; ANIMALS; CELL LINE, TUMOR; CELL PROLIFERATION; CELL TRANSFORMATION, NEOPLASTIC; GENE EXPRESSION REGULATION; GENES, TUMOR SUPPRESSOR; HELA CELLS; HMGA2 PROTEIN; HUMANS; MICE; MICE, NUDE; MICRORNAS; NEOPLASMS, EXPERIMENTAL; NIH 3T3 CELLS; ONCOGENES; TRANSFECTION; TRANSLOCATION, GENETIC;

MAMMALIA;

EID: 33947431322     PISSN: 00368075     EISSN: 10959203     Source Type: Journal    
DOI: 10.1126/science.1137999     Document Type: Article

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29. We thank M. Narita and S. Lowe for providing the Hmga2 antibody, and C. Jan, A. Grimson, and M. Narita for helpful discussions and advice. Supported by grants from the Deutsche Forschungsgemeinschaft (C.M.) and the NIH (D.B.). D.B. is a Howard Hughes Medical Institute Investigator.