Point mutation in AML1 disrupts subnuclear targeting, prevents myeloid differentiation, and effects a transformation-like phenotype

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

Volumn 102, Issue 20, 2005, Pages 7174-7179

  Vradii, Diana ^a   Zaidi, Sayyed K ^a   Lian, Jane B ^a   Van Wijnen, Andre J ^a   Stein, Janet L ^a   Stein, Gary S ^a  

^a UNIVERSITY OF MASSACHUSETTS MEDICAL SCHOOL   (United States)

Author keywords

Acute myeloid leukemia; AML1 ETO fusion protein; Nuclear matrix; Subnuclear organization

Indexed keywords

TRANSCRIPTION FACTOR RUNX1;

AMINO ACID SUBSTITUTION; ANIMAL CELL; ARTICLE; BONE MARROW CELL; CARBOXY TERMINAL SEQUENCE; CELL COMPARTMENTALIZATION; CELL DIFFERENTIATION; CELL PROLIFERATION; CELL STRUCTURE; CELLULAR DISTRIBUTION; CHROMOSOME 21; CHROMOSOME 8; CHROMOSOME TRANSLOCATION; CONTROLLED STUDY; GRANULOCYTE; LEUKEMOGENESIS; MOUSE; NONHUMAN; PHENOTYPE; POINT MUTATION; PRIORITY JOURNAL; PROTEIN EXPRESSION; PROTEIN FUNCTION; PROTEIN LOCALIZATION; PROTEIN TARGETING; SIGNAL TRANSDUCTION;

ACUTE DISEASE; ANIMALS; BLOTTING, WESTERN; CELL DIFFERENTIATION; CELL FRACTIONATION; CELL LINE; CELL NUCLEUS; CELL TRANSFORMATION, NEOPLASTIC; COLONY-FORMING UNITS ASSAY; CORE BINDING FACTOR ALPHA 2 SUBUNIT; DNA-BINDING PROTEINS; FLOW CYTOMETRY; FLUORESCENT ANTIBODY TECHNIQUE; LEUKEMIA, MYELOID; MICE; MYELOID PROGENITOR CELLS; PEROXIDASE; POINT MUTATION; PROTO-ONCOGENE PROTEINS; TRANSCRIPTION FACTORS; TRANSDUCTION, GENETIC;

EID: 18844442856     PISSN: 00278424     EISSN: None     Source Type: Journal    
DOI: 10.1073/pnas.0502130102     Document Type: Article

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