作者: S Meyers , J R Downing , S W Hiebert
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摘要: The AML1 gene on chromosome 21 is disrupted in the (8;21)(q22;q22) translocation associated with acute myelogenous leukemia and encodes a protein central 118-amino-acid domain 69% homology to Drosophila pair-rule gene, runt. We demonstrate that AML-1 DNA-binding which specifically interacts sequence belonging group of enhancer core motifs, TGT/cGGT. Electrophoretic mobility shift analysis cell extracts identified two AML-1-containing protein-DNA complexes whose electrophoretic mobilities were slower than those formed produced vitro. Mixing vitro-produced prior gel resulted formation higher-order complexes. Deletion mutagenesis revealed runt mediates both sequence-specific DNA binding protein-protein interactions. hybrid product, AML-1/ETO, results from (8;21) retains domain, recognizes consensus other cellular proteins.