作者: C E Ibanez , J S Lipsick
DOI: 10.1128/JVI.62.6.1981-1988.1988
关键词: Mutant 、 Cell nucleus 、 Acute myelomonocytic leukemia 、 Nuclear protein 、 MYB 、 Transformation (genetics) 、 Cell division 、 Nuclear transport 、 Molecular biology 、 Biology 、 Immunology 、 Insect Science 、 Microbiology 、 Virology
摘要: The v-myb oncogene of avian myeloblastosis virus causes acute myelomonocytic leukemia in vivo and transforms only myeloid cells vitro. Its product, p48v-myb, is a nuclear protein unknown function. To determine structure-function relationships for this protein, we constructed series deletion mutants v-myb, expressed them retroviral vectors, studied their biochemical biological properties. We used these to identify two separate domains p48v-myb which had distinct roles its accumulation the cell nucleus. showed that viral sequences normally encode both termini were dispensible transformation. In contrast, copies highly conserved amino-terminal repeat required also identified carboxyl-terminal domain was growth v-myb-transformed myeloblasts soft agar but not morphological