Abstract
p300, which was originally cloned as a nuclear binding target of the adenovirus E1A oncoprotein, forms a family with cyclic-AMP response element binding protein (CREB)-binding protein (CBP). p300/CBP are considered to be transcriptional coactivators that connect the basal transcriptional machinery to various DNA-binding transcriptional factors. p300/CBP are implicated in both cell differentiation and regulation of cell-cycle. We identify here that the p300 gene is fused to the MLL gene and that in-frame MLL-p300 fusion protein is generated in acute myeloid leukemia (AML) with t(11;22)(q23;q13). These finding suggest that the basis for the leukemogenesis of t(11;22)-AML is the inability of p300 to regulate cell-cycle end cell differentiation after fusion with MLL.
Original language | English |
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Pages (from-to) | 4699-4704 |
Number of pages | 6 |
Journal | Blood |
Volume | 90 |
Issue number | 12 |
DOIs | |
Publication status | Published - 15-12-1997 |
Externally published | Yes |
All Science Journal Classification (ASJC) codes
- Biochemistry
- Immunology
- Hematology
- Cell Biology