| Literature DB >> 9389684 |
K Ida1, I Kitabayashi, T Taki, M Taniwaki, K Noro, M Yamamoto, M Ohki, Y Hayashi.
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 findings suggest that the basis for the leukemogenesis of t(11; 22)-AML is the inability of p300 to regulate cell-cycle and cell differentiation after fusion with MLL.Entities:
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Year: 1997 PMID: 9389684
Source DB: PubMed Journal: Blood ISSN: 0006-4971 Impact factor: 22.113