抄録
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.
| 本文言語 | 英語 |
|---|---|
| ページ(範囲) | 4699-4704 |
| ページ数 | 6 |
| ジャーナル | Blood |
| 巻 | 90 |
| 号 | 12 |
| DOI | |
| 出版ステータス | 出版済み - 15-12-1997 |
| 外部発表 | はい |
All Science Journal Classification (ASJC) codes
- 生化学
- 免疫学
- 血液学
- 細胞生物学
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「Adenoviral E1A-associated protein p300 is involved in acute myeloid leukemia with t(11;22)(q23;q13)」の研究トピックを掘り下げます。これらがまとまってユニークなフィンガープリントを構成します。引用スタイル
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