Physical and functional link of the leukemia-associated factors AML1 and PML
Physical and functional link of the leukemia-associated factors AML1 and PML
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DOI：
10.1182/blood-2004-03-1185
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发表时间：
2005-01-01
期刊：
影响因子：
20.3
通讯作者：
Kitabayashi, I
中科院分区：
文献类型：
--
作者：
Nguyen, LA;Pandolfi, PP;Kitabayashi, I
AML1-CBFβ转录因子复合体是急性髓系白血病(AML)中最常见的特异性染色体易位靶点。早幼粒细胞白血病(PML)基因也经常参与AML相关易位。在这里，我们报告了特定的异构体PML I与AML1形成络合物。PML I能够在PML核小体中募集AML1和辅活化子p300，并在p300存在的情况下增强AML1介导的转录。发现PML I的特定C末端区域和AML1的C末端区域对于它们在核体中的结合和共定位都是必需的。PML I的过度表达刺激髓系细胞分化。这些结果表明，PML I可以作为AML1及其辅活化子p300/CBP的介体，组装成功能复合体，从而激活AML1依赖的转录和髓系细胞分化。(C)2005年，由美国血液病学会提供。
The AML1-CBFbeta transcription factor complex is the most frequent target of specific chromosome translocations in acute myeloid leukemia (AML). The promyelocytic leukemia (PML) gene is also frequently involved in AML-associated translocation. Here we report that a specific isoform PML I forms a complex with AML1. PML I was able to recruit AML1 and coactivator p300 in PML nuclear bodies and enhance the AML1-mediated transcription in the presence of p300. A specific C-terminal region of PML I and a C-terminal region of AML1 were found to be required for both their association and colocalization in the nuclear bodies. Overexpression of PML I stimulates myeloid cells to differentiate. These results suggest that PML I could act as a mediator for AML1 and its coactivator p300/CBP to assemble into functional complexes and, consequently, activate AML1-dependent transcription and myeloid cell differentiation. (C) 2005 by The American Society of Hematology.