共查询到20条相似文献,搜索用时 15 毫秒
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The Elongation Domain of ELL Is Dispensable but Its ELL-Associated Factor 1 Interaction Domain Is Essential for MLL-ELL-Induced Leukemogenesis 下载免费PDF全文
Roger T. Luo Catherine Lavau Changchun Du Federico Simone Paul E. Polak Shin Kawamata Michael J. Thirman 《Molecular and cellular biology》2001,21(16):5678-5687
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Goto NK Zor T Martinez-Yamout M Dyson HJ Wright PE 《The Journal of biological chemistry》2002,277(45):43168-43174
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Chromatin-related properties of CBP fused to MLL generate a myelodysplastic-like syndrome that evolves into myeloid leukemia 总被引:16,自引:0,他引:16 下载免费PDF全文
As a result of the recurring translocation t(11;16) (q23;p13.3), MLL (mixed-lineage leukemia) is fused in frame to CBP (CREB binding protein). This translocation has been documented almost exclusively in cases of acute leukemia or myelodysplasia secondary to therapy with drugs that target DNA topo isomerase II. The minimal chimeric protein that is produced fuses MLL to the bromodomain, histone acetyltransferase (HAT) domain, EIA-binding domain and steroid-receptor coactivator binding domains of CBP. We show that transplantation of bone marrow retrovirally transduced with MLL-CBP induces myeloid leukemias in mice that are preceded by a long preleukemic phase similar to the myelodysplastic syndrome (MDS) seen in many t(11;16) patients but unusual for other MLL translocations. Structure-function analysis demonstrated that fusion of both the bromodomain and HAT domain of CBP to the amino portion of MLL is required for full in vitro transformation and is sufficient to induce the leukemic phenotype in vivo. This suggests that the leukemic effect of MLL-CBP results from the fusion of the chromatin association and modifying activities of CBP with the DNA binding activities of MLL. 相似文献
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Multiple mixed lineage leukemia (MLL) fusion proteins suppress p53-mediated response to DNA damage 总被引:3,自引:0,他引:3
Wiederschain D Kawai H Shilatifard A Yuan ZM 《The Journal of biological chemistry》2005,280(26):24315-24321
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为了研究 C B P在胰岛 H I T 细胞中调节基因转录的机制,将不同的 C B P片段瞬时转染到细胞中,观察其转录活性.实验表明,在胰岛 H I T 细胞中,膜去极化及 c A M P 均可诱导 C B P30( C R E B结合功能区)转录活性增强,并有协同效应. P K C对 C B P30 的转录活性无影响;与 C R E B有更强结合力的 C B P K I X S/ B(氨基酸序列短于 C B P30 的 C R E B结合功能区)其基本转录活性及膜去极化、c A M P诱导下的转录活性均比 C B P30 更强.反义 C R E B 的过度表达可降低 c A M P诱导的 C B P的转录活性.提示在胰岛 H I T 细胞中,膜去极化及 c A M P对共转录因子 C B P转录活性的调节作用通过 C R E B介导. 相似文献
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