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首页> 外文期刊>Oncogene >The MN1-TEL myeloid leukemia-associated fusion protein has a dominant-negative effect on RAR-RXR-mediated transcription
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The MN1-TEL myeloid leukemia-associated fusion protein has a dominant-negative effect on RAR-RXR-mediated transcription

机译：MN1-TEL髓样白血病相关融合蛋白对RAR-RXR介导的转录具有显性负作用

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The translocation t(12;22)(p13;q11) creates an MN1-TEL fusion gene leading to acute myeloid leukemia. MN1 is a transcription coactivator of the retinoic acid and vitamin D receptors, and TEL (ETV6) is a member of the E26-transformation-specific family of transcription factors. In MN1-TEL, the transactivating domains of MN1 are combined with the DNA-binding domain of TEL. We show that MN1-TEL inhibits retinoic acid receptor (RAR)-mediated transcription, counteracts coactivators such as p160 and p300, and acts as a dominant-negative mutant of MN1. Compared to MN1, the same transactivation domains in MN1-TEL are poorly stimulated by p160, p300 or histone deacetylase inhibitors, indicating that the block of RAR-mediated transcription by MN1-TEL is caused by dysfunctional transactivation domains rather than by recruitment of corepressors. The mechanism leading to myeloid leukemia in t(12;22) thus differs from the translocations that involve RAR itself.
机译：易位t（12; 22）（p13; q11）创建了导致急性髓性白血病的MN1-TEL融合基因。 MN1是视黄酸和维生素D受体的转录共激活因子，而TEL（ETV6）是E26转化特异性转录因子家族的成员。在MN1-TEL中，MN1的反式激活域与TEL的DNA结合域结合在一起。我们表明，MN1-TEL抑制视黄酸受体（RAR）介导的转录，抵消诸如p160和p300等共激活因子，并充当MN1的显性负突变体。与MN1相比，p160，p300或组蛋白脱乙酰基酶抑制剂很难刺激MN1-TEL中相同的反式激活域，这表明MN1-TEL对RAR介导的转录阻滞是由功能失调的反式激活域引起的，而不是由募集的presspressor引起的。因此，t（12; 22）中导致髓样白血病的机制不同于涉及RAR自身的易位。

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