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首页> 美国卫生研究院文献>Proceedings of the National Academy of Sciences of the United States of America >Switch from Myc/Max to Mad1/Max binding and decrease in histone acetylation at the telomerase reverse transcriptase promoter during differentiation of HL60 cells
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Switch from Myc/Max to Mad1/Max binding and decrease in histone acetylation at the telomerase reverse transcriptase promoter during differentiation of HL60 cells

机译：从Myc / Max绑定更改为Mad1 / Max绑定并减少 端粒酶逆转时的组蛋白乙酰化 HL60细胞分化过程中的转录酶启动子

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Recent evidence suggests that the Myc and Mad1 proteins are implicated in the regulation of the gene encoding the human telomerase reverse transcriptase (hTERT), the catalytic subunit of telomerase. We have analyzed the in vivo interaction between endogenous c-Myc and Mad1 proteins and the hTERT promoter in HL60 cells with the use of the chromatin immunoprecipitation assay. The E-boxes at the hTERT proximal promoter were occupied in vivo by c-Myc in exponentially proliferating HL60 cells but not in cells induced to differentiate by DMSO. In contrast, Mad1 protein was induced and bound to the hTERT promoter in differentiated HL60 cells. Concomitantly, the acetylation of the histones at the promoter was significantly reduced. These data suggest that the reciprocal E-box occupancy by c-Myc and Mad1 is responsible for activation and repression of the hTERT gene in proliferating and differentiated HL60 cells, respectively. Furthermore, the histone deacetylase inhibitor trichostatin A inhibited deacetylation of histones at the hTERT promoter and attenuated the repression of hTERT transcription during HL60 cell differentiation. In addition, trichostatin A treatment activated hTERT transcription in resting human lymphocytes and fibroblasts. Taken together, these results indicate that acetylation/deacetylation of histones is operative in the regulation of hTERT expression.
机译：最近的证据表明，Myc和Mad1蛋白与编码人类端粒酶逆转录酶（hTERT）（端粒酶的催化亚基）的基因有关。我们已经使用染色质免疫沉淀分析法分析了HL60细胞中内源性c-Myc和Mad1蛋白与hTERT启动子之间的体内相互作用。 c-Myc在体内将hTERT近端启动子处的E-boxs在指数增殖的HL60细胞中占据，但在DMSO诱导分化的细胞中则没有。相反，Mad1蛋白被诱导并与分化的HL60细胞中的hTERT启动子结合。伴随地，在启动子上组蛋白的乙酰化显着降低。这些数据表明c-Myc和Mad1在E-box上的相互占用分别负责增殖和分化的HL60细胞中hTERT基因的激活和抑制。此外，组蛋白脱乙酰基酶抑制剂曲古抑菌素A抑制 hTERT启动子处组蛋白的去乙酰化 减弱了hTERT转录的抑制 HL60细胞分化。此外，曲古抑素A治疗 静息人类中激活的hTERT转录 淋巴细胞和成纤维细胞。综上所述，这些结果表明 组蛋白的乙酰化/去乙酰化在 hTERT表达的调控。

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