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c-Myc是一种泛在性的转录因子,它调控着许多涉及细胞增殖、分化、凋亡等生命活动的基因.实验结果表明在骨肉瘤细胞U2OS中过表达c-Myc和Nbs1都能减弱阿霉素降低集落形成的能力.进一步的实验证实c-Myc的这种作用与Nbs1有关,Nbs1是c-Myc的靶基因.染色质免疫沉淀实验显示,c-Myc招募组蛋白乙酰化酶p300复合物到Nbs1启动子区,引起了组蛋白H4的乙酰化,定位在Nbs1启动子区的相邻的两个E-box对c-Myc的结合是必要的.上述结果说明c-Myc减弱阿霉素的作用部分是通过调控Nbs1来实现的.这也提示了c-Myc在阿霉素诱导的DNA损伤修复中起作用。
c-Myc is a ubiquitous transcription factor, which regulates many genes involved in cell proliferation, differentiation, apoptosis and other life activities.Experimental results show that overexpression of c-Myc and Nbs1 in osteosarcoma U2OS can be weakened Adriamycin reduced the ability of colony formation.Further experiments confirmed that this role of c-Myc and Nbs1, Nbs1 c-Myc target gene.Chromatin immunoprecipitation experiments showed that c-Myc recruits histone acetylase p300 Complex to the Nbs1 promoter region, resulting in the acetylation of histone H4, which is necessary for the binding of c-Myc to two adjacent E-boxes located in the Nbs1 promoter region. The effect of mycotoxin is partly through the regulation of Nbs1, which also suggests that c-Myc plays a role in doxorubicin-induced DNA damage repair.