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Mol Cell：科学家发现不需要E3连接酶的泛素化过程

2016-07-11 佚名 生物谷

E3连接酶
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癌症包含了超过100种不同的疾病，但所有癌症都是由于细胞和基因脱离了正常的分裂过程，在体内按照自身计划进行复制所导致。遗传学和分子生物学的发展为研究人员提供导致癌症发生的基因突变或细胞变化信息之外，也提供了一些信息可以用于癌症预防措施和治疗方法的开发。来自美国Moffitt癌症中心的研究人员最近发现了一种调节蛋白活性的新机制，这种叫做SETDB1的组蛋白甲基转移酶的活性能够受到该机制调控，该蛋白在


癌症包含了超过100种不同的疾病，但所有癌症都是由于细胞和基因脱离了正常的分裂过程，在体内按照自身计划进行复制所导致。遗传学和分子生物学的发展为研究人员提供导致癌症发生的基因突变或细胞变化信息之外，也提供了一些信息可以用于癌症预防措施和治疗方法的开发。

来自美国Moffitt癌症中心的研究人员最近发现了一种调节蛋白活性的新机制，这种叫做SETDB1的组蛋白甲基转移酶的活性能够受到该机制调控，该蛋白在多种癌症类型中都存在表达上调的情况。相关研究结果发表在国际学术期刊Molecular Cell上。

研究人员发现的这种控制蛋白功能的新机制叫做单泛素化。一般情况下蛋白质能够受到泛素化过程调控，泛素化修饰能够导致许多不同效应：将许多泛素分子添加到蛋白上可以引导蛋白发生降解，但是添加单个泛素分子（单泛素化）可以激活蛋白信号途径或促进其他蛋白发生泛素化。通常泛素化过程的发生需要三种酶的协同作用：E1活化酶，E2结合酶和E3连接酶。

SETDB1能够调节DNA的缩合水平和基因表达，当SETDB1处于活跃状态，其靶基因的表达会受到抑制，由于SETDB1在调节基因表达方面发挥重要作用，因此SETDB1必须受到精准调控确保基因表达得以合理进行。

Moffitt的研究人员进行了分子生物学分析，首次发现SETDB1能够受到单个泛素分子的修饰，并且泛素化过程由E1和E2两种分子直接介导，不需要E3连接酶的参与，并且这种单泛素化修饰可以促进SETDB1活性，抑制靶基因表达。

研究人员表示，这项研究首次证明不需要E3泛素连接酶的参与就可以完成单泛素化修饰，同时表明E2结合酶是开发癌症治疗新方法的一类非常有吸引力的新靶点。

原始出处

Lidong Sun1, Jia Fang1.E3-Independent Constitutive Monoubiquitination Complements Histone Methyltransferase Activity of SETDB1.Mol Cell.2016

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    2016-11-16 ms1779634646866130

    #E3连接酶#

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    2017-04-06 zhaozhouchifen

    #Cell#

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    2016-12-24 lishiwen

    #连接酶#

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    2017-01-26 维他命

    #CEL#

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    2017-01-17 旅苦化文_208

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