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Smyd1是心脏和肌肉特异表达的组蛋白甲基转移酶,含有SET结构域,是组蛋白H3上第四位赖氨酸的甲基转移酶,具有激活下游基因转录的功能,可促进肌肉细胞成熟、分化。近来研究发现,Smyd1基因可选择性剪接,选择性剪接体为Smyd1a和Smyd1b,二者在时间和空间上的表达方式完全不同。基因的选择性剪接是产生数量众多蛋白质的主要方式,但机制未明。组蛋白修饰在选择性剪接中可能发挥重要作用。抗阻运动训练能够使Smyd基因发生选择性剪接,首先快速剪接表达Smyd1a,然后剪接转换表达Smyd1b(Smyd1-△Exon5),通过转换表达,能够使Smyd1a和Smyd1b保持相当长时间的生物学作用,他们均可以激活肌卫星细胞并促进其增殖。卫星细胞一旦被激活,即会增殖、分化,然后与已存在的肌纤维融合,通过这样的过程为肌纤维提供新的细胞核,并使各种基因的表达发生改变,实现肌纤维所需纤维蛋白含量的比率,使肌肉卫星(干)细胞库得到更新,对肌肉质量和功能的持续维持和增加起到重要作用。故了解Smyd1基因选择性剪接体的作用及其组蛋白的修饰作用对阐明骨骼肌质量变化过程的分子生物学机制具有重要意义,对预防长期伤残患者骨骼肌发生萎缩至关重要,同时为治疗与骨骼肌萎缩相关的其他疾病提供有效途径。
Smyd1 is a cardiac and muscle-specific histone methyltransferase that contains the SET domain and is the fourth lysine methyltransferase in histone H3 with the ability to activate downstream gene transcription to promote muscle cell maturation , Differentiation. Recent studies have found that Smyd1 gene alternative splicing, alternative splicing body Smyd1a and Smyd1b, both in time and space in a completely different way of expression. Alternative splicing of genes is the main way to produce a large number of proteins, but the mechanism is unclear. Histone modification may play an important role in alternative splicing. Anti-resistance exercise training can selectively spliced Smyd gene. Firstly, Smyd1a was spliced rapidly and spliced to Smyd1b (Smyd1-△ Exon5). Smyd1a and Smyd1b can be transformed for a long time by transforming expression. Can activate muscle satellite cells and promote their proliferation. Once activated, satellite cells proliferate, differentiate, and then fuse with preexisting muscle fibers, providing new nuclei to the muscle fibers and altering the expression of various genes to achieve the desired fibrin content of the muscle fibers , To update muscular satellite (stem) cell banks and play an important role in the sustained maintenance and increase of muscle mass and function. Therefore, it is important to understand the role of Smyd1 alternative spliceosome and its histone modification in elucidating the molecular biological mechanism of skeletal muscle mass change, and it is important to prevent skeletal muscle atrophy in long-term disabled patients and to treat Other diseases associated with skeletal muscle atrophy provide an effective approach.