甲调节S-adenosylmethionine生物合成和单碳代谢
在PubMed上查看摘要
概括
此摘要是机器生成的。甲通过向MAT1A来抑制S- 腺甲 (SAM) 的产生,影响单碳代谢和表观遗传调节. 这项研究揭示了一个反循环,细胞补偿了FA诱导的SAM耗尽.
科学领域
- 生物化学
- 表观遗传学
- 细胞代谢
背景情况
- 一碳代谢对细胞功能至关重要,包括表观遗传调节.
- 甲 (FA) 是一种来自内源和环境的单碳单位.
- 在细胞中,S-adenosylmethionine (SAM) 是主要的甲基供体.
研究的目的
- 研究甲 (FA) 如何影响单碳代谢和SAM生物合成.
- 阐明FA影响SAM产生的分子机制.
- 探索FA暴露对表观遗传修饰的影响.
主要方法
- 研究了FA与蛋白质中的囊残留物的反应,特别是MAT1A.
- 在体外评估了FA对MAT1A活性和SAM产生的影响.
- 我们使用了长期FA过载的基因小鼠模型.
- 在体内分析了SAM水平,基因甲基化和基因表达.
主要成果
- 通过向MAT1A,FA抑制了SAM生物合成,具有MAT异型特异性.
- 在MAT1A中,FA与氨酸残留物,包括Cys120发生反应.
- 在小鼠中,慢性FA过载导致SAM水平下降和基因组/基因甲基化发生改变.
- 细胞激活表观遗传和转录机制以补偿FA诱导的SAM耗尽.
结论
- 甲通过抑制SAM的产生直接影响单碳代谢.
- 由FA引起的SAM耗尽会影响基因组和基因水平的表观遗传调节.
- 在单碳代谢中,甲和SAM之间存在生物化学反循环.
相关概念视频
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