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Sequence-specific Labeling of Nucleic Acids and Proteins with Methyltransferases and Cofactor Analogues
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在METTL3中介的m.

Yuting Tang1, Fangling Hong1, Siyang Ding2

  • 1Department of Medical Genetics, Nanjing Medical University, Longmian Road 101, Nanjing 211166, P.R. China; Jiangsu Key Laboratory of Xenotransplantation, Nanjing Medical University, Longmian Road 101, Nanjing 211166, P.R. China.

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|June 4, 2023
PubMed
概括
此摘要是机器生成的。

长非编码RNAIGFBP7-OT通过增加IGFBP7表达和软骨退化来促进骨关节炎 (OA). 它的N6-甲基氨酸修饰为OA治疗提供了潜在的治疗标.

关键词:
CP: 免疫学 免疫学通过DNA甲基化.IGFBP7 IGFBP7 IGFBP7 IGFBP7 IGFBP7 IGFBP7 IGFBP7 IGFBP7在IGFBP7-OT中使用.在METTL3中,METTL3是METTL3的第一个类型.骨关节炎是一种关节炎.

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科学领域:

  • 生物化学 生物化学
  • 分子生物学分子生物学
  • 遗传学 遗传学 是一个

背景情况:

  • 骨关节炎 (OA) 是一种影响老年人的流行性退行性关节疾病.
  • 长非编码RNAs (lncRNAs) 越来越多地被认为是它们在疾病发病过程中的角色.

研究的目的:

  • 研究 lncRNA IGFBP7-OT 在骨关节炎中的作用.
  • 阐明IGFBP7-OT在OA中的功能背后的分子机制.

主要方法:

  • 分析IGFBP7-OT和IGFBP7在骨关节性软骨中的表达.
  • 在体外研究状细胞活力,细胞亡和细胞外基质.
  • 在小鼠模型中使用OA表型的体内评估.
  • 涉及DNA甲基化和m6A修饰的机制研究.

主要成果:

  • 在OA软骨中,IGFBP7-OT和IGFBP7的上调和正相关.
  • 过度表达IGFBP7-OT抑制了冠状细胞的活力,促进了细胞亡,并减少了细胞外基质.
  • 然而,IGFBP7-OT的降解产生了相反的效果,改善了OA的表型.
  • 通过抑制DNMT1/DNMT3a甲基化,IGFBP7-OT通过上调IGFBP7促进OA.
  • 通过METTL3介导的m6A修饰部分控制了OA中的IGFBP7-OT上调.

结论:

  • 通过DNMT1/DNMT3a-IGFBP7轴,IGFBP7-OT促进了OA的进展.
  • 通过METTL3介导的IGFBP7-OT的m6A修饰参与了OA的发病.
  • IGFBP7-OT代表了骨关节炎的潜在治疗标.