...
  • 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>Journal of cellular physiology. >PARP1 inhibition enhances reactive oxygen species on gut microbiota
【24h】

PARP1 inhibition enhances reactive oxygen species on gut microbiota

机译：PARP1 抑制增强肠道菌群中的活性氧

获取原文
获取原文并翻译 | 示例
           
页面导航
  • 摘要
  • 著录项
  • 相似文献
  • 相关主题

摘要

Abstract Poly(ADP‐ribose) polymerase 1 (PARP1) plays a key role in genome stability by modulating DNA‐damage responses. Activated by DNA interruptions through ultraviolet (UV) exposure, PARylation is synthesized by PARP1 and serves as a survival mechanism for cancer and metabolic diseases. Several strategies including ROS and antimicrobial peptides?(AMPs) function in host defenses, while the targeted tissue and mechanism under DNA damage are unknown. Here, we show that DNA damage induces responses specifically in the gut tissue. The knockdown of PARP1 reduces the activation of PARylation. Parp1 knockdown under DNA damage results in over‐accumulated ROS and secretion of AMPs through the regulation of Relish, a subunit of nuclear factor‐κB?(NF‐κB). Double‐knockdown of Parp1 and Relish specifically in the gut inhibits AMP secretion. In conclusion, the host defense is achieved through ROS accumulation rather than the AMPs under DNA damage. In contrast, the knockdown of PARP1 exacerbates ROS accumulation to a harmful level. Under this circumstance, NF‐κb targeted AMP secretion is provoked for host defense. Microbiome and functional analysis provide evidence for the hazard of DNA damage and show variations in the metabolic pathways following Parp1 inhibition. Our findings suggest the notion that PARP1 inhibition contributes to ROS accumulation under DNA damage and its role in NF‐κb activation for host defense.
机译：摘要聚ADP核糖应承担的)聚合酶1 (PARP1)在基因组稳定中发挥着关键作用调节DNA损伤反应。通过紫外(UV)接触中断,PARylation合成PARP1和作为癌症和新陈代谢的生存机制疾病。抗菌肽?(安培)功能主机防御,而有针对性的组织和机制在DNA损伤是未知的。特别是在DNA损伤诱发响应肠道组织。PARylation激活。活性氧积累和DNA损伤的结果通过调节分泌安培喜欢,一个亚基的核因子κB ? (NF必经κB)。Parp1和享受的双重必经击倒在肠道抑制腺苷酸分泌。宿主防御是通过活性氧积累而不是安培在DNA损害。加剧了活性氧积累到有害水平。在这种情况下,NFκb有针对性的AMP分泌引起宿主防御。提供微生物和功能分析DNA损伤的危害并展示证据变化后的代谢途径Parp1抑制。PARP1抑制导致活性氧积累下的DNA损伤及其作用NF必经κb激活宿主防御。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
获取原文

客服邮箱：kefu@zhangqiaokeyan.com

京公网安备：11010802029741号 ICP备案号：京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有

  • 客服微信

  • 服务号