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相关概念视频

Allosteric Proteins-ATCase01:19

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Binding sites linkages can regulate a protein's function.  For example, enzyme activity is often regulated through a feedback mechanism where the end product of the biochemical process serves as an inhibitor.
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通过结合TAF1减少LncR-GAS5的腺因基转移酶表达,以增加CIH造成的脏损伤.

Wei Liu1,2, Wukaiyang Liang1,2, CunTai Zhang1,2

  • 1Department of Geriatrics, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, 1095 Jiefang Avenue, Wuhan, 430030, China.

Heliyon
|July 12, 2024
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概括

长非编码RNA GAS5与TAF1结合,抑制APRT,使老鼠的慢性间歇性缺氧诱导的损伤恶化. 减少GAS5或增加APRT可以缓解损伤,亡和纤维化.

关键词:
APRT APRT APRT 的意思是什么意思一个CIH的CIH是一个CIH.造成脏损伤的人.在TAF1中,TAF1是TAF1.在cRNA GAS5 中.

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科学领域:

  • 腎臟病學 (nephrology) 是一種醫學專業.
  • 分子生物学分子生物学
  • 遗传学 是一个遗传学.

背景情况:

  • 阻塞性睡眠呼吸暂停-呼吸暂停综合征 (OSAHS) 通过慢性间歇性缺氧 (CIH) 诱导的损伤引起慢性病 (CKD).
  • 在CIH诱导的损伤中,长非编码RNA (lncRNA) GAS5和腺因基转移酶 (APRT) 之间的相互作用尚不清楚.

研究的目的:

  • 在CIH诱导的损伤的背景下,研究lncRNA GAS5和APRT之间的相互作用.
  • 阐明CIH诱导的损伤背后的分子机制,涉及GAS5和APRT.

主要方法:

  • 建立了慢性间歇性缺氧 (CIH) 的大鼠模型.
  • 使用了转录组测序,等离子体转染 (sh-GAS5,OE-APRT),RT-qPCR,西部涂抹和TUNEL染色.
  • 执行RNA拉下,RIP和ChIP测试以验证分子相互作用.

主要成果:

  • 在大鼠脏中,CIH显著增加TAF1并降低APRT表达.
  • GAS5抑制或APRT过度表达减轻了CIH诱导的损伤,降低了BUN和肌素水平.
  • 发现GAS5和TAF1对APRT转录有负面调节,其中GAS5与TAF1.1结合.

结论:

  • lncRNA GAS5与TAF1相互作用以抑制APRT转录.
  • 这种相互作用加剧了老鼠的慢性间歇性缺氧诱导的损伤.
  • 针对GAS5-TAF1-APRT轴可能为CIH相关脏疾病提供治疗潜力.