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相关概念视频

NF-κB-dependent Signaling Pathway02:26

NF-κB-dependent Signaling Pathway

The transcription factor NF-κB was discovered in 1986 in the lab of Nobel laureate Professor David Baltimore, for its interaction with the immunoglobulin light chain enhancer in B-cells. After more than three decades of study, it is now evident that NF-κB regulates the expression of over 100 genes. Most of these genes play an essential role in the innate and adaptive immune responses as well as the inflammatory responses of animals.
NF-κB-dependent Signaling Mechanism
The heterodimer of NF-κB...
Nitric Oxide Signaling Pathway01:28

Nitric Oxide Signaling Pathway

Nitric oxide (NO), an inorganic gas, acts as a potent second messenger in most animal and plant tissues. NO diffuses out of the cells that produce it and enters the neighboring cells to generate a downstream response. NO synthase (NOS) catalyzes NO production by the deamination of the amino acid arginine. There are three isoforms of NOS. Endothelial cells have endothelial NOS (eNOS), nerve and muscle cells have neuronal NOS (nNOS), and macrophages produce inducible NOS (iNOS) upon exposure to...

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相关实验视频

Updated: May 10, 2026

Two-photon Imaging of Intracellular Ca2+ Handling and Nitric Oxide Production in Endothelial and Smooth Muscle Cells of an Isolated Rat Aorta
08:08

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氧化会通过一种依赖于cGMP的途径,在成年猫类心肌中引起瘤缩因子-α的表达.

D Kalra1, G Baumgarten, Z Dibbs

  • 1Winters Center for Heart Failure Research, Cardiology Section, Department of Medicine, Veterans Administration Medical Center and Baylor College of Medicine, Houston, TX 77030, USA.

Circulation
|September 12, 2000
PubMed
概括
此摘要是机器生成的。

氧化 (NO) 通过一种依赖cGMP的途径在心脏衰竭中触发瘤缩因子-α (TNF-alpha) 的产生. 这表明NO和TNF-alpha可能会在心力衰竭中产生自我维持的炎症反循环.

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En Face Detection of Nitric Oxide and Superoxide in Endothelial Layer of Intact Arteries
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相关实验视频

Last Updated: May 10, 2026

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08:08

Two-photon Imaging of Intracellular Ca2+ Handling and Nitric Oxide Production in Endothelial and Smooth Muscle Cells of an Isolated Rat Aorta

Published on: June 10, 2015

En Face Detection of Nitric Oxide and Superoxide in Endothelial Layer of Intact Arteries
08:58

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Application of Genetically Encoded Fluorescent Nitric Oxide (NO•) Probes, the geNOps, for Real-time Imaging of NO• Signals in Single Cells

Published on: March 16, 2017

科学领域:

  • 心血管研究研究心血管研究
  • 分子生物学分子生物学
  • 免疫学 免疫学 免疫学

背景情况:

  • 瘤亡因子-α (TNF-α) 和氧化 (NO) 在失败的心脏中持续的同时表达尚未得到充分理解.
  • 驱动这种同时表达的精确机制仍然难以捉摸.

研究的目的:

  • 为了调查氧化 (NO) 是否足以诱导心脏中的瘤亡因子-α (TNF-alpha) 生物合成.
  • 阐明涉及NO介导的TNF-α生成的信号通路.

主要方法:

  • 使用缓冲器穿透的Langendorff心脏来自成年猫,接受了NO供体 (S-nitroso-N-acetylpenicillamine,SNAP) 的治疗.
  • 使用NO灭剂 (C-PTIO),cGMP类似物 (8--cGMP) 和对抗剂 (ODQ,Rp-8-Br-cGMPS) 来剖析NO信号通路.
  • 执行电泳运动转移测试 (EMSA) 来评估转录因子激活 (NF-kappaB,AP-1).
  • 在孤立的心脏肌细胞中研究了IkappaBalpha的蛋白质修饰 (酸化,降解).

主要成果:

  • 随着SNAP治疗剂量和时间的依赖,心肌TNF-alpha mRNA和蛋白质的增加.
  • NO诱导的TNF-α生物合成是由cGMP途径调解的,涉及蛋白激酶G (PKG).
  • 通过促进IkappaBalpha酸化和降解,SNAP和cGMP激活了NF-kappaB.

结论:

  • 氧化 (NO) 通过一种依赖cGMP的途径引起TNF-α生物合成.
  • 这种机制表明,NO和TNF-alpha可能会在失败的心脏中建立自我维持的炎症反回路.