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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...
The Extrinsic Apoptotic Pathway01:17

The Extrinsic Apoptotic Pathway

The extrinsic apoptotic pathway is initiated when extracellular death-inducing signals, such as specific cytokines, activate the death receptors expressed on the cell surface. The immune cells involved in this pathway are natural killer cells (NK cells) and cytotoxic T-lymphocytes. NK cells are critical in innate immune response, while cytotoxic T-lymphocytes are associated with adaptive immune response. These cells recognize specific receptors expressed on the altered cells and activate...
Amplifying Signals via Enzymatic Cascade01:22

Amplifying Signals via Enzymatic Cascade

When a ligand binds to a cell-surface receptor, the receptor's intracellular domain changes shape, which may either activate its enzyme function or allow its binding to other molecules. The initial signal is amplified by most signal transduction pathways. This means that a single ligand molecule can activate multiple molecules of a downstream target. Proteins that relay a signal are most commonly phosphorylated at one or more sites, activating or inactivating the protein. Kinases catalyze the...
The JAK-STAT Signaling Pathway01:20

The JAK-STAT Signaling Pathway

Several cytokine receptors have tightly bound Janus kinase or JAK proteins attached at their cytosolic tail. Small signaling molecules such as cytokines, growth hormones, or prolactins bind to the cytokine receptors and initiate their dimerization. The dimerization brings the cytosolic JAKs together that trans-phosphorylate and activates each other. The activated JAKs now phosphorylate cytosolic tails of the cytokine receptors, which serve as binding sites for adaptor proteins such as  SH2...
TGF - β Signaling Pathway01:16

TGF - β Signaling Pathway

The TGF-β signaling pathway regulates cell growth, differentiation, adhesion, motility, and development. TGF-β ligands that induce TGF-β signaling are synthesized in their latent form. Several proteases or cell surface receptors such as integrins act upon the latent form, releasing the active ligand. There are three types of mammalian TGF-βs: (TGF-β1, TGF-β2, and TGF-β3) that bind as homodimers or heterodimers to TGF-β receptors. The TGF-β receptors are of three kinds RI, RII, and RIII. The RI...
NF-kB-dependent Signaling Pathway02:26

NF-kB-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
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相关实验视频

Updated: May 26, 2026

A Guide to Production, Crystallization, and Structure Determination of Human IKK1/α
11:27

A Guide to Production, Crystallization, and Structure Determination of Human IKK1/α

Published on: November 2, 2018

通过NF-kappaB诱导gadd45beta会降低对亲细胞亡的JNK信号的调节.

E De Smaele1, F Zazzeroni, S Papa

  • 1The Gwen Knapp Center for Lupus and Immunology research, The University of Chicago, Illinois 60637, USA.

Nature
|November 20, 2001
PubMed
概括

核因子-kappaB (NF-kappaB) 转录因子通过降低c-Jun氨基终端激酶 (JNK) 途径来促进细胞存活. 这种NF-kappaB介导的JNK信号的抑制对于控制细胞死亡至关重要.

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科学领域:

  • 分子生物学分子生物学
  • 细胞生物学 细胞生物学
  • 免疫学 免疫学 免疫学

背景情况:

  • 核因子-kappaB (NF-kappaB) 转录因子调节免疫反应,炎症和细胞存活.
  • NF-kappaB的激活对抗由各种触发因素诱导的亡,包括TNF受体的参与.
  • 在癌症中NF-kappaB的抗亡作用是显著的,有助于瘤发生和对治疗的抗性.

研究的目的:

  • 阐明NF-kappaB抗亡活性背后的分子机制.
  • 建立NF-kappaB信号传递与c-Jun氨基终端激酶 (JNK) 途径之间的联系.
  • 确定NF-kappaB在调节细胞死亡途径中的作用.

主要方法:

  • 研究了NF-kappaB和JNK信号级联之间的相互作用.
  • 分析了参与压力和亡的基因的转录调节.
  • 利用TNF受体信号作为研究细胞死亡的模型系统.

主要成果:

  • 证明NF-kappaB复合体降低了JNK级联的下调.
  • 确定了Gadd45beta/Myd118作为一个关键的NF-kappaB上调基因,可以抑制JNK信号传递.
  • 表明NF-kappaB依赖于JNK的抑制对于预防TNF-α诱导的亡至关重要.

结论:

  • 建立了NF-kappaB和JNK通路之间的直接联系,揭示了一个新的细胞保护机制.
  • 突出了NF-kappaB介导的JNK信号抑制在控制编程细胞死亡中的重要性.
  • 表明持续的JNK激活有助于亡反应,特别是在TNF-alpha信号传递的背景下.