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相关概念视频

NF-κB-dependent Signaling Pathway02:26

NF-κB-dependent Signaling Pathway

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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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Genome-wide association studies or GWAS are used to identify whether common SNPs are associated with certain diseases. Suppose specific SNPs are more frequently observed in individuals with a particular disease than those without the disease. In that case, those SNPs are said to be associated with the disease. Chi-square analysis is performed to check the probability of the allele likely to be associated with the disease.
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Signaling cascades usually lack linearity. Multiple pathways interact and regulate one another, allowing cells to integrate and respond to diverse environmental stimuli.
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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...
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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...
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Screening for Functional Non-coding Genetic Variants Using Electrophoretic Mobility Shift Assay EMSA and DNA-affinity Precipitation Assay DAPA
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综合性分析确定了一个cGAS-STING路径驱动的签名,在系统性红斑狼中具有上下文依赖的角色.

Lele Zhang1, Ming-Ju Amy Lyu1,2, Ze Hong3

  • 1Central Laboratory, Innovation and Incubation Center, Shanghai Pulmonary Hospital, School of Medicine, Tongji University, Shanghai, China.

Advanced science (Weinheim, Baden-Wurttemberg, Germany)
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概括
此摘要是机器生成的。

干扰素基因 (cGAS-STING) 的循环GMP-AMP合成酶刺激通路在全身性红斑狼 (SLE) 中至关重要. 一个新的M7core基因签名量化了途径活性,有助于诊断和预测SLE患者的STING抗剂治疗反应.

关键词:
- / - 小鼠.在Trex1−/−小鼠中.Zbp1−/− 的小鼠.原始诱导的类似狼的小鼠.系统性红血性狼 (Systemic Lupus Erythematosus) 是一种全身性狼.这就是cGAS-STING路径.

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科学领域:

  • 免疫学 免疫学 免疫学
  • 遗传学 是一个遗传学.
  • 类风湿病学 类风湿病学

背景情况:

  • 干扰素基因 (cGAS-STING) 循环GMP-AMP合成酶刺激通路越来越多地被认为是系统性红斑狼 (SLE) 发病的关键因素.
  • 了解这种途径的确切作用和活性对于开发向疗法至关重要.

研究的目的:

  • 在SLE中描述cGAS-STING路径签名.
  • 开发一种定量生物标志物,用于评估cGAS-STING通路活动.
  • 评估这种生物标志物对STING抗剂治疗反应的预测价值.

主要方法:

  • 利用大规模的转录组学,基于细胞的测试和两种狼类小鼠模型.
  • 确定了一种依赖于STING的基因特征 (M7core) 用于对cGAS-STING通路活性进行定量评估.
  • 在十个独立的队列中验证了M7core,并与干扰素刺激的基因特征进行了比较.

主要成果:

  • 鉴定了M7core,一种依赖于STING的基因特征,可以对SLE中的cGAS-STING通路活性进行定量评估.
  • 在70.4%的SLE样本中,M7core显示了广泛的激活,并在74.1%的患者中预测了对STING抗剂的治疗反应.
  • M7core的表现优于现有的签名,与疾病活动标志物相关,并且通过氧化治疗减少.
  • 在小鼠模型中,施用STING抗剂改善了病理,抑制了M7core基因,包括ZBP1,一个关键的促进者.

结论:

  • M7core 作为一种强大的诊断和机械生物标志物,用于SLE中cGAS-STING通路活性.
  • 评估cGAS-STING通路活性对于在SLE患者中指导针对STING的治疗选择至关重要.
  • ZBP1在狼的发病过程中扮演着上下文依赖的角色,这突显了它在cGAS-STING介导的炎症中的重要性.