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相关概念视频

NF-κB-dependent Signaling Pathway02:26

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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.
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Multivesicular bodies (MVBs) are mature endosomes that sort ubiquitinated proteins and then fuse with lysosomes to degrade the sorted proteins. Epidermal growth factor (EGF) and its receptor (EGFR) form a complex that can be internalized through endocytosis, sorted into an MVB, and later degraded.
The EGFR can initiate signaling pathways that  lead to cell proliferation, migration, and differentiation. Overexpression of EGFR  stimulates cells to proliferate. Excessive  EGFR...
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Gene transcription is regulated by the synergistic action of several proteins that form a complex at a gene regulatory site. This is observed in eukaryotes, where the regulation of gene expression is a complex process. Regulatory proteins in eukaryotes can broadly be classified into two types – regulators that bind directly to specific DNA sequences and co-regulators that associate with regulatory proteins but cannot directly bind to the DNA. These co-regulators are further divided into...
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The human X chromosome contains over ten times the number of genes as in the Y chromosome. Since males have only one X chromosome, and females have two, one might expect females to produce twice as many of the proteins, with undesirable results.
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Methods for the Modulation and Analysis of NF-κB-dependent Adult Neurogenesis
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通过DcR3抑制NF-κB和下游XBP1,有助于降低抗体分泌.

Po-Chun Liu1, Szu-Ying Huang1, Kuo-I Lin2

  • 1Institute of Microbiology and Immunology, National Yang Ming Chiao Tung University, Taipei City, Taiwan.

Journal of immunology (Baltimore, Md. : 1950)
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概括

诱惑受体3 (DcR3) 通过降低B细胞中的X盒结合蛋白1 (XBP1) 表达来损害抗体的产生. 这种机制涉及抑制NF-κB激活,最终降低抗体分泌.

关键词:
这就是NF-κBB.在X盒结合蛋白1中,X盒结合蛋白1抗体分泌 抗体分泌诱惑受体 3 诱惑受体 3 诱惑受体幽默反应是一种幽默反应.

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科学领域:

  • 免疫学 免疫学 免疫学
  • 分子生物学分子生物学

背景情况:

  • 诱受体3 (DcR3) 是一种可溶性受体,调节免疫细胞功能.
  • 已知DcR3可以抑制B细胞增殖并改善自身免疫性疾病.
  • DcR3在调节抗体产生中的确切作用尚不清楚.

研究的目的:

  • 研究DcR3调节抗体生成的机制.
  • 为了确定DcR3是否影响T细胞依赖性抗体反应.
  • 阐明参与DcR3介导的抗体分泌调节的分子途径.

主要方法:

  • 在体内研究中使用了DcR3转基因小鼠模型.
  • 使用DcR3-Fc与B细胞融合蛋白进行了体外试验.
  • 评估了T细胞依赖性抗体反应,B细胞增殖和抗体分泌.
  • 分析了分泌Igh,Xbp1和NF-κB活动的表达.
  • 研究了X盒结合蛋白1 (XBP1) 在DcR3中介作用中的作用.

主要成果:

  • DcR3转基因小鼠表现出受损的T细胞依赖抗体反应.
  • 在体外,DcR3-Fc融合蛋白减弱的T细胞依赖抗体的产生.
  • 在激活的B细胞中,DcR3-Fc减少了分泌Igh和Xbp1的表达.
  • DcR3-Fc抑制了NF-κB活性和XBP1促进体活性,这对Xbp1表达至关重要.
  • 恢复拼接的XBP1部分挽救了抗体生产缺陷.

结论:

  • DcR3通过抑制NF-κB激活和随后在B细胞中的XBP1表达,损害了抗体的产生.
  • 这种XBP1的减少导致抗体分泌的减少,无论是体外还是体内.
  • DcR3的作用超出了抑制增殖的范围,直接影响抗体生产机制.