相关实验视频

Updated: Jun 28, 2025

Isolation and Th17 Differentiation of Naïve CD4 T Lymphocytes

Isolation and Th17 Differentiation of Naïve CD4 T Lymphocytes

Published on: September 26, 2013

通过UHRF1-MAP4K3轴,UHRF1P通过IL-17A介导的系统性红斑狼产生作用

Huai-Chia Chuang¹, Kuei-Yuan Lan², Pu-Ming Hsu¹

¹Immunology Research Center, National Health Research Institutes, Zhunan, Taiwan.

Journal of autoimmunity

|April 21, 2024

概括

一种新型假基因UHRF1P在全身性红斑狼 (SLE) 患者的T细胞中过度表达. UHRF1P通过抑制其母蛋白来驱动自身免疫性炎症.

科学领域:

免疫学免疫学免疫学
遗传学是一个遗传学.
分子生物学分子生物学

背景情况:

炎症T细胞在诸如系统性红斑狼 (SLE) 等自身免疫性疾病中起着关键作用.
识别SLE的新生物标志物和致病机制对于了解疾病进展至关重要.

研究的目的:

使用T细胞转录组学识别SLE的新生物标志物.
阐明SLE期间T细胞中新发现的假基因UHRF1P的致病作用.

主要方法:

使用机器学习分析来自SLE患者队伍的T细胞转录组学数据.
产生T细胞特异的UHRF1P转基因小鼠和MAP4K3淘汰小鼠.
研究涉及UHRF1,UHRF1P和MAP4K3.3的蛋白质相互作用和降解途径.

主要成果:

伪基UHRF1P被确定为SLE的新生物标志物.
UHRF1P蛋白在SLE患者的T细胞中过度表达,并且缺乏其父 UHRF1蛋白的关键域.
在T细胞中UHRF1P的过度表达会通过防止MAP4K3降解来诱导IL-17A的产生和自身免疫性炎症.
在UHRF1P转基因小鼠中,MAP4K3淘汰消除了IL-17A诱导和自身免疫表型.

结论:

UHRF1P是T细胞中的一种致病驱动物,有助于导致SLE等自身免疫性疾病.
UHRF1P通过抑制UHRF1的E3结合酶活性来起作用,从而导致异常的MAP4K3稳定和IL-17A诱导.
准UHRF1P或其下游途径可能为SLE和其他自身免疫疾病提供治疗策略.

关键词:

在MAP4K3/GLK中使用.一个小小的东西.在T细胞,T细胞.在UHRF1中,UHRF1是这就是UHRF1P1P.

更多相关视频

The bm12 Inducible Model of Systemic Lupus Erythematosus SLE in C57BL/6 Mice

The bm12 Inducible Model of Systemic Lupus Erythematosus SLE in C57BL/6 Mice

Published on: November 1, 2015

Native Polyacrylamide Gel Electrophoresis Immunoblot Analysis of Endogenous IRF5 Dimerization

Native Polyacrylamide Gel Electrophoresis Immunoblot Analysis of Endogenous IRF5 Dimerization

Published on: October 6, 2019

相关概念视频

T Cell Types and Functions

T Cell Types and Functions

When T cells with CD4 markers are activated, they give rise to two types of effector cells: helper T cells and regulatory T cells. Meanwhile, T cells with CD8 markers differentiate into effector cytotoxic T cells. The differentiation of CD4 T cells into helper T cell subsets, such as Th1, Th2, and Th17 cells, is dependent on the antigen type, antigen-presenting cell, and regulatory cytokines.
Th1 cells stimulate dendritic cells to express necessary co-stimulatory molecules on their surfaces for...

Regulation of the Unfolded Protein Response

Regulation of the Unfolded Protein Response

Inositol-requiring kinase one or IRE1 is the most conserved eukaryotic unfolded protein response (UPR) receptor. It is a type I transmembrane protein kinase receptor with a distinctive site-specific RNase activity. As the binding mechanics of the misfolded proteins with the N-terminal domain of IRE-1 are unclear, three binding models — direct, indirect, and allosteric -- are proposed for receptor activation. Nevertheless, it is known that once a misfolded protein associates with IRE1, it...

The JAK-STAT Signaling Pathway

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...