三方基序蛋白(TRIM)在调节免疫系统反应中的作用:关注自身免疫性疾病。

IF 3.3 3区 生物学 Q3 CELL BIOLOGY
Subasini Uthirapathy, Abdulrahman T Ahmed, Mahmood Jawad, Vicky Jain, Suhas Ballal, Hussein Riyadh Abdul Kareem Al-Hetty, Gaurav Khandelwal, Renu Arya, Muthena Kariem, Yasser Fakri Mustafa
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引用次数: 0

摘要

三方基序(TRIM)蛋白是许多过程的重要调节因子,包括对与免疫反应相关的几种途径的调节。大多数 TRIM 家族成员都能通过作为 E3 泛素连接酶对目标蛋白质进行多泛素化。根据目前的研究,TRIMs 通过修饰转录因子、模式识别受体(PRR)和先天性免疫中的关键适配蛋白,在先天性免疫反应中发挥着关键作用。越来越清楚的是,TRIMs 在适应性免疫反应中发挥着重要作用,尤其是在刺激和促进 T 细胞方面。我们强调了 TRIMs 在与自身免疫疾病相关的 PRRs 轴中的 E3 泛素连接酶功能。通过聚焦 TRIM 家族成员,我们还阐明了调节免疫反应以缓解自身免疫疾病的新方法。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Tripartite motif (TRIM) proteins roles in the regulation of immune system responses: Focus on autoimmune diseases.

The tripartite motif (TRIM) proteins are well-studied as essential modulators of many processes, including the modulation of several pathways linked to immunological reactions. Most TRIM family members can polyubiquitinate the targeted proteins by acting as E3 ubiquitin ligases. According to current research, TRIMs play a critical role in innate immune response via modifying transcription factors, pattern recognition receptors (PRRs), and key adaptor proteins within innate immunity. It is becoming clearer that TRIMs play important roles in adaptive immune response, especially in the stimulation and promotion of T cells. We highlight the E3 ubiquitin ligase functions of TRIMs in the PRRs axis linked to autoimmune disorders. By focusing on TRIM family members, we also clarify the new approaches to regulating immunological reactions to alleviate autoimmunity.

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来源期刊
Experimental cell research
Experimental cell research 医学-细胞生物学
CiteScore
7.20
自引率
0.00%
发文量
295
审稿时长
30 days
期刊介绍: Our scope includes but is not limited to areas such as: Chromosome biology; Chromatin and epigenetics; DNA repair; Gene regulation; Nuclear import-export; RNA processing; Non-coding RNAs; Organelle biology; The cytoskeleton; Intracellular trafficking; Cell-cell and cell-matrix interactions; Cell motility and migration; Cell proliferation; Cellular differentiation; Signal transduction; Programmed cell death.
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