关键词: IFN-induced genes IFP35 bZIP leucine-zipper proteins multiple sclerosis zinc-finger proteins

来  源:   DOI:10.3390/biology10121325

Abstract:
Discovered in 1993 by Bange et al., the 35-kDa interferon-induced protein (IFP35) is a highly conserved cytosolic interferon-induced leucine zipper protein with a 17q12-21 coding gene and unknown function. Belonging to interferon stimulated genes (ISG), the IFP35 reflects the type I interferon (IFN) activity induced through the JAK-STAT phosphorylation, and it can homodimerize with N-myc-interactor (NMI) and basic leucine zipper transcription factor (BATF), resulting in nuclear translocation and a functional expression. Casein kinase 2-interacting protein-1 (CKIP-1), retinoic acid-inducible gene I (RIG-I), and laboratory of genetics and physiology 2 Epinephelus coioides (EcLGP2) are thought to regulate IFP35, via the innate immunity pathway. Several in vitro and in vivo studies on fish and mammals have confirmed the IFP35 as an ISG factor with antiviral and antiproliferative functions. However, in a mice model of sepsis, IFP35 was found working as a damage associated molecular pattern (DAMP) molecule, which enhances inflammation by acting in the innate immune-mediated way. In human pathology, the IFP35 expression level predicts disease outcome and response to therapy in Multiple Sclerosis (MS), reflecting IFN activity. Specifically, IFP35 was upregulated in Lupus Nephritis (LN), Rheumatoid Arthritis (RA), and untreated MS. However, it normalized in the MS patients undergoing therapy. The considered data indicate IFP35 as a pleiotropic factor, suggesting it as biologically relevant in the innate immunity, general pathology, and human demyelinating diseases of the central nervous system.
摘要:
1993年由Bange等人发现。,35-kDa干扰素诱导蛋白(IFP35)是一种高度保守的胞浆干扰素诱导亮氨酸拉链蛋白,具有17q12-21编码基因,功能未知.属于干扰素刺激基因(ISG),IFP35反映了通过JAK-STAT磷酸化诱导的I型干扰素(IFN)活性,它可以与N-myc相互作用子(NMI)和碱性亮氨酸拉链转录因子(BATF)同源二聚化,导致核易位和功能性表达。酪蛋白激酶2相互作用蛋白-1(CKIP-1),视黄酸诱导基因I(RIG-I),和遗传学和生理学实验室2石斑鱼(EcLGP2)被认为通过先天免疫途径调节IFP35。对鱼类和哺乳动物的一些体外和体内研究已经证实IFP35是具有抗病毒和抗增殖功能的ISG因子。然而,在脓毒症小鼠模型中,IFP35被发现是一种损伤相关分子模式(DAMP)分子,通过先天免疫介导的方式增强炎症。在人类病理学中,IFP35表达水平预测多发性硬化(MS)的疾病结果和对治疗的反应,反映IFN活性。具体来说,狼疮性肾炎(LN)IFP35上调,类风湿性关节炎(RA),和未经处理的女士然而,在接受治疗的MS患者中恢复正常。所考虑的数据表明IFP35是一种多效性因子,表明它在先天免疫中具有生物学相关性,一般病理学,和人类中枢神经系统的脱髓鞘疾病。
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