大肠杆菌鼠李糖调节子

大肠杆菌（Escherichia coil）L-鼠李糖（rha）调节子由三个功能相关的操纵子（operon）组成,位于大肠杆菌染色体基因组中。它编码大肠杆菌吸收和利用L-鼠李糖的蛋白,即一个鼠李糖运输蛋白（RhaT）、三个鼠李糖代谢酶（RhaB、RhaA、RhaD）以及两个调节蛋白（RhaS、RhaR）。三个操纵子均受到L-鼠李糖本身的诱导,同时以调控蛋白RhaS、RhaR和CRP（cAMP受体蛋白）为中介的正调控也参与调节。     

DEAD-box RNA解旋酶家族在天然免疫应答信号通路中的作用

病毒入侵宿主细胞时,宿主细胞启动抑制病毒复制的免疫机制.同样,病毒也会利用多种手段去逃避先天免疫感应机制的监测以及宿主细胞对外来者的降解,同时还会操纵宿主细胞为自身的增殖提供便利.DEAD-box解旋酶家族是一类存在于宿主细胞中的功能蛋白,它们在转录、剪接、mRNA的合成和翻译等多种细胞过程中起着关键作用.该家族成员拥...     

微 RNA 研究进展

近年来,相继发现一些具有调控功能的非编码微RNA,长度约22nt,与基因,细胞周期乃至个体发育过程密切相关,可能对基因功能研究,人类疾病防治及生物进化探索有重要意义。     

环状RNA:潜在的新型miRNA活性调控分子

环状RNA(circular RNA,circRNA)是近年来RNA领域最新的研究热点.它是一类由特殊的选择性剪切产生且在真核细胞中广泛表达的环形内源性RNA分子.研究发现,circRNA富含microRNA(miRNA)结合位点,可以发挥竞争性内源RNA作用,作为miRNA"海绵"来解除对其靶基因的抑制效应.近年来,circRNA作为一种新型调控分子调控miRNA功能的发挥,受到众多研究者的青睐.本文综述circRNA的产生机制,及其调控miRNA的最新研究进展与研究方法等.     

细菌抗氧化系统-oxyR调节子研究进展

细菌抗氧化系统是细菌抵抗呼吸作用及环境因素导致的氧化损伤的一套防卫系统.oxyR调节子是最早发现的具有抗氧化作用的系统之一,由OxyR调节蛋白的编码基因oxyR及其调控的基因和操纵子所构成.oxyR调节子参与了细菌的抗氧化作用、抑制自发突变、致病性、铁代谢及外膜蛋白相变等多种生理代谢作用,这些发现促进了该调节子在细菌耐药性以及致突变物质筛查等方面的研究应用.作者主要从细菌oxyR调节子的结构组成、参与的生理代谢作用、OxyR调控转录的分子机制及影响因素等方面结合最新研究成果展开了介绍,以期对开展细菌抗药性研究及致突变物质的筛查等提供参考.     

细胞外微RNA:一种新型的肺癌分子生物标志物

尽管癌症的早期诊断和治疗在不断发展和进步,但寻找一种敏感、准确和微创的分子生物标志物,用于肿瘤的诊断仍是一项艰巨任务。微RNA(miRNA)是一类长约21～24个核甘酸的内源性非编码小分子RNA。细胞外miRNA作为一种新型的分子生物标志物,在癌症诊断方面具有微创、高灵敏度和高特异性等许多潜在特征。近年来,细胞外miRNA研究成果颇丰。文章就细胞外miRNA的来源、功能、检测以及作为分子标志物在肺癌诊断中的作用和目前存在的一些问题进行了综述。     

微RNA通过调节上皮间质转化影响肿瘤转移

肿瘤细胞向远处转移受多因素调控, 涉及多个基因, 需要经历一系列连续的、可选择的级联事件。上皮间质转化(Epithelial-mesenchymal transition, EMT)是肿瘤细胞转移中的关键步骤, 但肿瘤发生 EMT的机制至今尚不完全明确。微RNA (MicroRNA, miRNA)是一类内源性、非编码小分子RNA, 可在转录后水平负调控EMT相关基因的表达, 在肿瘤转移中发挥重要作用。文章主要就EMT与肿瘤转移的关系、影响EMT的转录因子, 以及miRNA通过靶向EMT相关的转录因子影响肿瘤转移等方面进行了综述。     

长链非编码RNA在肿瘤发生和天然免疫中的功能与调控机制

摘要:长链非编码RNA(Long non-coding RNA,lncRNA)是长度大于200个核苷酸的不具有编码蛋白质能力的RNA分子。长链非编码RNA一度被认为是转录“噪音”。然而,近年来大量的实验证据表明长链非编码RNA通过表观遗传修饰与转录调控、转录后加工、翻译调控等多种机制,在细胞生命活动中发挥重要作用。lncRNA的异常表达和调控往往与肿瘤发生、宿主抗病原微生物感染的天然免疫应答密切相关,本文就这些方面研究进展进行综述。     

铁摄取调节子在细菌铁离子代谢中的调节及其机制

铁离子是大多数细菌生存所必需的营养物质,但是过多的铁离子通过芬顿反应产生的活性氧（reactive oxygen species, ROS）对细菌造成损伤。因此,细菌必须严格控制体内铁离子浓度。铁摄取调节子（ferric uptake regulator,Fur）是细菌铁离子代谢中最重要的调节子。Fur通过抑制或者激活基因的转录,来调节与铁摄取、利用和储存相关的基因,维持胞内铁离子浓度动态平衡。此外,Fur还参与细菌的氧化应激、抗酸能力、毒力和能量代谢等多种生物过程的调节。本文对Fur参与的生物过程及调节机制进行介绍,以期为进一步研究其他细菌Fur的调节机制,以及Fur在细菌应对环境变化中所起作用提供参考。     

Macrophage migration inhibitory factor: a regulator of innate immunity

For more than a quarter of a century, macrophage migration inhibitory factor (MIF) has been a mysterious cytokine. In recent years, MIF has assumed an important role as a pivotal regulator of innate immunity. MIF is an integral component of the host antimicrobial alarm system and stress response that promotes the pro-inflammatory functions of immune cells. A rapidly increasing amount of literature indicates that MIF is implicated in the pathogenesis of sepsis, and inflammatory and autoimmune diseases, suggesting that MIF-directed therapies might offer new treatment opportunities for human diseases in the future.     

MicroRNA in innate immunity and autophagy during mycobacterial infection

The fine‐tuning of innate immune responses is an important aspect of host defenses against mycobacteria. MicroRNAs (miRNAs), small non‐coding RNAs, play essential roles in regulating multiple biological pathways including innate host defenses against various infections. Accumulating evidence shows that many miRNAs regulate the complex interplay between mycobacterial survival strategies and host innate immune pathways. Recent studies have contributed to understanding the role of miRNAs, the levels of which can be modulated by mycobacterial infection, in tuning host autophagy to control bacterial survival and innate effector function. Despite considerable efforts devoted to miRNA profiling over the past decade, further work is needed to improve the selection of appropriate biomarkers for tuberculosis. Understanding the roles and mechanisms of miRNAs in regulating innate immune signaling and autophagy may provide insights into new therapeutic modalities for host‐directed anti‐mycobacterial therapies. Here, we present a comprehensive review of the recent literature regarding miRNA profiling in tuberculosis and the roles of miRNAs in modulating innate immune responses and autophagy defenses against mycobacterial infections.     

GPA-9 is a novel regulator of innate immunity against Escherichia coli foods in adult Caenorhabditis elegans

Innate immune responses to pathogens are governed by the nervous system. Here, we investigated the molecular mechanism underlying innate immunity in Caenorhabditis elegans against Escherichia coli OP50, a standard laboratory C. elegans food. Longevity was compared in worms fed live or UV‐killed OP50 at low or high density food condition (HDF). Expression of the antimicrobial gene lys‐8 was approximately 5‐fold higher in worms fed live OP50, suggesting activation of innate immunity upon recognition of OP50 metabolites. Lifespan was extended and SOD‐3 mRNA levels were increased in gpa‐9‐overexpressing gpa‐9XS worms under HDF in association with robust induction of insulin/IGF‐1 signaling (IIS). Expression of ins‐7 and daf‐28 that control lys‐8 expression was reduced in gpa‐9XS, indicating that GPA‐9‐mediated immunity is due in part to ins‐7 and daf‐28 downregulation. Our results suggest that OP50 metabolites in amphid neurons elicit innate immunity through the IIS pathway, and identify GPA‐9 as a novel regulator of both the immune system and aging in C. elegans.     

Rosiglitazone as a regulator of innate immunity in a cell model of hyperglycemia

Epidemiological studies have shown that severe inflammatory responses occur in patients with hyperglycemia. The molecular nature of these changes is currently under intense investigations. A central role of nuclear receptors PPAR has been shown in the regulation of metabolic changes associated with hyperglycemia, a selective agonist of nuclear receptor PPARγ rosiglitazone is used as a hypoglycemic drug. Rosiglitazone is known to have anti-inflammatory effects, but its properties as an anti-inflammatory drug in hyperglycemic conditions have not been studied. This was an aim of our work. We used a human cell culture model of hyperglycemia: HeLa cells incubated in the conditions of 25 mM glucose for 3 days. Control cells were incubated with 5 mM glucose. The cells were stimulated with lipopolysaccharide (LPS) that is known to trigger innate immune response through activation of Toll-like receptor 4 and influence mRNA expression levels of three of PPAR (α, β/δ, γ) isotypes as well as cyclooxygenase (COX-1 and COX-2). We have shown that under hyperglycemic conditions expression levels of PPARα and PPARβ/δ decreased almost twofold, expression level of COX-2 also decreased, while expression levels of COX-1 and PPARγ remained unchanged compared to those under normal glucose concentration. LPS administration in control cells leads to a 1.5–2.5-fold stimulation of expression of COX-2 and PPAR isotypes. In contrast, under hyperglycemia, LPS exhibited no effect on expression of COX-2 and the PPAR isotypes, which indicates potential mechanisms of hyperglycemia-related alterations in innate immunity. Rosiglitazone, an agonist of PPARγ, decreased expression level of PPARβ/δ and abolished the effect of LPS under hyperglycemia. Rosiglitazone also reduced expression level of COX-1 and COX-2, which indicates on the agonist possible role as an anti-inflammatory agent under high glucose concentrations. These data broaden applicability of rosiglitazone as an anti-inflammatory agent in hyperglycemic conditions.     

NLRP1, a regulator of innate immunity associated with vitiligo

Some familial forms of the dermatological condition vitiligo have recently been linked to polymorphisms in the innate immunity gene, NLRP1. Here, we review what is currently known about the mechanisms that regulate activation of the NLRP1 protein and the downstream effects of NLRP1 on pathways impacting inflammation and apoptosis. How polymorphic variants of the NLRP1 gene contribute to the pathogenesis of vitiligo remains mysterious, requiring further investigation.     

Trypanosome lytic factors: novel mediators of human innate immunity

A novel trypanosome lytic factor (TLF) has been characterized that protects humans from infection by Trypanosoma brucei brucei. The mechanism of trypanolysis is unknown; contrary to one hypothesis, TLF does not kill trypanosomes by generating oxygen radicals. However, these trypanosomes become human-infective when they express a serum-resistance-associated gene.