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Biomarkers for aging in Caenorhabditis elegans high throughput screening. 高通量筛选草履虫衰老生物标志物。
IF 3.8 3区 生物学 Q2 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2024-06-26 DOI: 10.1042/BST20231303
Victoria R Yarmey, Adriana San-Miguel

Aging is characterized by a functional decline in organism fitness over time due to a complex combination of genetic and environmental factors [ 1-4]. With an increasing elderly population at risk of age-associated diseases, there is a pressing need for research dedicated to promoting health and longevity through anti-aging interventions. The roundworm Caenorhabditis elegans is an established model organism for aging studies due to its short life cycle, ease of culture, and conserved aging pathways. These benefits also make the worm well-suited for high-throughput screening (HTS) methods to study biomarkers of the molecular changes, cellular dysfunction, and physiological decline associated with aging. Within this review, we offer a summary of recent advances in HTS techniques to study biomarkers of aging in C. elegans.

衰老的特点是,由于遗传和环境因素的复杂组合,机体的机能随着时间的推移而下降[ 1-4]。随着面临老年相关疾病风险的老年人口不断增加,迫切需要通过抗衰老干预措施来促进健康和长寿的研究。蛔虫秀丽隐杆线虫(Caenorhabditis elegans)因其生命周期短、易于培养和保守的衰老途径而成为衰老研究的成熟模式生物。这些优点也使该蠕虫非常适合采用高通量筛选(HTS)方法来研究与衰老相关的分子变化、细胞功能障碍和生理衰退的生物标志物。在这篇综述中,我们总结了用于研究优雅虫衰老生物标志物的 HTS 技术的最新进展。
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引用次数: 0
Exploring mechanisms of mupirocin resistance and hyper-resistance. 探索莫匹罗星抗药性和超抗药性的机制。
IF 3.8 3区 生物学 Q2 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2024-06-26 DOI: 10.1042/BST20230581
Igor Zivkovic, Ita Gruic-Sovulj

Mupirocin is a broad-spectrum antibiotic that acts predominantly against Gram-positive bacteria. It is produced by Pseudomonas fluorescens NCIMB 10586 and has been clinically used to treat primary and secondary skin infections and to eradicate nasal colonisation of methicillin-resistant Staphylococcus aureus strains. Mupirocin inhibits protein synthesis by blocking the active site of isoleucyl-tRNA synthetase (IleRS), which prevents the enzyme from binding isoleucine and ATP for Ile-tRNAIle synthesis. Two types of IleRS are found in bacteria - while IleRS1 is susceptible to mupirocin inhibition, IleRS2 provides resistance to cells. These two types belong to distinct evolutionary clades which likely emerged from an early gene duplication in bacteria. Resistance in IleRS2 is based on the loss of interactions that govern mupirocin binding to IleRS1, such as hydrogen bonding to the carboxylate moiety of mupirocin. IleRS2 enzymes with Ki in the millimolar range have recently been discovered. These hyper-resistant IleRS2 variants surprisingly have a non-canonical version of the catalytic motif, which serves as a signature motif of class I aminoacyl-tRNA synthetases to which IleRS belongs. The non-canonical motif, in which the 1st and 3rd positions are swapped, is key for hyper-resistance and can be accommodated without abolishing enzyme activity in IleRS2 but not in IleRS1. Clinical use of mupirocin led to the emergence of resistance in S. aureus. Low-level resistance arises by mutations of the housekeeping IleRS1, while high-level resistance develops by the acquisition of the resistant IleRS2 on a plasmid. There is no evidence that hyper-resistant variants have been found in clinical isolates.

莫匹罗星是一种广谱抗生素,主要针对革兰氏阳性菌。它由荧光假单胞菌 NCIMB 10586 产生,临床上用于治疗原发性和继发性皮肤感染,以及根除耐甲氧西林金黄色葡萄球菌菌株的鼻腔定植。莫匹罗星通过阻断异亮氨酰-tRNA 合成酶(IleRS)的活性位点,阻止该酶结合异亮氨酸和 ATP 进行 Ile-tRNAIle 合成,从而抑制蛋白质合成。细菌中有两种类型的 IleRS:IleRS1 易受莫匹罗星抑制,而 IleRS2 对细胞具有抗性。这两种类型属于不同的进化支系,很可能是细菌中早期基因复制产生的。IleRS2 的抗性是基于失去了莫匹罗星与 IleRS1 结合的相互作用,例如与莫匹罗星羧基的氢键结合。最近发现了 Ki 在毫摩尔范围内的 IleRS2 酶。这些抗性超强的 IleRS2 变体令人惊讶地具有非规范版本的催化基团,该基团是 IleRS 所属的 I 类氨基酰-tRNA 合成酶的标志性基团。非规范基团的第 1 位和第 3 位对调,是产生超抗性的关键所在,IleRS2 可以在不影响酶活性的情况下适应这种非规范基团,而 IleRS1 则不行。莫匹罗星的临床使用导致了金黄色葡萄球菌耐药性的出现。低水平的耐药性是由看家的 IleRS1 基因突变产生的,而高水平的耐药性则是由质粒上的耐药 IleRS2 基因产生的。没有证据表明在临床分离株中发现了超耐药性变种。
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引用次数: 0
Deubiquitinases in muscle physiology and disorders. 肌肉生理学和疾病中的去泛素酶。
IF 3.8 3区 生物学 Q2 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2024-06-26 DOI: 10.1042/BST20230562
Cyriel S Olie, Darragh P O'Brien, Hannah B L Jones, Zhu Liang, Andreas Damianou, Ilknur Sur-Erdem, Adán Pinto-Fernández, Vered Raz, Benedikt M Kessler

In vivo, muscle and neuronal cells are post-mitotic, and their function is predominantly regulated by proteostasis, a multilayer molecular process that maintains a delicate balance of protein homeostasis. The ubiquitin-proteasome system (UPS) is a key regulator of proteostasis. A dysfunctional UPS is a hallmark of muscle ageing and is often impacted in neuromuscular disorders (NMDs). Malfunction of the UPS often results in aberrant protein accumulation which can lead to protein aggregation and/or mis-localization affecting its function. Deubiquitinating enzymes (DUBs) are key players in the UPS, controlling protein turnover and maintaining the free ubiquitin pool. Several mutations in DUB encoding genes are linked to human NMDs, such as ATXN3, OTUD7A, UCHL1 and USP14, whilst other NMDs are associated with dysregulation of DUB expression. USP5, USP9X and USP14 are implicated in synaptic transmission and remodeling at the neuromuscular junction. Mice lacking USP19 show increased maintenance of lean muscle mass. In this review, we highlight the involvement of DUBs in muscle physiology and NMDs, particularly in processes affecting muscle regeneration, degeneration and inflammation following muscle injury. DUBs have recently garnered much respect as promising drug targets, and their roles in muscle maturation, regeneration and degeneration may provide the framework for novel therapeutics to treat muscular disorders including NMDs, sarcopenia and cachexia.

在体内,肌肉和神经细胞处于后有丝分裂期,其功能主要受蛋白稳态调节,这是一个多层次的分子过程,可维持蛋白质稳态的微妙平衡。泛素-蛋白酶体系统(UPS)是蛋白稳态的关键调节器。泛素-蛋白酶体系统功能失调是肌肉老化的标志,神经肌肉疾病(NMDs)也常常受到影响。UPS 功能失常通常会导致蛋白质异常积累,从而导致蛋白质聚集和/或错误定位,影响其功能。去泛素化酶(Dubiquitinating enzymes,DUBs)是 UPS 的关键角色,负责控制蛋白质周转和维持游离泛素池。DUB 编码基因的一些突变与人类 NMDs 有关,如 ATXN3、OTUD7A、UCHL1 和 USP14,而其他 NMDs 则与 DUB 表达失调有关。USP5、USP9X 和 USP14 与神经肌肉接头处的突触传递和重塑有关。缺乏 USP19 的小鼠显示瘦肌肉的维持能力增强。在这篇综述中,我们将重点介绍 DUBs 参与肌肉生理学和 NMD 的情况,尤其是参与影响肌肉再生、变性和肌肉损伤后炎症的过程。最近,DUBs 作为有前景的药物靶点受到了广泛关注,它们在肌肉成熟、再生和变性中的作用可能为治疗 NMDs、肌肉疏松症和恶病质等肌肉疾病的新型疗法提供了框架。
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引用次数: 0
Three-dimensional cardiac models: a pre-clinical testing platform. 三维心脏模型:临床前测试平台。
IF 3.8 3区 生物学 Q2 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2024-06-26 DOI: 10.1042/BST20230444
Eline Groen, Christine L Mummery, Loukia Yiangou, Richard P Davis

Major advancements in human pluripotent stem cell (hPSC) technology over recent years have yielded valuable tools for cardiovascular research. Multi-cell type 3-dimensional (3D) cardiac models in particular, are providing complementary approaches to animal studies that are better representatives than simple 2-dimensional (2D) cultures of differentiated hPSCs. These human 3D cardiac models can be broadly divided into two categories; namely those generated through aggregating pre-differentiated cells and those that form self-organizing structures during their in vitro differentiation from hPSCs. These models can either replicate aspects of cardiac development or enable the examination of interactions among constituent cell types, with some of these models showing increased maturity compared with 2D systems. Both groups have already emerged as physiologically relevant pre-clinical platforms for studying heart disease mechanisms, exhibiting key functional attributes of the human heart. In this review, we describe the different cardiac organoid models derived from hPSCs, their generation methods, applications in cardiovascular disease research and use in drug screening. We also address their current limitations and challenges as pre-clinical testing platforms and propose potential improvements to enhance their efficacy in cardiac drug discovery.

近年来,人类多能干细胞(hPSC)技术的重大进步为心血管研究提供了宝贵的工具。特别是多细胞型三维(3D)心脏模型,为动物研究提供了补充方法,比简单的二维(2D)培养分化 hPSC 更具代表性。这些人类三维心脏模型大致可分为两类,即通过聚集预分化细胞生成的模型和在体外分化 hPSCs 过程中形成自组织结构的模型。这些模型可以复制心脏发育的各个方面,也可以检查组成细胞类型之间的相互作用,其中一些模型与二维系统相比显示出更高的成熟度。这两类模型已成为研究心脏疾病机制的生理学临床前平台,展示了人类心脏的关键功能属性。在这篇综述中,我们将介绍源自 hPSCs 的不同心脏类器官模型、它们的生成方法、在心血管疾病研究中的应用以及在药物筛选中的使用。我们还讨论了它们作为临床前测试平台目前存在的局限性和挑战,并提出了潜在的改进措施,以提高它们在心脏药物发现中的功效。
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引用次数: 0
Dopamine synthesis and transport: current and novel therapeutics for parkinsonisms. 多巴胺的合成和转运:治疗帕金森病的现有疗法和新疗法。
IF 3.8 3区 生物学 Q2 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2024-06-26 DOI: 10.1042/BST20231061
Mary Dayne Sia Tai, Gloria Gamiz-Arco, Aurora Martinez

Parkinsonism is the primary type of movement disorder in adults, encompassing a set of clinical symptoms, including rigidity, tremors, dystonia, bradykinesia, and postural instability. These symptoms are primarily caused by a deficiency in dopamine (DA), an essential neurotransmitter in the brain. Currently, the DA precursor levodopa (synthetic L-DOPA) is the standard medication to treat DA deficiency, but it only addresses symptoms rather than provides a cure. In this review, we provide an overview of disorders associated with DA dysregulation and deficiency, particularly Parkinson's disease and rare inherited disorders leading predominantly to dystonia and/or parkinsonism, even in childhood. Although levodopa is relatively effective for the management of motor dysfunctions, it is less effective for severe forms of parkinsonism and is also associated with side effects and a loss of efficacy over time. We present ongoing efforts to reinforce the effect of levodopa and to develop innovative therapies that target the underlying pathogenic mechanisms affecting DA synthesis and transport, increasing neurotransmission through disease-modifying approaches, such as cell-based therapies, nucleic acid- and protein-based biologics, and small molecules.

帕金森病是成人运动障碍的主要类型,包括一系列临床症状,包括僵直、震颤、肌张力障碍、运动迟缓和姿势不稳。这些症状主要是由于缺乏多巴胺(DA)引起的,多巴胺是大脑中一种重要的神经递质。目前,DA 前体左旋多巴(合成 L-DOPA)是治疗 DA 缺乏症的标准药物,但它只能缓解症状,而不能治愈疾病。在这篇综述中,我们将概述与DA调节失调和缺乏有关的疾病,尤其是帕金森病和罕见的遗传性疾病,这些疾病主要导致肌张力障碍和/或帕金森病,甚至在儿童时期就已出现。虽然左旋多巴对运动功能障碍的治疗相对有效,但对严重帕金森病的治疗效果较差,而且随着时间的推移,还伴有副作用和疗效减退。我们正在努力加强左旋多巴的疗效,并开发针对影响 DA 合成和转运的潜在致病机制的创新疗法,通过基于细胞的疗法、基于核酸和蛋白质的生物制剂以及小分子药物等疾病调节方法增加神经传递。
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引用次数: 0
The high-affinity tryptophan uptake transport system in human cells. 人体细胞中的高亲和性色氨酸吸收转运系统。
IF 3.8 3区 生物学 Q2 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2024-06-26 DOI: 10.1042/BST20230742
Keisuke Wakasugi, Takumi Yokosawa

The L-tryptophan (Trp) transport system is highly selective for Trp with affinity in the nanomolar range. This transport system is augmented in human interferon (IFN)-γ-treated and indoleamine 2,3-dioxygenase 1 (IDO1)-expressing cells. Up-regulated cellular uptake of Trp causes a reduction in extracellular Trp and initiates immune suppression. Recent studies demonstrate that both IDO1 and tryptophanyl-tRNA synthetase (TrpRS), whose expression levels are up-regulated by IFN-γ, play a pivotal role in high-affinity Trp uptake into human cells. Furthermore, overexpression of tryptophan 2,3-dioxygenase (TDO2) elicits a similar effect as IDO1 on TrpRS-mediated high-affinity Trp uptake. In this review, we summarize recent findings regarding this Trp uptake system and put forward a possible molecular mechanism based on Trp deficiency induced by IDO1 or TDO2 and tryptophanyl-AMP production by TrpRS.

L-色氨酸(Trp)转运系统对 Trp 具有高度选择性,亲和力在纳摩尔范围内。在经干扰素(IFN)-γ 处理和表达吲哚胺-2,3-二氧化酶 1(IDO1)的细胞中,这种转运系统会增强。细胞对 Trp 吸收的上调会导致细胞外 Trp 的减少,并引发免疫抑制。最近的研究表明,IDO1 和色氨酸-tRNA 合成酶(TrpRS)的表达水平受 IFN-γ 上调,它们在人类细胞吸收高亲和性 Trp 的过程中起着关键作用。此外,色氨酸 2,3-二氧合酶(TDO2)的过表达对 TrpRS 介导的高亲和性 Trp 摄取也有类似于 IDO1 的作用。在这篇综述中,我们总结了有关这一 Trp 摄取系统的最新发现,并提出了一种可能的分子机制,该机制基于 IDO1 或 TDO2 诱导的 Trp 缺乏以及 TrpRS 产生的色氨酸-AMP。
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引用次数: 0
Lessons from natural molecular glue degraders. 天然分子胶降解剂的启示
IF 3.8 3区 生物学 Q2 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2024-06-26 DOI: 10.1042/BST20230836
Shiyun Cao

Molecular glue (MG) degraders include plant hormones and therapeutic drugs and have become a hot topic in drug discovery. Unlike bivalent proteolysis targeting chimeras (PROTACs), monovalent MGs can trigger the degradation of non-ligandable proteins by enhancing their interaction with E3 ubiquitin ligases. Here, I analyze the characteristics of natural MG degraders, contrast them with synthetic ones, and provide a rationale for optimizing MGs. In natural MG-based degradation systems, a stable complex is only formed when all three partners (MG, E3 ligase, and substrate) are present, while the affinities between any two components are either weak or undetectable. After the substrate is degraded, the MG will dissociate from its receptor (E3 ligase) due to their low micromolar affinity. In contrast, synthetic MGs, such as immunomodulatory drugs (IMiDs) and CR8, are potent inhibitors of their receptors by blocking the CRBN-native substrate interaction or by occupying the active site of CDK12. Inspired by nature, the affinities of IMiDs to CRBN can be reduced to make those compounds degraders without the E3-inhibitory activity, therefore, minimizing the interference with the physiological substrates of CRBN. Similarly, the CR8-CDK interaction can be weakened to uncouple the degrader function from the kinase inhibition. To mimic natural examples and reduce side effects, future development of MG degraders that lack the inhibitory activity should be considered.

分子胶(MG)降解剂包括植物激素和治疗药物,已成为药物发现领域的热门话题。与二价蛋白水解靶向嵌合体(PROTACs)不同,单价MGs可以通过增强非配体蛋白与E3泛素连接酶的相互作用来触发非配体蛋白的降解。在这里,我分析了天然MG降解剂的特点,将它们与合成的MG降解剂进行了对比,并为优化MGs提供了理论依据。在基于天然 MG 的降解系统中,只有当所有三个伙伴(MG、E3 连接酶和底物)都存在时,才能形成稳定的复合物,而任何两个成分之间的亲和力要么很弱,要么无法检测到。底物降解后,由于 MG 与其受体(E3 连接酶)之间的亲和力很低,因此 MG 会与其受体解离。相反,人工合成的 MG,如免疫调节药物(IMiDs)和 CR8,通过阻断 CRBN 与原生底物的相互作用或占据 CDK12 的活性位点,成为其受体的强效抑制剂。受自然界的启发,IMiDs 与 CRBN 的亲和力可以降低,使这些化合物成为没有 E3 抑制活性的降解剂,从而最大限度地减少对 CRBN 生理底物的干扰。同样,也可以削弱 CR8 与 CDK 的相互作用,使降解剂功能与激酶抑制作用脱钩。为了模仿自然实例并减少副作用,未来应考虑开发缺乏抑制活性的 MG 降解剂。
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引用次数: 0
Reprogrammed mitochondria: a central hub of cancer cell metabolism. 重编程线粒体:癌细胞新陈代谢的中心枢纽。
IF 3.8 3区 生物学 Q2 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2024-06-26 DOI: 10.1042/BST20231090
Fabio Ciccarone, Maria Rosa Ciriolo

Mitochondria represent the metabolic hub of normal cells and play this role also in cancer but with different functional purposes. While cells in differentiated tissues have the prerogative of maintaining basal metabolism and support the biosynthesis of specialized products, cancer cells have to rewire the metabolic constraints imposed by the differentiation process. They need to balance the bioenergetic supply with the anabolic requirements that entail the intense proliferation rate, including nucleotide and membrane lipid biosynthesis. For this aim, mitochondrial metabolism is reprogrammed following the activation of specific oncogenic pathways or due to specific mutations of mitochondrial proteins. The main process leading to mitochondrial metabolic rewiring is the alteration of the tricarboxylic acid cycle favoring the appropriate orchestration of anaplerotic and cataplerotic reactions. According to the tumor type or the microenvironmental conditions, mitochondria may decouple glucose catabolism from mitochondrial oxidation in favor of glutaminolysis or disable oxidative phosphorylation for avoiding harmful production of free radicals. These and other metabolic settings can be also determined by the neo-production of oncometabolites that are not specific for the tissue of origin or the accumulation of metabolic intermediates able to boost pro-proliferative metabolism also impacting epigenetic/transcriptional programs. The full characterization of tumor-specific mitochondrial signatures may provide the identification of new biomarkers and therapeutic opportunities based on metabolic approaches.

线粒体是正常细胞的代谢枢纽,在癌症细胞中也发挥着这一作用,但功能目的不同。分化组织中的细胞拥有维持基础代谢和支持特化产品生物合成的特权,而癌细胞则必须重新连接分化过程带来的代谢限制。它们需要平衡生物能供应与高增殖率带来的合成代谢需求,包括核苷酸和膜脂的生物合成。为此,线粒体新陈代谢会在特定致癌途径激活或线粒体蛋白发生特定突变后重新编程。导致线粒体新陈代谢重构的主要过程是三羧酸循环的改变,这种改变有利于适当地协调无氧反应和有氧反应。根据肿瘤类型或微环境条件,线粒体可将葡萄糖分解与线粒体氧化分离,转而进行谷氨酰胺溶解,或使氧化磷酸化失效,以避免产生有害的自由基。这些和其他代谢环境还可由新产生的非原发组织特异性代谢产物或代谢中间产物的积累决定,这些代谢中间产物可促进增殖性代谢,并影响表观遗传/转录程序。对肿瘤特异性线粒体特征的全面描述,可为确定新的生物标记物和基于代谢方法的治疗机会提供依据。
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引用次数: 0
Research progress of ZIC5 for tumor metastasis. ZIC5治疗肿瘤转移的研究进展。
IF 3.8 3区 生物学 Q2 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2024-06-26 DOI: 10.1042/BST20231263
Yiming Zhong, Shangzhi Yang, Xianli Wang, Chuanyu Sun

The zinc finger protein of the cerebellum (ZIC) family comprises five members (ZIC1-5), homologous with the odd-paired (OPA) gene in Drosophila melanogila. These transcription factors contain five Cys2His zinc finger domains, constituting one of the most abundant transcription factor families in human cells. ZIC proteins significantly contribute to transcriptional regulation and chromatin remodeling. As a member of the ZIC family, ZIC5 is essential for animal growth and development. Numerous studies have investigated the connection between ZIC proteins and cancer as well as tumor metastases in recent years. Many studies have found that within tumor tissues, the transcription and translation processes increase the expression of ZIC5 which is linked to tumor aggressiveness. This review aims to provide an objective summary of the impact of ZIC5 on tumor metastasis and consider the potential application of ZIC5 targets in both tumor therapy and the early detection of cancer.

小脑锌指蛋白(ZIC)家族由五个成员(ZIC1-5)组成,与黑腹果蝇的奇数配对(OPA)基因同源。这些转录因子含有五个 Cys2His 锌指结构域,是人类细胞中最丰富的转录因子家族之一。ZIC 蛋白对转录调控和染色质重塑有重要贡献。作为 ZIC 家族的一员,ZIC5 对动物的生长和发育至关重要。近年来,许多研究都在探讨 ZIC 蛋白与癌症以及肿瘤转移之间的联系。许多研究发现,在肿瘤组织中,转录和翻译过程会增加 ZIC5 的表达,而这与肿瘤的侵袭性有关。本综述旨在客观总结 ZIC5 对肿瘤转移的影响,并探讨 ZIC5 靶点在肿瘤治疗和癌症早期检测中的潜在应用。
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引用次数: 0
Proofreading mechanisms of the innate immune receptor RIG-I: distinguishing self and viral RNA. 先天性免疫受体 RIG-I 的校对机制:区分自身和病毒 RNA。
IF 3.8 3区 生物学 Q2 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2024-06-26 DOI: 10.1042/BST20230724
Mihai Solotchi, Smita S Patel

The RIG-I-like receptors (RLRs), comprising retinoic acid-inducible gene I (RIG-I), melanoma differentiation-associated gene 5 (MDA5), and laboratory of genetics and physiology 2 (LGP2), are pattern recognition receptors belonging to the DExD/H-box RNA helicase family of proteins. RLRs detect viral RNAs in the cytoplasm and respond by initiating a robust antiviral response that up-regulates interferon and cytokine production. RIG-I and MDA5 complement each other by recognizing different RNA features, and LGP2 regulates their activation. RIG-I's multilayered RNA recognition and proofreading mechanisms ensure accurate viral RNA detection while averting harmful responses to host RNAs. RIG-I's C-terminal domain targets 5'-triphosphate double-stranded RNA (dsRNA) blunt ends, while an intrinsic gating mechanism prevents the helicase domains from non-specifically engaging with host RNAs. The ATPase and RNA translocation activity of RIG-I adds another layer of selectivity by minimizing the lifetime of RIG-I on non-specific RNAs, preventing off-target activation. The versatility of RIG-I's ATPase function also amplifies downstream signaling by enhancing the signaling domain (CARDs) exposure on 5'-triphosphate dsRNA and promoting oligomerization. In this review, we offer an in-depth understanding of the mechanisms RIG-I uses to facilitate viral RNA sensing and regulate downstream activation of the immune system.

RIG-I 样受体(RLRs)包括视黄酸诱导基因 I(RIG-I)、黑色素瘤分化相关基因 5(MDA5)和遗传与生理学实验室 2(LGP2),是属于 DExD/H-box RNA 螺旋酶家族的模式识别受体。RLRs 可检测到细胞质中的病毒 RNA,并通过启动强有力的抗病毒反应,上调干扰素和细胞因子的产生。RIG-I 和 MDA5 通过识别不同的 RNA 特征来相互补充,而 LGP2 则调节它们的激活。RIG-I 的多层 RNA 识别和校对机制可确保准确检测病毒 RNA,同时避免对宿主 RNA 产生有害反应。RIG-I 的 C 端结构域靶向 5'-triphosphate 双链 RNA (dsRNA) 的钝末端,而内在的门控机制可防止螺旋酶结构域与宿主 RNA 发生非特异性结合。RIG-I 的 ATPase 和 RNA 转位活性可最大限度地减少 RIG-I 在非特异性 RNA 上的停留时间,防止脱靶激活,从而增加了另一层选择性。RIG-I 的 ATPase 功能还能增强信号结构域(CARDs)在 5'-triphosphate dsRNA 上的暴露,促进寡聚化,从而扩大下游信号传导。在这篇综述中,我们将深入了解 RIG-I 用来促进病毒 RNA 感知和调节下游免疫系统激活的机制。
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