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Advances in Muscle Research in Health and Disease. 健康与疾病中的肌肉研究进展》。
IF 5.1 2区 生物学 Q2 CELL BIOLOGY Pub Date : 2024-10-14 DOI: 10.3390/cells13201694
Wan Lee

Muscle tissue plays a vital role in the maintenance of overall health, contributing to essential body functions such as locomotion, respiration, blood circulation, and metabolic regulation [...].

肌肉组织在维持整体健康方面发挥着至关重要的作用,对运动、呼吸、血液循环和新陈代谢调节等身体基本功能做出了贡献[......]。
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引用次数: 0
Generation of a Biotin-Tagged Dual-Display Phage. 生成生物素标记的双显示噬菌体。
IF 5.1 2区 生物学 Q2 CELL BIOLOGY Pub Date : 2024-10-14 DOI: 10.3390/cells13201696
Laura Maria De Plano, Salvatore Oddo, David Bikard, Antonella Caccamo, Sabrina Conoci

Phage display is widely used in biomedical research. One of the great advantages of phage display is the specificity of the connection of a foreign peptide exposed outside the capsid to the intended target. Secondary detection systems, which are often laborious and costly, are required to identify and quantify the peptide/target interaction. In this study, we generated a novel dual-display phage to facilitate the detection and quantification of the peptide/target interaction. First, we generated a biotin-tagged phage by adding a small biotin-accepting peptide (sBT) to gene-3 of the M13K07 helper phage. Subsequently, we enhanced the M13K07 biotin-tagged phage by incorporating a selective peptide on gene-8, which is then exposed to the phage capsid. The exposed peptide acts as a probe to bind to a selective molecular target, whose interaction can be readily visualized thanks to the biotinylated phage. Our versatile dual-display phage exhibits high flexibility; by swapping the displayed peptide/probe, one can change the phage target while retaining the sBT gene in-frame with the pIII. We expect the generated biotin-tagged dual phages to be used as a multifunctional probe to couple with several streptavidin-biotin-based systems.

噬菌体展示被广泛应用于生物医学研究。噬菌体展示的一大优势是将暴露在噬菌体外壳外的外来肽与预定靶标特异性地连接起来。要识别和量化肽/靶相互作用,需要二级检测系统,而二级检测系统通常既费力又昂贵。在本研究中,我们生成了一种新型双显示噬菌体,以促进肽/靶相互作用的检测和量化。首先,我们在 M13K07 辅助噬菌体的基因-3 中添加了一个小的生物素接受肽(sBT),生成了一个生物素标记的噬菌体。随后,我们在基因 8 上加入了选择性多肽,从而增强了 M13K07 生物素标记噬菌体的能力,使其暴露在噬菌体的囊膜上。暴露的多肽可作为探针与选择性分子靶标结合,由于噬菌体上有生物素标记,因此可以很容易地观察到它们之间的相互作用。我们的多功能双显示噬菌体具有很高的灵活性;通过交换显示的肽/探针,可以改变噬菌体的靶标,同时保留与 pIII 同源的 sBT 基因。我们希望生成的生物素标记双噬菌体能用作多功能探针,与多种基于链霉亲和素-生物素的系统结合使用。
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引用次数: 0
Phase Separation Mediated Sub-Nuclear Compartmentalization of Androgen Receptors. 相分离介导的雄激素受体核下区隔化
IF 5.1 2区 生物学 Q2 CELL BIOLOGY Pub Date : 2024-10-13 DOI: 10.3390/cells13201693
Selçuk Yavuz, Tsion E Abraham, Adriaan B Houtsmuller, Martin E van Royen

The androgen receptor (AR), a member of the nuclear steroid hormone receptor family of transcription factors, plays a crucial role not only in the development of the male phenotype but also in the development and growth of prostate cancer. While AR structure and AR interactions with coregulators and chromatin have been studied in detail, improving our understanding of AR function in gene transcription regulation, the spatio-temporal organization and the role of microscopically discernible AR foci in the nucleus are still underexplored. This review delves into the molecular mechanisms underlying AR foci formation, focusing on liquid-liquid phase separation and its role in spatially organizing ARs and their binding partners within the nucleus at transcription sites, as well as the influence of 3D-genome organization on AR-mediated gene transcription.

雄激素受体(AR)是转录因子核类固醇激素受体家族的成员,它不仅在男性表型的形成过程中起着关键作用,而且在前列腺癌的发生和生长过程中也起着关键作用。虽然对 AR 的结构以及 AR 与核心调控因子和染色质的相互作用进行了详细研究,从而提高了我们对 AR 在基因转录调控中的功能的认识,但对细胞核中显微镜下可辨认的 AR 病灶的时空组织和作用的研究仍然不足。这篇综述深入探讨了 AR 病灶形成的分子机制,重点是液-液相分离及其在转录位点的核内空间组织 AR 及其结合伙伴的作用,以及三维基因组组织对 AR 介导的基因转录的影响。
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引用次数: 0
Unveiling a Surgical Revolution: The Use of Conventional Histology versus Ex Vivo Fusion Confocal Microscopy in Breast Cancer Surgery. 揭开外科革命的面纱:传统组织学与体内外融合共聚焦显微镜在乳腺癌手术中的应用。
IF 5.1 2区 生物学 Q2 CELL BIOLOGY Pub Date : 2024-10-12 DOI: 10.3390/cells13201692
Daniel Humaran, Javiera Pérez-Anker, Pedro L Fernández, Lidia Blay, Iciar Pascual, Eva Castellà, Laia Pérez, Susana Puig, Josep Malvehy, Joan F Julián

Ex vivo fusion confocal microscopy (EVFCM) enables the rapid examination of breast tissue and has the potential to reduce the surgical margins and the necessity for further surgeries. Traditional methods, such as frozen section analysis, are limited by the distortion of tissue and artefacts, leading to false negatives and the need for additional surgeries. This study on observational diagnostic accuracy evaluated the ability of EVFCM to detect breast cancer. A total of 36 breast tissue samples, comprising 20 non-neoplastic and 16 neoplastic cases, were analysed using EVFCM and compared to the results obtained from routine histopathology. A Mohs surgeon experienced in EVFCM (evaluator A) and two breast pathologists unfamiliar with EVFCM (evaluators B and C) performed blinded analyses. EVFCM showed high concordance with the histopathology and the detection of neoplasia, with significant kappa values (p < 0.001). Evaluator A achieved 100% sensitivity and specificity. Evaluators B and C achieved a sensitivity of >87%, a specificity of >94%, positive predictive values of >95%, and negative predictive values of 81% and 94%, respectively. EVFCM therefore offers a promising technique for the assessment of margins in breast-conserving surgery. Its widespread adoption could significantly reduce re-excisions, lower healthcare costs, and improve cosmetic and oncological outcomes.

体外融合共聚焦显微镜(EVFCM)可对乳腺组织进行快速检查,并有可能减少手术切缘和进一步手术的必要性。传统方法(如冷冻切片分析)受到组织变形和伪影的限制,导致假阴性和需要进行额外手术。这项关于观察诊断准确性的研究评估了 EVFCM 检测乳腺癌的能力。共有 36 份乳腺组织样本(包括 20 个非肿瘤性病例和 16 个肿瘤性病例)使用 EVFCM 进行了分析,并与常规组织病理学的结果进行了比较。一名在 EVFCM 方面经验丰富的莫氏外科医生(评估员 A)和两名不熟悉 EVFCM 的乳腺病理学家(评估员 B 和 C)进行了盲法分析。EVFCM 与组织病理学和肿瘤的检测结果高度一致,卡帕值显著(p < 0.001)。评估员 A 的灵敏度和特异性均达到 100%。评估者 B 和 C 的灵敏度>87%,特异性>94%,阳性预测值>95%,阴性预测值分别为 81% 和 94%。因此,EVFCM 为保乳手术的边缘评估提供了一种前景广阔的技术。它的广泛应用可大大减少再次切除,降低医疗成本,改善美容和肿瘤效果。
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引用次数: 0
Long-Term Human Immune Reconstitution, T-Cell Development, and Immune Reactivity in Mice Lacking the Murine Major Histocompatibility Complex: Validation with Cellular and Gene Expression Profiles. 缺乏小鼠主要组织相容性复合体的小鼠的长期人类免疫重建、T 细胞发育和免疫反应性:细胞和基因表达谱的验证。
IF 5.1 2区 生物学 Q2 CELL BIOLOGY Pub Date : 2024-10-12 DOI: 10.3390/cells13201686
Milita Darguzyte, Philipp Antczak, Daniel Bachurski, Patrick Hoelker, Nima Abedpour, Rahil Gholamipoorfard, Hans A Schlößer, Kerstin Wennhold, Martin Thelen, Maria A Garcia-Marquez, Johannes Koenig, Andreas Schneider, Tobias Braun, Frank Klawonn, Michael Damrat, Masudur Rahman, Jan-Malte Kleid, Sebastian J Theobald, Eugen Bauer, Constantin von Kaisenberg, Steven R Talbot, Leonard D Shultz, Brian Soper, Renata Stripecke

Background: Humanized mice transplanted with CD34+ hematopoietic cells (HPCs) are broadly used to study human immune responses and infections in vivo and for testing therapies pre-clinically. However, until now, it was not clear whether interactions between the mouse major histocompatibility complexes (MHCs) and/or the human leukocyte antigens (HLAs) were necessary for human T-cell development and immune reactivity.

Methods: We evaluated the long-term (20-week) human hematopoiesis and human T-cell development in NOD Scid Gamma (NSG) mice lacking the expression of MHC class I and II (NSG-DKO). Triplicate experiments were performed with HPCs obtained from three donors, and humanization was confirmed in the reference strain NOD Rag Gamma (NRG). Further, we tested whether humanized NSG-DKO mice would respond to a lentiviral vector (LV) systemic delivery of HLA-A*02:01, HLA-DRB1*04:01, human GM-CSF/IFN-α, and the human cytomegalovirus gB antigen.

Results: Human immune reconstitution was detectable in peripheral blood from 8 to 20 weeks after the transplantation of NSG-DKO. Human single positive CD4+ and CD8+ T-cells were detectable in lymphatic tissues (thymus, bone marrow, and spleen). LV delivery harnessed the detection of lymphocyte subsets in bone marrow (αβ and γδ T-cells and NK cells) and the expression of HLA-DR. Furthermore, RNA sequencing showed that LV delivery increased the expression of different human reactome pathways, such as defense responses to other organisms and viruses.

Conclusions: Human T-cell development and reactivity are independent of the expression of murine MHCs in humanized mice. Therefore, humanized NSG-DKO is a promising new model for studying human immune responses, as it abrogates the xenograft mouse MHC interference.

背景:移植了 CD34+ 造血细胞(HPCs)的人源化小鼠被广泛用于研究人体免疫反应和体内感染,以及临床前的疗法测试。然而,到目前为止,小鼠主要组织相容性复合物(MHC)和/或人类白细胞抗原(HLA)之间的相互作用是否是人类T细胞发育和免疫反应所必需的还不清楚:我们评估了缺乏 MHC I 类和 II 类表达的 NOD Scid Gamma(NSG)小鼠(NSG-DKO)的长期(20 周)人类造血和人类 T 细胞发育情况。我们使用从三位供体获得的 HPCs 进行了一式三份的实验,并在参考品系 NOD Rag Gamma (NRG) 中确认了人源化。此外,我们还测试了人源化 NSG-DKO 小鼠是否会对 HLA-A*02:01、HLA-DRB1*04:01、人 GM-CSF/IFN-α、人巨细胞病毒 gB 抗原的慢病毒载体(LV)系统递送产生反应:结果:NSG-DKO移植后8至20周,外周血中可检测到人类免疫重建。淋巴组织(胸腺、骨髓和脾脏)中可检测到人类单个阳性 CD4+ 和 CD8+ T 细胞。LV 递送利用了骨髓中淋巴细胞亚群(αβ 和 γδ T 细胞和 NK 细胞)的检测和 HLA-DR 的表达。此外,RNA测序显示,LV递送增加了不同人类反应组通路的表达,如对其他生物和病毒的防御反应:结论:人T细胞的发育和反应性与人源化小鼠中鼠MHC的表达无关。因此,人源化 NSG-DKO 是研究人类免疫反应的一种很有前途的新模型,因为它能消除异种移植小鼠 MHC 的干扰。
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引用次数: 0
The Extracellular Matrix and Cardiac Pressure Overload: Focus on Novel Treatment Targets. 细胞外基质与心脏压力超负荷:关注新的治疗目标。
IF 5.1 2区 生物学 Q2 CELL BIOLOGY Pub Date : 2024-10-12 DOI: 10.3390/cells13201685
Matthijs Snelders, Meltem Yildirim, A H Jan Danser, Ingrid van der Pluijm, Jeroen Essers

Heart failure is a significant health issue in developed countries, often stemming from conditions like hypertension, which imposes a pressure overload on the heart. Despite various treatment strategies for heart failure, many lack long-term effectiveness. A critical aspect of cardiac disease is the remodeling of the heart, where compensatory changes in the extracellular matrix exacerbate disease progression. This review explores the processes and changes occurring in the pressure-overloaded heart with respect to the extracellular matrix. It further summarizes current treatment strategies, and then focuses on novel treatment targets for maladaptive cardiac remodeling, derived from transverse aortic constriction-induced pressure overload animal models.

在发达国家,心力衰竭是一个重要的健康问题,通常源于高血压等疾病,因为高血压会导致心脏压力超负荷。尽管针对心力衰竭有多种治疗策略,但许多策略都缺乏长期疗效。心脏疾病的一个重要方面是心脏的重塑,细胞外基质的代偿性变化会加剧疾病的进展。本综述探讨了压力过大的心脏在细胞外基质方面发生的过程和变化。它进一步总结了当前的治疗策略,然后重点介绍了适应性心脏重塑的新型治疗靶点,这些靶点来自横向主动脉收缩诱导的压力超负荷动物模型。
{"title":"The Extracellular Matrix and Cardiac Pressure Overload: Focus on Novel Treatment Targets.","authors":"Matthijs Snelders, Meltem Yildirim, A H Jan Danser, Ingrid van der Pluijm, Jeroen Essers","doi":"10.3390/cells13201685","DOIUrl":"https://doi.org/10.3390/cells13201685","url":null,"abstract":"<p><p>Heart failure is a significant health issue in developed countries, often stemming from conditions like hypertension, which imposes a pressure overload on the heart. Despite various treatment strategies for heart failure, many lack long-term effectiveness. A critical aspect of cardiac disease is the remodeling of the heart, where compensatory changes in the extracellular matrix exacerbate disease progression. This review explores the processes and changes occurring in the pressure-overloaded heart with respect to the extracellular matrix. It further summarizes current treatment strategies, and then focuses on novel treatment targets for maladaptive cardiac remodeling, derived from transverse aortic constriction-induced pressure overload animal models.</p>","PeriodicalId":9743,"journal":{"name":"Cells","volume":null,"pages":null},"PeriodicalIF":5.1,"publicationDate":"2024-10-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11505996/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142495950","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Role of ACSBG1 in Brain Lipid Metabolism and X-Linked Adrenoleukodystrophy Pathogenesis: Insights from a Knockout Mouse Model. ACSBG1 在脑脂质代谢和 X-连锁肾上腺白质营养不良症发病机制中的作用:基因敲除小鼠模型的启示。
IF 5.1 2区 生物学 Q2 CELL BIOLOGY Pub Date : 2024-10-12 DOI: 10.3390/cells13201687
Xiaoli Ye, Yuanyuan Li, Domingo González-Lamuño, Zhengtong Pei, Ann B Moser, Kirby D Smith, Paul A Watkins

"Bubblegum" acyl-CoA synthetase (ACSBG1) is a pivotal player in lipid metabolism during mouse brain development, facilitating the activation of long-chain fatty acids (LCFA) and their incorporation into lipid species that are crucial for brain function. ACSBG1 converts LCFA into acyl-CoA derivatives, supporting vital metabolic processes. Fruit fly mutants lacking ACSBG1 exhibited neurodegeneration and had elevated levels of very long-chain fatty acids (VLCFA), characteristics of human X-linked adrenoleukodystrophy (XALD). To explore ACSBG1's function and potential as a therapeutic target in XALD, we created an ACSBG1 knockout (Acsbg1-/-) mouse and examined the effects on brain FA metabolism during development. Phenotypically, Acsbg1-/- mice resembled wild type (w.t.) mice. ACSBG1 expression was found mainly in tissue affected pathologically in XALD, namely the brain, adrenal gland and testis. ACSBG1 depletion did not significantly reduce the total ACS enzyme activity in these tissue types. In adult mouse brain, ACSBG1 expression was highest in the cerebellum; the low levels detected during the first week of life dramatically increased thereafter. Unexpectedly, lower, rather than higher, saturated VLCFA levels were found in cerebella from Acsbg1-/- vs. w.t. mice, especially after one week of age. Developmental changes in monounsaturated ω9 FA and polyunsaturated ω3 FA levels also differed between w.t. and Acsbg1-/- mice. ACSBG1 deficiency impacted the developmental expression of several cerebellar FA metabolism enzymes, including those required for the synthesis of ω3 polyunsaturated FA, precursors of bioactive signaling molecules like eicosanoids and docosanoids. These changes in membrane lipid FA composition likely affect membrane fluidity and may thus influence the body's response to inflammation. We conclude that, despite compelling circumstantial evidence, it is unlikely that ACSBG1 directly contributes to the pathology of XALD, decreasing its potential as a therapeutic target. Instead, the effects of ACSBG1 knockout on processes regulated by eicosanoids and/or docosanoids should be further investigated.

"泡泡糖 "酰基-CoA 合成酶(ACSBG1)在小鼠大脑发育过程中的脂质代谢中起着关键作用,可促进长链脂肪酸(LCFA)的活化并将其转化为对大脑功能至关重要的脂质物种。ACSBG1 将 LCFA 转化为酰基-CoA 衍生物,支持重要的代谢过程。缺乏 ACSBG1 的果蝇突变体表现出神经变性和超长链脂肪酸(VLCFA)水平升高,这是人类 X 连锁肾上腺白质营养不良症(XALD)的特征。为了探索 ACSBG1 的功能和作为 XALD 治疗靶点的潜力,我们创建了一只 ACSBG1 基因敲除(Acsbg1-/-)小鼠,并研究了其在发育过程中对大脑脂肪酸代谢的影响。从表型上看,Acsbg1-/-小鼠与野生型(w.t. )小鼠相似。ACSBG1主要在XALD中受病理影响的组织中表达,即大脑、肾上腺和睾丸。删除 ACSBG1 并不会显著降低这些组织类型中 ACS 酶的总活性。在成年小鼠的大脑中,小脑中的 ACSBG1 表达量最高;出生后第一周检测到的低表达量随后急剧增加。出乎意料的是,在 Acsbg1-/- 与 w.t. 小鼠的小脑中,饱和的 VLCFA 含量更低而不是更高,尤其是在一周龄之后。单不饱和ω9脂肪酸和多不饱和ω3脂肪酸水平的发育变化在w.t.小鼠和Acsbg1-/-小鼠之间也存在差异。ACSBG1缺乏影响了几种小脑FA代谢酶的发育表达,包括合成ω3多不饱和FA所需的酶,而ω3多不饱和FA是二十酸类和二十二酸类等生物活性信号分子的前体。膜脂质不饱和脂肪酸组成的这些变化可能会影响膜的流动性,从而影响机体对炎症的反应。我们的结论是,尽管有令人信服的间接证据,但 ACSBG1 不太可能直接导致 XALD 的病理变化,从而降低其作为治疗靶点的潜力。相反,应进一步研究 ACSBG1 基因敲除对二十酸类和/或二十二酸类调控过程的影响。
{"title":"Role of ACSBG1 in Brain Lipid Metabolism and X-Linked Adrenoleukodystrophy Pathogenesis: Insights from a Knockout Mouse Model.","authors":"Xiaoli Ye, Yuanyuan Li, Domingo González-Lamuño, Zhengtong Pei, Ann B Moser, Kirby D Smith, Paul A Watkins","doi":"10.3390/cells13201687","DOIUrl":"10.3390/cells13201687","url":null,"abstract":"<p><p>\"Bubblegum\" acyl-CoA synthetase (ACSBG1) is a pivotal player in lipid metabolism during mouse brain development, facilitating the activation of long-chain fatty acids (LCFA) and their incorporation into lipid species that are crucial for brain function. ACSBG1 converts LCFA into acyl-CoA derivatives, supporting vital metabolic processes. Fruit fly mutants lacking ACSBG1 exhibited neurodegeneration and had elevated levels of very long-chain fatty acids (VLCFA), characteristics of human X-linked adrenoleukodystrophy (XALD). To explore ACSBG1's function and potential as a therapeutic target in XALD, we created an ACSBG1 knockout (Acsbg1<sup>-/-</sup>) mouse and examined the effects on brain FA metabolism during development. Phenotypically, Acsbg1<sup>-/-</sup> mice resembled wild type (w.t.) mice. ACSBG1 expression was found mainly in tissue affected pathologically in XALD, namely the brain, adrenal gland and testis. ACSBG1 depletion did not significantly reduce the total ACS enzyme activity in these tissue types. In adult mouse brain, ACSBG1 expression was highest in the cerebellum; the low levels detected during the first week of life dramatically increased thereafter. Unexpectedly, lower, rather than higher, saturated VLCFA levels were found in cerebella from Acsbg1<sup>-/-</sup> vs. w.t. mice, especially after one week of age. Developmental changes in monounsaturated ω9 FA and polyunsaturated ω3 FA levels also differed between w.t. and Acsbg1<sup>-/-</sup> mice. ACSBG1 deficiency impacted the developmental expression of several cerebellar FA metabolism enzymes, including those required for the synthesis of ω3 polyunsaturated FA, precursors of bioactive signaling molecules like eicosanoids and docosanoids. These changes in membrane lipid FA composition likely affect membrane fluidity and may thus influence the body's response to inflammation. We conclude that, despite compelling circumstantial evidence, it is unlikely that ACSBG1 directly contributes to the pathology of XALD, decreasing its potential as a therapeutic target. Instead, the effects of ACSBG1 knockout on processes regulated by eicosanoids and/or docosanoids should be further investigated.</p>","PeriodicalId":9743,"journal":{"name":"Cells","volume":null,"pages":null},"PeriodicalIF":5.1,"publicationDate":"2024-10-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11506745/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142495946","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
The Versatile Role of Peroxisome Proliferator-Activated Receptors in Immune-Mediated Intestinal Diseases. 过氧化物酶体增殖物激活受体在免疫介导的肠道疾病中的多种作用。
IF 5.1 2区 生物学 Q2 CELL BIOLOGY Pub Date : 2024-10-12 DOI: 10.3390/cells13201688
Edit Posta, Istvan Fekete, Istvan Varkonyi, Eva Zold, Zsolt Barta

Peroxisome proliferator-activated receptors (PPARs) are nuclear receptors that sense lipophilic molecules and act as transcription factors to regulate target genes. PPARs have been implicated in the regulation of innate immunity, glucose and lipid metabolism, cell proliferation, wound healing, and fibrotic processes. Some synthetic PPAR ligands are promising molecules for the treatment of inflammatory and fibrotic processes in immune-mediated intestinal diseases. Some of these are currently undergoing or have previously undergone clinical trials. Dietary PPAR ligands and changes in microbiota composition could modulate PPARs' activation to reduce inflammatory responses in these immune-mediated diseases, based on animal models and clinical trials. This narrative review aims to summarize the role of PPARs in immune-mediated bowel diseases and their potential therapeutic use.

过氧化物酶体增殖激活受体(PPARs)是一种核受体,能感知亲脂分子,并作为转录因子调节靶基因。PPAR 与先天性免疫、葡萄糖和脂质代谢、细胞增殖、伤口愈合和纤维化过程的调节有关。一些合成的 PPAR 配体是治疗免疫介导的肠道疾病中炎症和纤维化过程的有前途的分子。其中一些正在进行或已经进行过临床试验。根据动物模型和临床试验,膳食 PPAR 配体和微生物群组成的变化可调节 PPAR 的活化,从而减轻这些免疫介导疾病的炎症反应。本综述旨在总结 PPARs 在免疫介导的肠道疾病中的作用及其潜在的治疗用途。
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引用次数: 0
Atypical Exon 2/3 Mutants G48C, Q43K, and E37K Present Oncogenic Phenotypes Distinct from Characterized NRAS Variants. 非典型 2/3 外显子突变体 G48C、Q43K 和 E37K 的致癌表型与特征 NRAS 变体不同。
IF 5.1 2区 生物学 Q2 CELL BIOLOGY Pub Date : 2024-10-12 DOI: 10.3390/cells13201691
Mark Anthony G Fran, Dominique Mickai G Leaño, James Allen D de Borja, Charles John T Uy, Aleq Adrianne R Andresan, Dennis L Sacdalan, Reynaldo L Garcia

NRAS belongs to the RAS family of GTPases. In colorectal cancer (CRC), NRAS mutations are rare compared to KRAS, but may lead to worse outcomes. We report the functional characterization of the novel NRAS mutants-G48C, Q43K, and E37K-identified in Filipino young-onset CRC patients. Unlike previously characterized NRAS mutants with no apparent effects on cell proliferation, these mutants enhanced proliferation of both HCT116 and NIH3T3 cells. This was confirmed in 3D spheroid assays to mimic the spatial organization of cells. G48C and E37K showed apoptosis resistance in both cell lines, and Q43K showed resistance in HCT116 cells. All three showed no effect on cellular migration in NIH3T3, but G48C enhanced the migration rate of HCT116 cells. Actin staining of NIH3T3 cells expressing the mutants showed a shrunken cytoplasm and transient structures associated with motility and invasiveness. Docking simulations show that GDP is only able to bind fully within the binding pocket of wild-type NRAS, but not in the mutants. Further, G48C, Q43K, and E37K all have less negative ΔG values, indicating a weaker GDP-binding affinity compared to wild-type NRAS. Taken together, the results suggest that oncogenic readouts of NRAS mutants are codon- and mutation-specific, with potential repercussions on the aggressiveness, resistance, and therapeutic response.

NRAS 属于 RAS GTPase 家族。在结直肠癌(CRC)中,NRAS突变比KRAS罕见,但可能会导致更坏的结果。我们报告了在菲律宾年轻发病的 CRC 患者中发现的新型 NRAS 突变体--G48C、Q43K 和 E37K 的功能特征。与之前对细胞增殖无明显影响的 NRAS 突变体不同,这些突变体增强了 HCT116 和 NIH3T3 细胞的增殖。这一点在模拟细胞空间组织的三维球状实验中得到了证实。G48C 和 E37K 在两种细胞系中都表现出抗凋亡性,Q43K 在 HCT116 细胞中表现出抗凋亡性。三者对 NIH3T3 细胞的迁移都没有影响,但 G48C 提高了 HCT116 细胞的迁移率。表达突变体的 NIH3T3 细胞的肌动蛋白染色显示细胞质缩小,并出现与运动性和侵袭性相关的瞬时结构。对接模拟显示,GDP 只能完全与野生型 NRAS 的结合袋结合,而不能与突变体结合。此外,G48C、Q43K 和 E37K 的 ΔG 值均为负值,表明与野生型 NRAS 相比,它们的 GDP 结合亲和力较弱。综上所述,研究结果表明,NRAS突变体的致癌基因读数具有密码子和突变的特异性,对侵袭性、耐药性和治疗反应具有潜在的影响。
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引用次数: 0
Interleukin-1 Receptor-Associated Kinase 1 in Cancer Metastasis and Therapeutic Resistance: Mechanistic Insights and Translational Advances. 白细胞介素-1 受体相关激酶 1 在癌症转移和治疗抗药性中的作用:机理洞察与转化进展》(Mechanistic Insights and Translational Advances)。
IF 5.1 2区 生物学 Q2 CELL BIOLOGY Pub Date : 2024-10-12 DOI: 10.3390/cells13201690
Mariana K Najjar, Munazza S Khan, Chuling Zhuang, Ankush Chandra, Hui-Wen Lo

Interleukin-1 Receptor Associated Kinase 1 (IRAK1) is a serine/threonine kinase that plays a critical role as a signaling transducer of the activated Toll-like receptor (TLR)/Interleukin-1 receptor (IL-1R) signaling pathway in both immune cells and cancer cells. Upon hyperphosphorylation by IRAK4, IRAK1 forms a complex with TRAF6, which results in the eventual activation of the NF-κB and MAPK pathways. IRAK1 can translocate to the nucleus where it phosphorylates STAT3 transcription factor, leading to enhanced IL-10 gene expression. In immune cells, activated IRAK1 coordinates innate immunity against pathogens and mediates inflammatory responses. In cancer cells, IRAK1 is frequently activated, and the activation is linked to the progression and therapeutic resistance of various types of cancers. Consequently, IRAK1 is considered a promising cancer drug target and IRAK1 inhibitors have been developed and evaluated preclinically and clinically. This is a comprehensive review that summarizes the roles of IRAK1 in regulating metastasis-related signaling pathways of importance to cancer cell proliferation, cancer stem cells, and dissemination. This review also covers the significance of IRAK1 in mediating cancer resistance to therapy and the underlying molecular mechanisms, including the evasion of apoptosis and maintenance of an inflammatory tumor microenvironment. Finally, we provide timely updates on the development of IRAK1-targeted therapy for human cancers.

白细胞介素-1受体相关激酶1(IRAK1)是一种丝氨酸/苏氨酸激酶,在免疫细胞和癌细胞中作为激活的Toll样受体(TLR)/白细胞介素-1受体(IL-1R)信号通路的信号转导物发挥着关键作用。IRAK4过度磷酸化后,IRAK1与TRAF6形成复合物,最终激活NF-κB和MAPK通路。IRAK1 可转位到细胞核,在那里磷酸化 STAT3 转录因子,导致 IL-10 基因表达增强。在免疫细胞中,活化的 IRAK1 可协调先天性免疫,抵御病原体,并介导炎症反应。在癌细胞中,IRAK1 经常被激活,这种激活与各种癌症的进展和抗药性有关。因此,IRAK1 被认为是一个很有前景的癌症药物靶点,IRAK1 抑制剂已被开发出来并进行了临床前和临床评估。本文是一篇综合性综述,总结了IRAK1在调节转移相关信号通路中的作用,这些信号通路对癌细胞增殖、癌症干细胞和扩散具有重要意义。本综述还涵盖了 IRAK1 在介导癌症抗药性方面的重要作用以及其潜在的分子机制,包括逃避凋亡和维持炎症性肿瘤微环境。最后,我们将及时提供有关开发针对人类癌症的 IRAK1 靶向疗法的最新进展。
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