Biochimica et biophysica acta. General subjects最新文献_第10页

Baicalein benefits amyotrophic lateral sclerosis via reduction of Intraneuronal misfolded protein 黄芩素通过减少神经元内错误折叠蛋白对肌萎缩性侧索硬化症有益

IF 2.8 3区生物学 Q3 BIOCHEMISTRY & MOLECULAR BIOLOGY

Biochimica et biophysica acta. General subjects

Pub Date : 2025-07-01 Epub Date: 2025-06-06 DOI: 10.1016/j.bbagen.2025.130831

Chen-Hung Ting , Shao-Ting Tai , Hsiang-Yu Chang , Po-Ya Huang , Lo-Fan Cheng , Hsing-Jung Lai , Yih-Chih Kuo , Chia-Hsin Kao , I-Fan Wang , Li-Kai Tsai

Amyotrophic lateral sclerosis (ALS) is a rapidly progressive neurodegenerative disease characterized by muscle weakness and atrophy, with limited treatment options. The accumulation of misfolded proteins, such as misfolded superoxide dismutase 1 (mSOD1), contributes significantly to neuronal degeneration in ALS. Therapies targeting misfolded proteins represent a promising strategy. Baicalein, a flavonoid compound with neuroprotective properties, has shown efficacy in clearing misfolded proteins and improving behaviors in rodent models of Alzheimer's and Parkinson's diseases. However, its effects in ALS remain largely unexplored. This study demonstrated that baicalein treatment reduced total and misfolded SOD1 protein levels in both soluble and insoluble fractions of a motor neuron cell line overexpressing mutant SOD1. Baicalein also reduced intracellular SOD1 aggregates in cultured motor neurons transfected with SOD1/G93A, preserving neurite length. In an ALS mouse model expressing the SOD1/G93A transgene, baicalein treatment decreased mSOD1 aggregation, increased spinal motor neuron density, and reduced neuromuscular junction denervation. Furthermore, baicalein partially improved motor behaviors, as assessed by the rotarod test. These findings highlight baicalein's potential as a therapeutic agent for ALS, targeting intraneuronal misfolded proteins to ameliorate pathological changes and preserve motor function.

肌萎缩性侧索硬化症（ALS）是一种以肌肉无力和萎缩为特征的快速进展性神经退行性疾病，治疗选择有限。错误折叠蛋白的积累，如错误折叠的超氧化物歧化酶1 (mSOD1)，对ALS的神经元变性有重要作用。靶向错误折叠蛋白的治疗是一种很有前途的策略。黄芩素是一种具有神经保护作用的类黄酮化合物，在阿尔茨海默病和帕金森病的啮齿动物模型中显示出清除错误折叠蛋白质和改善行为的功效。然而，它对ALS的影响在很大程度上仍未被探索。该研究表明，黄芩素处理降低了过表达SOD1突变体的运动神经元细胞系的可溶性和不溶性部分的总SOD1蛋白和错误折叠的SOD1蛋白水平。黄芩苷还能降低转染SOD1/G93A的运动神经元细胞内SOD1聚集，保持神经突长度。在表达SOD1/G93A转基因的ALS小鼠模型中，黄芩苷处理降低了mSOD1聚集，增加了脊髓运动神经元密度，减少了神经肌肉接点的去神经控制。此外，黄芩素部分改善运动行为，通过旋转测试评估。这些发现突出了黄芩素作为ALS治疗药物的潜力，它可以靶向神经元内错误折叠蛋白来改善病理改变并保持运动功能。

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引用次数: 0

The role of mesenchymal stem cells and their exosomes in radiotherapy: A new opportunity or a potential threat 间充质干细胞及其外泌体在放射治疗中的作用：一个新的机会或潜在的威胁

IF 2.8 3区生物学 Q3 BIOCHEMISTRY & MOLECULAR BIOLOGY

Biochimica et biophysica acta. General subjects

Pub Date : 2025-07-01 Epub Date: 2025-05-26 DOI: 10.1016/j.bbagen.2025.130823

Fatemeh Zeinalzadeh , Seyedeh Nasibeh Mousavikia , Mohammad Taghi Bahreyni Toossi , Hosein Azimian

Cancer remains a major global health problem characterized by complex biological mechanisms and diverse clinical manifestations. Radiotherapy is a key element in cancer treatment. However, radioresistance is a major obstacle to achieving optimal results. This resistance is associated with several factors, including genetic and epigenetic changes in tumor cells that allow cancer cells to survive and proliferate despite radiation exposure. In this context, mesenchymal stem cells (MSCs) play an important role in the tumor microenvironment. Due to their unique properties such as self-renewal, migration to tumors via the bloodstream and involvement in paracrine signaling, they are important for understanding cancer biology and treatment responses. MSCs can release exosomes that can promote intercellular communication and influence tumor response to radiotherapy. However, the role of MSCs in cancer is complex and sometimes contradictory. In some contexts they may exhibit tumor suppressive effects, while in others they promote tumor growth and metastasis. This duality raises important questions about their overall impact on cancer therapy, particularly in relation to radiotherapy. This review will first explore the multifaceted role of MSCs and their exosomes as key mediators of cellular communication within the tumor microenvironment, and then assess the implications of these interactions for radiotherapy, focusing on how MSCs may influence treatment efficacy and the potential to harness their properties to improve therapeutic outcomes.

癌症仍然是一个主要的全球健康问题，其特点是生物学机制复杂，临床表现多样。放射治疗是癌症治疗的一个关键因素。然而，辐射阻力是实现最佳结果的主要障碍。这种抗性与几个因素有关，包括肿瘤细胞的遗传和表观遗传变化，这些变化使癌细胞能够在辐射照射下存活和增殖。在这种情况下，间充质干细胞（MSCs）在肿瘤微环境中发挥着重要作用。由于其独特的特性，如自我更新，通过血液迁移到肿瘤和参与旁分泌信号，它们对了解癌症生物学和治疗反应非常重要。MSCs可以释放外泌体，促进细胞间通讯并影响肿瘤对放疗的反应。然而，间充质干细胞在癌症中的作用是复杂的，有时是矛盾的。在某些情况下，它们可能表现出肿瘤抑制作用，而在其他情况下，它们促进肿瘤生长和转移。这种双重性提出了关于它们对癌症治疗的总体影响的重要问题，特别是与放射治疗有关的问题。本综述将首先探讨间质干细胞及其外泌体作为肿瘤微环境中细胞通讯的关键介质的多方面作用，然后评估这些相互作用对放射治疗的影响，重点关注间质干细胞如何影响治疗效果以及利用其特性改善治疗结果的潜力。

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引用次数: 0

Cyanobacterial KdpD modulates in vivo and in vitro activities of a membrane-anchored histidine kinase 蓝藻KdpD调节膜锚定组氨酸激酶的体内和体外活性。

IF 2.8 3区生物学 Q3 BIOCHEMISTRY & MOLECULAR BIOLOGY

Biochimica et biophysica acta. General subjects

Pub Date : 2025-07-01 Epub Date: 2025-05-11 DOI: 10.1016/j.bbagen.2025.130817

Anand Ballal , Shree Kumar Apte

The prokaryotic KdpATPAse complex, encoded by the kdpABC operon, is an inducible, high-affinity K⁺ transporter. In E. coli, the operon is transcriptionally regulated by a two-component sensor-kinase response-regulator system, constituted by the KdpD and KdpE proteins. In contrast, cyanobacteria exhibit a truncated kdpD gene that encodes a KdpD homolog that is similar to the N-terminal domain (NTD) of E. coli KdpD, but lacks the transmitter, histidine kinase-containing, C-terminal domain (CTD). Here we show that the cyanobacterium Anabaena sp. strain L-31 constitutively transcribes the short kdpD gene, but synthesizes KdpATPase only during potassium starvation. However, unlike E. coli., expression of the kdpD gene remains unaffected by K⁺ limitation in Anabaena. To gain insight into the possible role of Anabaena KdpD, the chimeric Anacoli KdpD protein, wherein the NTD of E. coli KdpD was replaced with Anabaena KdpD, was functionally analyzed. Detailed investigation has revealed that the Anacoli KdpD (a) responds to a much lower threshold of external K⁺ than the E. coli KdpD (b) exhibits much reduced ability to induce kdp in response to ionic osmolytes than E. coli KdpD, and is therefore unable to sustain optimal growth in the presence of these osmolytes and (c) displays higher in vitro phosphatase activity than the wild type E. coli KdpD. Thus, Anabaena KdpD modulates properties of E. coli KdpD-CTD in a manner that is quite distinct from the E. coli KdpD-NTD. Based on these evidences, a model for kdp regulation by the short KdpD is proposed.

由kdpABC操纵子编码的原核生物KdpATPAse复合物是一种可诱导的高亲和力K+转运体。在大肠杆菌中，操纵子受由KdpD和KdpE蛋白组成的双组分传感器-激酶反应调节系统的转录调节。相比之下，蓝藻细菌表现出截断的kdpD基因，该基因编码的kdpD同源物与大肠杆菌kdpD的n端结构域（NTD）相似，但缺乏递质，含组氨酸激酶的c端结构域（CTD）。本研究表明，蓝藻Anabaena菌株L-31可组成性地转录kdpD短基因，但仅在缺钾状态下合成KdpATPase。然而，不像大肠杆菌。， kdpD基因的表达不受K+限制的影响。为了深入了解Anabaena KdpD的可能作用，我们对大肠杆菌KdpD的NTD被Anabaena KdpD取代的嵌合Anacoli KdpD蛋白进行了功能分析。详细的研究表明，Anacoli KdpD (a)对外部K+的反应阈值比大肠杆菌KdpD低得多(b)在离子渗透物诱导KdpD的能力比大肠杆菌KdpD低得多，因此在这些渗透物存在下生长较慢；(c)在体外磷酸酶活性比野生型大肠杆菌KdpD高。因此，Anabaena KdpD以一种与大肠杆菌KdpD- ntd截然不同的方式调节大肠杆菌KdpD- ctd的特性。在此基础上，本文提出了一个由短KdpD调控的kdp模型。

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引用次数: 0

Plasma-activated medium disrupts intercellular barrier function in HaCaT cells by suppressing claudin-1 expression via clathrin-dependent endocytosis 血浆活化培养基通过网格蛋白依赖内吞作用抑制claudin-1的表达，破坏HaCaT细胞间屏障功能

IF 2.8 3区生物学 Q3 BIOCHEMISTRY & MOLECULAR BIOLOGY

Biochimica et biophysica acta. General subjects

Pub Date : 2025-07-01 Epub Date: 2025-05-27 DOI: 10.1016/j.bbagen.2025.130826

Chika Miyamoto , Yuta Yoshino , Hiromasa Tanaka , Hirokazu Hara , Satoshi Endo , Akira Ikari

The skin plays a critical role in protecting against water loss from the inside and pathogen invasion from the outside. The expression levels and localization of claudin-1 (CLDN1) are responsible for the tight junction (TJ) barrier function in the epidermis. Nonthermal atmospheric pressure plasma (NTAPP) has recently received attention as a novel tool in life sciences, including dermatology. NTAPP application showed useful effects on the skin, including antimicrobial activity, wound healing promotion, and anticancer activity for melanoma. However, it remains unknown how NTAPP indirect irradiation affects skin cells. In this study, we used the human epidermal keratinocyte HaCaT cells to clarify the effect of NTAPP-irradiated medium (PAM) on the epidermal TJ barrier function. Treatment with 30 % of the medium irradiated no distance from NTAPP (PAM0) significantly decreased the expression levels of CLDN1 protein. PAM0 significantly decreased the localization of CLDN1 in the cell-cell contact area. After PAM0 treatment, further culture without PAM0 significantly restored the expression and localization of CLDN1 to the same level as in the control cells. The PAM0-induced changes in protein expression and localization of CLDN1 involve lysosome degradation via a clathrin-dependent endocytosis. Treatment with PAM0 decreases transepithelial electrical resistance and increases the intercellular permeability of low-molecular-weight compounds but not high-molecular-weight compounds. The present study shows that treatment with PAM0 weakens intercellular permeability by decreasing the TJ localization of CLDN1 protein in human epidermal keratinocytes. The technology using NTAPP may be useful to promote transdermal absorption of drugs that are difficult to permeate into the body.

皮肤在防止内部水分流失和外部病原体入侵方面起着关键作用。CLDN1的表达水平和定位与表皮的紧密连接屏障功能有关。近年来，非热大气压等离子体（NTAPP）作为一种新的生命科学工具受到了包括皮肤科学在内的广泛关注。NTAPP的应用显示出对皮肤的有益作用，包括抗菌活性、促进伤口愈合和黑色素瘤的抗癌活性。然而，NTAPP间接照射对皮肤细胞的影响尚不清楚。本研究以人表皮角质形成细胞HaCaT细胞为实验材料，研究了ntapp辐照介质（PAM）对表皮TJ屏障功能的影响。与NTAPP （PAM0）无距离辐照的30%培养基显著降低了CLDN1蛋白的表达水平。PAM0显著降低了CLDN1在细胞-细胞接触区域的定位。经PAM0处理后，不加PAM0的进一步培养，CLDN1的表达和定位明显恢复到与对照细胞相同的水平。pam0诱导的CLDN1蛋白表达和定位的变化涉及溶酶体通过网格蛋白依赖的内吞作用降解。PAM0降低了经上皮电阻，增加了低分子量化合物的细胞间渗透性，但对高分子量化合物没有作用。本研究表明，PAM0通过降低人表皮角质形成细胞中CLDN1蛋白的TJ定位而减弱细胞间渗透性。使用NTAPP的技术可能有助于促进难以渗透到体内的药物的透皮吸收。

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引用次数: 0

Computational modelling of olfactory receptors 嗅觉受体的计算模型

IF 2.8 3区生物学 Q3 BIOCHEMISTRY & MOLECULAR BIOLOGY

Biochimica et biophysica acta. General subjects

Pub Date : 2025-07-01 Epub Date: 2025-05-27 DOI: 10.1016/j.bbagen.2025.130825

Chiemela S. Odoemelam, Volker Steuber, Michael Schmuker

Olfactory receptors (ORs), the largest subfamily of G protein-coupled receptors, are essential for detecting and interpreting environmental odorants in animals. Understanding their function is crucial for deciphering olfactory perception and exploring emerging roles in non-olfactory systems. With the recent surge in available sequence data and AI-based structural predictions, computational modelling has become indispensable for investigating OR structure, ligand binding, and activation mechanisms. This review provides a comprehensive overview of computational approaches used in OR research, including homology modelling, molecular docking, molecular dynamics simulations, free energy calculations, pharmacophore modelling, virtual screening, and machine learning-based predictions. Both ligand-based and structure-based pharmacophore modelling are discussed in detail, highlighting their respective applications, strengths, and limitations. While structure-based approaches have gained prominence due to advances in receptor structure prediction tools like AlphaFold, ligand-based pharmacophore modelling remains valuable in scenarios where structural data are limited or uncertain. Case studies illustrate how these techniques have been applied to identify novel OR–ligand interactions, explore receptor dynamics, and support drug discovery. Collectively, these computational strategies offer powerful tools for decoding OR function, guiding experimental validation, and expanding our understanding of olfactory signalling in health and disease.

嗅觉受体（ORs）是最大的G蛋白偶联受体亚家族，对动物检测和解释环境气味至关重要。了解它们的功能对于破译嗅觉感知和探索非嗅觉系统中的新角色至关重要。随着最近可用的序列数据和基于人工智能的结构预测的激增，计算建模已经成为研究OR结构、配体结合和激活机制不可或缺的工具。本文综述了用于OR研究的计算方法，包括同源建模、分子对接、分子动力学模拟、自由能计算、药效团建模、虚拟筛选和基于机器学习的预测。本文详细讨论了基于配体和基于结构的药效团建模，重点介绍了它们各自的应用、优势和局限性。虽然基于结构的方法由于AlphaFold等受体结构预测工具的进步而获得突出地位，但基于配体的药效团建模在结构数据有限或不确定的情况下仍然有价值。案例研究说明了这些技术如何应用于识别新的or配体相互作用、探索受体动力学和支持药物发现。总的来说，这些计算策略为解码OR功能提供了强大的工具，指导实验验证，并扩展了我们对健康和疾病嗅觉信号的理解。

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引用次数: 0

SLAMF9 aggravates myocardial ischemia reperfusion injury through activating the hippo-yap pathway SLAMF9通过激活海马-叶波通路加重心肌缺血再灌注损伤。

IF 2.8 3区生物学 Q3 BIOCHEMISTRY & MOLECULAR BIOLOGY

Biochimica et biophysica acta. General subjects

Pub Date : 2025-07-01 Epub Date: 2025-05-16 DOI: 10.1016/j.bbagen.2025.130821

Tingting Liu , Xiuli Guo , Yanhua Fu , Weili Zhang

Background

The objective was to investigate the impact of signaling lymphocyte activation molecule family member 9 (SLAMF9) on myocardial infarction (MI) and its mechanisms.

Methods

SLAMF9 expression in MI rats was firstly measured. SLAMF9 effect on cardiac functions, myocardial fibrosis, cardiomyocyte hypertrophy, cardiomyocyte apoptosis and inflammation in MI rats was explored using echocardiography, HE staining, masson staining, wheat germ agglutinin staining, western blot, TUNEL staining and qRT-PCR. Meanwhile, SLAMF9 effect on the viability, apoptosis, and inflammation in H9C2 cells was investigated by CCK-8 assay, TUNEL staining and western blot. Moreover, the potential mechanisms of SLAMF9 were investigated using western blot, ELISA and TUNEL staining after different treatment.

Results

SLAMF9 expression was upregulated in MI rats. SLAMF9 knockdown ameliorated heart damage, cardiomyocyte apoptosis and inflammatory response in MI rats. Similarly, SLAMF9 silencing in macrophages attenuated the apoptosis and inflammatory response in H/R-induced H9C2 cells. Moreover, SLAMF9 knockdown inhibited Hippo-Yap pathway in MI in vitro and in vivo. Besides, SLAMF9 knockdown in macrophages suppressed the activation of Hippo-Yap pathway in H9C2 cells by inhibiting TNF-α release. Additionally, LATS1 overexpression in H9C2 cells reversed the effect of SLAMF9 silencing on the apoptosis and inflammatory response in H/R-induced H9C2 cells. Meanwhile, PY-60 treatment in H9C2 cells reversed the effect of SLAMF9 overexpression on the apoptosis and inflammatory response in H/R-induced H9C2 cells.

Conclusion

The absence of SLAMF9 led to a reduction in TNF-α secretion in macrophages, consequently repressing Hippo-Yap pathway in cardiomyocytes, and ultimately ameliorating myocardial damage, cardiomyocyte apoptosis and inflammation in MI.

背景：目的是研究信号淋巴细胞活化分子家族成员9 （SLAMF9）对心肌梗死（MI）的影响及其机制。方法：首先测定心肌梗死大鼠中SLAMF9的表达。采用超声心动图、HE染色、masson染色、小麦胚凝集素染色、western blot、TUNEL染色、qRT-PCR等方法探讨SLAMF9对心肌梗死大鼠心功能、心肌纤维化、心肌细胞肥大、心肌细胞凋亡及炎症的影响。同时通过CCK-8法、TUNEL染色和western blot检测SLAMF9对H9C2细胞活力、凋亡和炎症的影响。此外，采用western blot、ELISA和TUNEL染色等方法研究不同处理后SLAMF9的潜在作用机制。结果：心肌梗死大鼠中SLAMF9表达上调。SLAMF9敲低可改善心肌梗死大鼠的心脏损伤、心肌细胞凋亡和炎症反应。同样，巨噬细胞中SLAMF9的沉默可以减轻H/ r诱导的H9C2细胞的凋亡和炎症反应。此外，在体外和体内实验中，SLAMF9敲低可抑制心肌梗死的Hippo-Yap通路。此外，巨噬细胞中SLAMF9敲低可通过抑制TNF-α释放抑制H9C2细胞中hipo - yap通路的激活。此外，LATS1在H9C2细胞中的过表达逆转了SLAMF9沉默对H/ r诱导的H9C2细胞凋亡和炎症反应的影响。同时，PY-60处理H9C2细胞逆转了SLAMF9过表达对H/ r诱导的H9C2细胞凋亡和炎症反应的影响。结论：SLAMF9缺失导致巨噬细胞分泌TNF-α减少，从而抑制心肌细胞的Hippo-Yap通路，最终改善心肌梗死的心肌损伤、心肌细胞凋亡和炎症。

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引用次数: 0

Mastering the plant growth symphony: The interplay between calcium sensing machinery and phytohormone signaling during abiotic stress 掌握植物生长交响曲：在非生物胁迫下钙感知机制和植物激素信号之间的相互作用。

IF 2.8 3区生物学 Q3 BIOCHEMISTRY & MOLECULAR BIOLOGY

Biochimica et biophysica acta. General subjects

Pub Date : 2025-07-01 Epub Date: 2025-05-17 DOI: 10.1016/j.bbagen.2025.130820

Tanashvi Seth, Shruti Saxena, Barkha Ravi, Girdhar K. Pandey

Climate change introduces a multitude of abiotic stressors, affecting plants' ability to thrive and produce. Abiotic stresses significantly impair plant growth, development, and production, jeopardizing food security. Despite extensive research on individual stress adaptation mechanisms, a critical gap remains in understanding the synergistic role of calcium (Ca²⁺) signaling and phytohormonal regulation in plant stress responses. Ca²⁺, a ubiquitous second messenger, plays a pivotal role in stress perception and signal transduction, while phytohormones regulate adaptive physiological and molecular responses. This review aims to bridge the knowledge gap by synthesizing recent advancements in Ca²⁺-phytohormone interactions and their combined role in enhancing plant resilience to abiotic stress. Hence, understanding these interconnected signaling cascades would pave the path for the development of innovative strategies for enhancing crop stress tolerance, thereby promoting sustainable agriculture in the face of climate change.

气候变化引入了大量的非生物压力源，影响了植物的生长和生产能力。非生物胁迫严重损害植物生长、发育和生产，危及粮食安全。尽管对个体胁迫适应机制进行了广泛的研究，但在了解钙（Ca2+）信号和植物激素调节在植物胁迫反应中的协同作用方面仍存在关键空白。Ca2+是一种普遍存在的第二信使，在胁迫感知和信号转导中起关键作用，而植物激素调节适应性生理和分子反应。本文旨在通过综合Ca2+-植物激素相互作用及其在增强植物抗非生物胁迫中的综合作用的最新进展来弥合这方面的知识差距。因此，了解这些相互关联的信号级联将为开发提高作物抗逆性的创新策略铺平道路，从而促进面对气候变化的可持续农业。

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引用次数: 0

N-glycosylation of CD4+ T cell changes with the development in Graves' disease and is sensitive to methimazole treatment CD4+ T细胞n -糖基化随graves病的发展而变化，对甲巯咪唑治疗敏感。

IF 2.8 3区生物学 Q3 BIOCHEMISTRY & MOLECULAR BIOLOGY

Biochimica et biophysica acta. General subjects

Pub Date : 2025-07-01 Epub Date: 2025-05-25 DOI: 10.1016/j.bbagen.2025.130824

Sara Trzos , Marta Szewczyk , Paweł Link-Lenczowski , Grzegorz Sokołowski , Małgorzata Trofimiuk-Müldner , Katarzyna Bocian , Ewa Pocheć

Graves' disease (GD) is one of the most common autoimmune disorders. Helper T (Th) cells, whose surface receptors are rich in glycans, are involved in the GD pathomechanism. N-glycosylation is altered during autoimmunity and can be modulated by pharmacotherapy. We hypothesized that changes in Th glycosylation accompany GD, and the glycome of these cells is sensitive to methimazole therapy. The study group consisted of patients with Graves' disease before (GD) and after (GD/T) restoring euthyroidism as a result of methimazole therapy. In the control group, healthy donors were recruited. Th cells were isolated from PBMCs and sorted into a subpopulation of CD4⁺CD25⁻ cells and those expressing the CD25 late activation marker (CD4⁺CD25⁺). MALDI-Tof MS was used for analysis of N-linked glycans, and the expression of glycosyltransferases was determined by RT-qPCR. The N-glycosylation profile of CD4⁺ cell subpopulations differed in the ratio of the complex-to-oligomannose N-glycans in GD. Complex N-glycans are partially replaced by oligomannose forms, and their structure is shortened by agalactosylation in CD4⁺CD25⁻ cells from GD. The rearrangement of N-glycans in CD4⁺CD25⁺ cells has the opposite direction, namely the ratio is shifted towards complex structures in GD. The changes in the N-glycan profile were reflected partly in MGAT5 and FUT8 expression. Methimazole to some extent normalized the glycosyltransferase levels and affected the N-linked glycans profile. Our study shows N-glycosylation changes in CD4⁺ T cells in GD development and methimazole therapy for the first time. Further studies are needed to determine the functional aspect of the identified glycosylation changes in thyroid autoimmunity.

格雷夫斯病（GD）是最常见的自身免疫性疾病之一。辅助性T （Th）细胞，其表面受体富含聚糖，参与GD的病理机制。n -糖基化在自身免疫过程中发生改变，可通过药物治疗进行调节。我们假设GD伴有Th糖基化的变化，这些细胞的糖基化对甲巯咪唑治疗敏感。研究组为经甲巯咪唑治疗恢复甲亢前（GD/T）和后（GD/T） Graves病患者。在对照组中，招募健康的供体。这些细胞从pbmc中分离出来，并分为CD4+CD25-细胞亚群和表达CD25晚期激活标志物（CD4+CD25+）的细胞亚群。采用MALDI-Tof质谱法分析n链聚糖，RT-qPCR法检测糖基转移酶的表达。CD4+细胞亚群的n -糖基化谱在GD中复合物与寡甘露糖n -聚糖的比例不同。在GD的CD4+CD25-细胞中，n -甘聚糖复合物部分被寡甘露糖形式所取代，其结构因无半乳糖化而缩短。CD4+CD25+细胞中n -聚糖的重排方向相反，即在GD中比例向复杂结构转移。n -聚糖谱的变化部分反映在MGAT5和FUT8的表达上。甲巯咪唑在一定程度上使糖基转移酶水平正常化，并影响n链聚糖谱。我们的研究首次揭示了GD发展和甲巯咪唑治疗中CD4+ T细胞n -糖基化的变化。需要进一步的研究来确定甲状腺自身免疫中糖基化变化的功能方面。

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引用次数: 0

There is more to scanning than meets the eye: Raster Image Correlation Spectroscopy 还有更多的扫描比满足眼睛：光栅图像相关光谱学。

IF 2.8 3区生物学 Q3 BIOCHEMISTRY & MOLECULAR BIOLOGY

Biochimica et biophysica acta. General subjects

Pub Date : 2025-07-01 Epub Date: 2025-05-10 DOI: 10.1016/j.bbagen.2025.130818

Irene Gialdini , Jelle Hendrix , Don C. Lamb

Raster Image Correlation Spectroscopy (RICS) is a confocal image analysis method that can measure the diffusion and interactions of fluorescently labeled molecules in real time in solution and in living cells. RICS is easy to implement on commercial confocal microscopes and allows detailed investigations of complex biological systems and pathways. The method is especially robust for measurements in living cells using commonly used labels such as fluorescent proteins. Moreover, since its invention in 2005, the robustness and applicability of RICS has been significantly increased to allow, e.g., straightforward kinetic analyses, advanced image segmentation, parameter mapping, and multi-species analysis. In this review, we describe the methodological principles of RICS in a manner that is accessible to a broad readership, position RICS in relation to other fluorescence fluctuation techniques, highlight recent methodological advances and present exemplary applications of the method. With this review, we hope to facilitate the implementation of this powerful method into the everyday repertoire of confocal imaging approaches.

光栅图像相关光谱（RICS）是一种共聚焦图像分析方法，可以实时测量荧光标记分子在溶液和活细胞中的扩散和相互作用。RICS很容易在商用共聚焦显微镜上实现，并且可以对复杂的生物系统和途径进行详细的研究。该方法尤其适用于使用荧光蛋白等常用标记对活细胞进行测量。此外，自2005年发明以来，RICS的鲁棒性和适用性得到了显著提高，可以进行直接的动力学分析、高级图像分割、参数映射和多物种分析。在这篇综述中，我们以一种通俗易懂的方式描述了RICS的方法学原理，将RICS与其他荧光波动技术进行了比较，强调了最近的方法学进展，并介绍了该方法的示例应用。通过这篇综述，我们希望促进这种强大的方法在共聚焦成像方法中的日常应用。

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引用次数: 0

Unraveling architectural RNAs: Structural and functional blueprints of membraneless organelles and strategies for genome-scale identification 结构rna：一类作为无膜细胞器支架的长链非编码rna。

IF 2.8 3区生物学 Q3 BIOCHEMISTRY & MOLECULAR BIOLOGY

Biochimica et biophysica acta. General subjects

Pub Date : 2025-07-01 Epub Date: 2025-05-08 DOI: 10.1016/j.bbagen.2025.130815

Naoko Fujiwara, Tsuyoshi Ueno, Tomohiro Yamazaki, Tetsuro Hirose

Architectural RNAs (arcRNAs) are long noncoding RNAs that serve as structural scaffolds for membraneless organelles (MLOs), facilitating cellular organization and dynamic responses to stimuli. Acting as blueprints for MLO assembly, arcRNAs recruit specific proteins and nucleic acids to establish and maintain the internal structure of MLOs while coordinating their spatial relationships with other organelles. This organized framework enables precise spatiotemporal regulation, allowing for targeted control of transcription, RNA processing, and cellular responses to stress. Notably, arcRNAs exhibit the “semi-extractable” feature, a property derived from their stable binding to cellular structures, making them partially resistant to conventional RNA extraction methods. This unique feature serves as a useful criterion for identifying novel arcRNAs, providing an opportunity to accelerate research in long noncoding RNAs and deepen our understanding of their functional roles in cellular processes.

建筑rna （arcRNAs）是一种长链非编码rna，作为无膜细胞器（MLOs）的结构支架，促进细胞组织和对刺激的动态反应。arcrna作为MLO组装的蓝图，招募特定的蛋白质和核酸来建立和维持MLO的内部结构，同时协调其与其他细胞器的空间关系。这种有组织的框架能够实现精确的时空调节，允许有针对性地控制转录，RNA加工和细胞对应激的反应。值得注意的是，arcRNAs表现出“半可提取”的特征，这一特性源于它们与细胞结构的稳定结合，使它们对传统的RNA提取方法具有部分抗性。这种独特的特征可以作为鉴定新型arcrna的有用标准，为加速长链非编码rna的研究提供了机会，并加深了我们对其在细胞过程中的功能作用的理解。

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