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Deubiquitinases in skeletal muscle - The Underappreciated Side of the Ubiquitination Coin. 骨骼肌中的去泛素酶--泛素化硬币中未被重视的一面。
IF 5 2区 生物学 Q2 CELL BIOLOGY Pub Date : 2024-09-30 DOI: 10.1152/ajpcell.00553.2024
Wayne X Du, Craig A Goodman, Paul Gregorevic

Ubiquitination is a post-translational modification that plays important roles in regulating protein stability, function, localization, and protein-protein interactions. Proteins are ubiquitinated via a process involving specific E1 activating enzymes, E2 conjugating enzymes, and E3 ligases. Simultaneously, protein ubiquitination is opposed by deubiquitinating enzymes (DUBs). DUB-mediated deubiquitination can change protein function or fate and recycle ubiquitin to maintain the free ubiquitin pool. Approximately 100 DUBs have been identified in the mammalian genome, and characterized into seven classes (USP, OTU, UCH, MJD, JAMM, MINDY and ZUP classes). Of these 100 DUBs, there has only been relatively limited investigation of 19 specifically in skeletal muscle cells, in vitro or in vivo, using overexpression, knockdown, and knockout models. To date, evidence indicates roles for individual DUBs in regulating aspects of myogenesis, protein turnover, muscle mass, and muscle metabolism. However, the exact mechanism by which these DUBs act (i.e. the specific targets of these DUBs and the type of ubiquitin chains they target) is still largely unknown, underscoring how little we know about DUBs in skeletal muscle. This review endeavors to comprehensively summarize the current state of knowledge of the function of DUBs in skeletal muscle and highlight the opportunities for gaining a greater understanding through further research into this important area of skeletal muscle and ubiquitin biology.

泛素化是一种翻译后修饰,在调节蛋白质的稳定性、功能、定位以及蛋白质与蛋白质之间的相互作用方面发挥着重要作用。蛋白质泛素化的过程涉及特定的 E1 激活酶、E2 连接酶和 E3 连接酶。与此同时,去泛素化酶(DUB)也会对抗蛋白质的泛素化。DUB 介导的去泛素化可以改变蛋白质的功能或命运,并回收泛素以维持游离泛素池。目前已在哺乳动物基因组中鉴定出约 100 种 DUB,并将其分为七类(USP、OTU、UCH、MJD、JAMM、MINDY 和 ZUP 类)。在这 100 种 DUBs 中,只有 19 种在体外或体内通过过表达、基因敲除和基因剔除模型专门针对骨骼肌细胞进行了相对有限的研究。迄今为止,有证据表明,个别 DUBs 在调节肌肉生成、蛋白质周转、肌肉质量和肌肉代谢等方面发挥作用。然而,这些 DUBs 作用的确切机制(即这些 DUBs 的特定靶标及其靶标泛素链的类型)在很大程度上仍不为人所知,这突出表明我们对骨骼肌中的 DUBs 知之甚少。本综述力图全面总结目前对骨骼肌中 DUBs 功能的认识,并强调通过进一步研究骨骼肌和泛素生物学这一重要领域来加深理解的机会。
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引用次数: 0
ZNF197-AS1/miR-425/GABARAPL1 Axis: A Novel Regulatory Mechanism in Uveal Melanoma. ZNF197-AS1/miR-425/GABARAPL1轴:葡萄膜黑色素瘤的新型调控机制
IF 5 2区 生物学 Q2 CELL BIOLOGY Pub Date : 2024-09-23 DOI: 10.1152/ajpcell.00457.2024
Chao Zhang, Shuai Wu

This study investigates the role of the long non-coding RNA (lncRNA) ZNF197-AS1 in uveal melanoma (UM), focusing on its function within a competing endogenous RNA (ceRNA) network. Utilizing the UM-related TCGA dataset, we analyzed the expression levels of ZNF197-AS1 and its correlation with miR-425 and GABARAPL1, an essential autophagy-related gene. Our analysis revealed that ZNF197-AS1 acts as a ceRNA by competitively binding to miR-425, resulting in the upregulation of GABARAPL1. This interaction plays a crucial role in the growth and metastasis of UM. The expression of GABARAPL1 showed a strong correlation with the clinical outcomes of UM patients. Furthermore, in vitro assays confirmed that ZNF197-AS1 impedes UM cell proliferation, migration, and invasion by modulating the miR-425/GABARAPL1 axis. These findings suggest that ZNF197-AS1 can effectively inhibit UM progression through this ceRNA regulatory network. This study provides valuable insights into the molecular mechanisms underlying UM and highlights the potential of targeting the ZNF197-AS1/miR-425/GABARAPL1 axis as a therapeutic strategy for UM.

本研究调查了长非编码 RNA(lncRNA)ZNF197-AS1 在葡萄膜黑色素瘤(UM)中的作用,重点研究了它在竞争性内源性 RNA(ceRNA)网络中的功能。利用 UM 相关的 TCGA 数据集,我们分析了 ZNF197-AS1 的表达水平及其与 miR-425 和 GABARAPL1(一种重要的自噬相关基因)的相关性。我们的分析表明,ZNF197-AS1 通过与 miR-425 竞争性结合,起到了 ceRNA 的作用,从而导致 GABARAPL1 的上调。这种相互作用在 UM 的生长和转移中起着至关重要的作用。GABARAPL1 的表达与 UM 患者的临床预后密切相关。此外,体外实验证实 ZNF197-AS1 通过调节 miR-425/GABARAPL1 轴阻碍了 UM 细胞的增殖、迁移和侵袭。这些发现表明,ZNF197-AS1 可通过这一 ceRNA 调控网络有效抑制 UM 的发展。这项研究为研究UM的分子机制提供了有价值的见解,并凸显了靶向ZNF197-AS1/miR-425/GABARAPL1轴作为UM治疗策略的潜力。
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引用次数: 0
The water channels Aquaporin-1 and Aquaporin-3 interact with and affect the cell polarity protein Scribble in 3D in vitro models of breast cancer 在乳腺癌三维体外模型中,水通道 Aquaporin-1 和 Aquaporin-3 与细胞极性蛋白 Scribble 相互作用并对其产生影响
IF 5.5 2区 生物学 Q2 CELL BIOLOGY Pub Date : 2024-09-16 DOI: 10.1152/ajpcell.00094.2024
Sarannya Edamana, Frédéric H. Login, Andreas Riishede, Vibeke S. Dam, Teresa Kirkegaard, Lene N. Nejsum
American Journal of Physiology-Cell Physiology, Ahead of Print.
美国生理学-细胞生理学杂志》,提前出版。
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引用次数: 0
Bone Marrow Stromal Cells Enhance Differentiation of Acute Myeloid Leukemia Induced by Pyrimidine Synthesis Inhibitors 骨髓基质细胞能增强嘧啶合成抑制剂诱导的急性髓性白血病的分化能力
IF 5.5 2区 生物学 Q2 CELL BIOLOGY Pub Date : 2024-09-16 DOI: 10.1152/ajpcell.00413.2024
Tomislav Smoljo, Hrvoje Lalic, Vilma Dembitz, Barbara Tomic, Josip Batinic, Radovan Vrhovac, Antonio Bedalov, Dora Visnjic
American Journal of Physiology-Cell Physiology, Ahead of Print.
美国生理学-细胞生理学杂志》,提前出版。
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引用次数: 0
Pik3c3 Expression Profiling in the Mouse Kidney and Its Role in Proximal Tubule Cell Physiology 小鼠肾脏中 Pik3c3 的表达谱分析及其在近端肾小管细胞生理学中的作用
IF 5.5 2区 生物学 Q2 CELL BIOLOGY Pub Date : 2024-09-09 DOI: 10.1152/ajpcell.00564.2023
Ting Liu, Jialing Yuan, Caihong Dai, Mystie X Chen, Jerry Fan, Benjamin D. Humphreys, David J. Fulton, Daniel T. Kleven, Xingjun Fan, Zheng Dong, Jian-Kang Chen
American Journal of Physiology-Cell Physiology, Ahead of Print.
美国生理学-细胞生理学杂志》,提前出版。
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引用次数: 0
Dual effects of targeting neuropilin-1 in lenvatinib-resistant hepatocellular carcinoma: inhibition of tumor growth and angiogenesis 在来伐替尼耐药肝细胞癌中靶向神经肽-1的双重作用:抑制肿瘤生长和血管生成
IF 5.5 2区 生物学 Q2 CELL BIOLOGY Pub Date : 2024-09-09 DOI: 10.1152/ajpcell.00511.2024
Junjie Ao, Na Qiang, Hiroaki Kanzaki, Masato Nakamura, Risa Kakiuchi, Jiaqi Zhang, Ryuta Kojima, Keisuke Koroki, Masanori Inoue, Naoya Kanogawa, Ryo Nakagawa, Takayuki Kondo, Sadahisa Ogasawara, Shingo Nakamoto, Ryosuke Muroyama, Jun Kato, Naoya Kato
American Journal of Physiology-Cell Physiology, Ahead of Print.
美国生理学-细胞生理学杂志》,提前出版。
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引用次数: 0
KLF3 impacts insulin sensitivity and glucose uptake in skeletal muscle KLF3 影响骨骼肌的胰岛素敏感性和葡萄糖摄取量
IF 5.5 2区 生物学 Q2 CELL BIOLOGY Pub Date : 2024-09-09 DOI: 10.1152/ajpcell.00085.2024
Shuying Fu, Xiaocheng Gong, Keying Liang, Ke Ding, Li Qiu, Huice Cen, Hongli Du
American Journal of Physiology-Cell Physiology, Ahead of Print.
美国生理学-细胞生理学杂志》,提前出版。
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引用次数: 0
Melatonin mitigates matrix stiffness-induced disc degenetation by inhibiting reactive oxygen species and melatonin receptor mediated-PI3K/AKT/NF-κB pathway 褪黑激素通过抑制活性氧和褪黑激素受体介导的PI3K/AKT/NF-κB通路,减轻基质僵化诱发的椎间盘退化
IF 5.5 2区 生物学 Q2 CELL BIOLOGY Pub Date : 2024-09-09 DOI: 10.1152/ajpcell.00630.2023
Zhihui Liang, Jia Song, Wen-ji Shangguan, Qiu-qi Zhang, Jiang Shao, Yue-hui Zhang
American Journal of Physiology-Cell Physiology, Ahead of Print.
美国生理学-细胞生理学杂志》,提前出版。
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引用次数: 0
Corrigendum for Hagen et al., volume 327, 2024, p. C372–C378 Hagen 等人的更正,第 327 卷,2024 年,第 C372-C378 页
IF 5.5 2区 生物学 Q2 CELL BIOLOGY Pub Date : 2024-09-09 DOI: 10.1152/ajpcell.00326.2024_cor
American Journal of Physiology-Cell Physiology, Volume 327, Issue 3, Page C867-C867, September 2024.
美国生理学杂志-细胞生理学》,第 327 卷第 3 期,第 C867-C867 页,2024 年 9 月。
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引用次数: 0
Involvement of the gut microbiota in cancer cachexia. 肠道微生物群对癌症恶病质的影响
IF 5 2区 生物学 Q2 CELL BIOLOGY Pub Date : 2024-09-01 Epub Date: 2024-07-09 DOI: 10.1152/ajpcell.00327.2024
Brandon N VanderVeen, Thomas D Cardaci, Brooke M Bullard, Michael Madden, Jie Li, Kandy T Velazquez, Jason L Kubinak, Daping Fan, E Angela Murphy

Cancer cachexia, or the unintentional loss of body weight in patients with cancer, is a multiorgan and multifactorial syndrome with a complex and largely unknown etiology; however, metabolic dysfunction and inflammation remain hallmarks of cancer-associated wasting. Although cachexia manifests with muscle and adipose tissue loss, perturbations to the gastrointestinal tract may serve as the frontline for both impaired nutrient absorption and immune-activating gut dysbiosis. Investigations into the gut microbiota have exploded within the past two decades, demonstrating multiple gut-tissue axes; however, the link between adipose and skeletal muscle wasting and the gut microbiota with cancer is only beginning to be understood. Furthermore, the most used anticancer drugs (e.g. chemotherapy and immune checkpoint inhibitors) negatively impact gut homeostasis, potentially exacerbating wasting and contributing to poor patient outcomes and survival. In this review, we 1) highlight our current understanding of the microbial changes that occur with cachexia, 2) discuss how microbial changes may contribute to adipose and skeletal muscle wasting, and 3) outline study design considerations needed when examining the role of the microbiota in cancer-induced cachexia.

癌症恶病质,即癌症患者无意中出现的体重减轻,是一种多器官、多因素综合征,病因复杂且大多不明;然而,代谢功能障碍和炎症仍然是癌症相关消瘦的标志。恶病质表现为肌肉和脂肪组织的损失,而胃肠道的紊乱可能是营养吸收受损和免疫激活性肠道菌群失调的前线。在过去的二十年中,对肠道微生物群的研究呈爆炸式增长,显示出多种肠道组织轴;然而,人们对脂肪和骨骼肌萎缩与肠道微生物群与癌症之间的联系才刚刚开始有所了解。此外,最常用的抗癌药物(如化疗、免疫检查点抑制剂)会对肠道稳态产生负面影响,可能会加剧消瘦并导致患者预后和生存率低下。在本综述中,我们将:1)重点介绍我们目前对恶病质发生的微生物变化的理解;2)讨论微生物变化如何可能导致脂肪和骨骼肌消瘦;3)概述在研究微生物群在癌症诱导的恶病质中的作用时需要考虑的研究设计因素。
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American journal of physiology. Cell physiology
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