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POGK is a domesticated KRAB domain-containing transposable element with tumor suppressive functions in breast cancer. POGK 是一种驯化的含 KRAB 结构域的转座元件,在乳腺癌中具有肿瘤抑制功能。
IF 13 1区 生物学 Q1 CELL BIOLOGY Pub Date : 2024-11-14 DOI: 10.1016/j.tcb.2024.11.002
Karen M Mann

Transposable elements (TEs) account for 50% of the human genome and have essential functions as gene promoters. A subset of TEs is expressed in normal cells and differentially expressed in cancers, yet their biological significance is understudied. In a recent article, Tu et al. describe the tumor suppressive function of POGK, an expressed TE with a KRAB domain, and its cooperation with TRIM28 to repress ribosomal gene transcription in triple-negative breast cancer (TNBC).

可转座元件(TEs)占人类基因组的 50%,具有基因启动子的基本功能。可转座元件的一个子集在正常细胞中表达,而在癌症中则有不同表达,但它们的生物学意义还未得到充分研究。在最近的一篇文章中,Tu 等人描述了具有 KRAB 结构域的表达 TE POGK 的肿瘤抑制功能,以及它与 TRIM28 合作抑制三阴性乳腺癌(TNBC)中核糖体基因转录的功能。
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引用次数: 0
Central role of the ER proteostasis network in healthy aging. ER蛋白稳态网络在健康老龄化中的核心作用。
IF 13 1区 生物学 Q1 CELL BIOLOGY Pub Date : 2024-11-14 DOI: 10.1016/j.tcb.2024.10.003
Claudio Hetz, Andrew Dillin

Aging trajectories vary among individuals, characterized by progressive functional decline, often leading to disease states. One of the central hallmarks of aging is the deterioration of proteostasis, where the function of the endoplasmic reticulum (ER) is dramatically affected. ER stress is monitored and adjusted by the unfolded protein response (UPR); a signaling pathway that mediates adaptive processes to restore proteostasis. Studies in multiple model organisms (yeast, worms, flies, and mice) in addition to human tissue indicates that adaptive UPR signaling contributes to healthy aging. Strategies to improve ER proteostasis using small molecules and gene therapy reduce the decline of organ function during normal aging in mammals. This article reviews recent advances in understanding the significance of the ER proteostasis network to normal aging and its relationship with other hallmarks of aging such as senescence.

衰老的轨迹因人而异,其特点是功能逐渐衰退,往往导致疾病状态。衰老的核心特征之一是蛋白稳态恶化,内质网(ER)的功能受到严重影响。未折叠蛋白反应(UPR)可监测和调节 ER 压力;UPR 是一种信号通路,可介导恢复蛋白稳态的适应过程。对多种模式生物(酵母、蠕虫、苍蝇和小鼠)以及人体组织的研究表明,适应性 UPR 信号传导有助于健康老化。利用小分子和基因疗法改善ER蛋白稳态的策略可减少哺乳动物正常衰老过程中器官功能的衰退。本文回顾了在理解ER蛋白稳态网络对正常衰老的意义及其与衰老的其他标志(如衰老)之间的关系方面的最新进展。
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引用次数: 0
TFEB links the cGAS-STING pathway to lysosome biogenesis. TFEB 将 cGAS-STING 通路与溶酶体生物生成联系起来。
IF 13 1区 生物学 Q1 CELL BIOLOGY Pub Date : 2024-11-14 DOI: 10.1016/j.tcb.2024.10.011
Yaping Meng, Xinran Li, Haoxing Xu

The cGAS-STING pathway senses the level of double-stranded (ds)DNA in the cytosol, and is required for innate immunity through its effector, TBK1. A recent study by Lv et al. reports that STING activation also simultaneously promotes lysosomal biogenesis by inducing nuclear translocation of the transcription factors TFEB/TFE3 independent of TBK1.

cGAS-STING 通路可感知细胞膜中双链 DNA 的水平,并通过其效应因子 TBK1 实现先天性免疫。Lv 等人最近的一项研究报告指出,STING 的激活还能通过诱导独立于 TBK1 的转录因子 TFEB/TFE3 的核转位,同时促进溶酶体的生物生成。
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引用次数: 0
The culture and application of circulating tumor cell-derived organoids. 循环肿瘤细胞衍生有机体的培养和应用。
IF 13 1区 生物学 Q1 CELL BIOLOGY Pub Date : 2024-11-09 DOI: 10.1016/j.tcb.2024.10.004
Can Pan, Xueping Wang, Chuan Yang, Kai Fu, Fang Wang, Liwu Fu

Circulating tumor cells (CTCs), which have the heterogeneity and histological properties of the primary tumor and metastases, are shed from the primary tumor and/or metastatic lesions into the vasculature and initiate metastases at remote sites. In the clinic, CTCs are used extensively in liquid biopsies for early screening, diagnosis, treatment, and prognosis. Current research focuses on using CTC-derived models to study tumor heterogeneity and metastasis, with 3D organoids emerging as a promising tool in cancer research and precision oncology. However, isolating and enriching CTCs from blood remains challenging due to their scarcity, exacerbated by the lack of an optimized culture medium for CTC-derived organoids (CTCDOs). In this review, we summarize the origin, isolation, enrichment, culture, validation, and clinical application of CTCs and CTCDOs.

循环肿瘤细胞(CTCs)具有原发肿瘤和转移灶的异质性和组织学特性,从原发肿瘤和/或转移灶脱落进入血管,并在远处引发转移。在临床上,CTCs 被广泛用于液体活检,以进行早期筛查、诊断、治疗和预后判断。目前的研究重点是利用 CTC 衍生的模型来研究肿瘤的异质性和转移性,其中三维组织器官是癌症研究和精准肿瘤学中一种很有前途的工具。然而,由于 CTCs 的稀缺性,从血液中分离和富集 CTCs 仍然具有挑战性,而缺乏用于 CTC 衍生有机体(CTCDOs)的优化培养基更加剧了这一挑战。在这篇综述中,我们总结了 CTC 和 CTCDOs 的起源、分离、富集、培养、验证和临床应用。
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引用次数: 0
Emerging roles of palmitoylation in pyroptosis. 棕榈酰化在高温变态反应中的新作用。
IF 13 1区 生物学 Q1 CELL BIOLOGY Pub Date : 2024-11-08 DOI: 10.1016/j.tcb.2024.10.005
Na Zhang, Yuanxin Yang, Daichao Xu

Pyroptosis is a lytic, proinflammatory type of programmed cell death crucial for the immune response to pathogen infections and internal danger signals. Gasdermin D (GSDMD) acts as the pore-forming protein in pyroptosis following inflammasome activation. While recent research has improved our understanding of pyroptosis activation and execution, many aspects regarding the molecular mechanisms controlling inflammasome and GSDMD activation remain to be elucidated. A growing body of literature has shown that S-palmitoylation, a reversible post-translational modification (PTM) that attaches palmitate to cysteine residues, contributes to multi-layered regulation of pyroptosis. This review summarizes the emerging roles of S-palmitoylation in pyroptosis research with a focus on mechanisms that regulate NLRP3 inflammasome and GSDMD activation.

裂解是一种溶解性、促炎性的程序性细胞死亡,对病原体感染和内部危险信号的免疫反应至关重要。炎症小体激活后,Gasdermin D(GSDMD)在裂解过程中充当孔形成蛋白。尽管最近的研究增进了我们对热蛋白沉积激活和执行的了解,但控制炎症小体和 GSDMD 激活的分子机制的许多方面仍有待阐明。越来越多的文献表明,S-棕榈酰化是一种可逆的翻译后修饰(PTM),它将棕榈酸盐连接到半胱氨酸残基上,有助于对热蛋白变性进行多层调控。本综述总结了 S-棕榈酰化在热蛋白变性研究中新出现的作用,重点关注调控 NLRP3 炎症小体和 GSDMD 激活的机制。
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引用次数: 0
MDM4 exon skipping upon dysfunctional ribosome assembly. 核糖体组装失调时的 MDM4 外显子跳转。
IF 13 1区 生物学 Q1 CELL BIOLOGY Pub Date : 2024-11-07 DOI: 10.1016/j.tcb.2024.10.006
Jennifer Jansen, Matthias Dobbelstein

Recent studies revealed how nucleolar stress enhances MDM4 exon skipping and activates p53 via the ribosomal protein L22 (RPL22; eL22). Tumor-associated L22 mutations lead to full-length MDM4 synthesis, overcoming tumor suppression by p53. This forum article explores how MDM4 splicing patterns integrate stress signaling to take p53-dependent cell fate decisions.

最近的研究揭示了核极应激如何通过核糖体蛋白 L22(RPL22;eL22)增强 MDM4 外显子跳越并激活 p53。肿瘤相关的 L22 突变会导致全长 MDM4 合成,从而克服 p53 对肿瘤的抑制。本论坛文章探讨了 MDM4 剪接模式如何整合应激信号,以作出依赖于 p53 的细胞命运决定。
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引用次数: 0
Increased O-GlcNAcylation connects metabolic to transcriptional reprogramming during pathophysiological cell activation. 在病理生理细胞激活过程中,O-GlcNAcylation 的增加将代谢与转录重编程联系起来。
IF 13 1区 生物学 Q1 CELL BIOLOGY Pub Date : 2024-11-07 DOI: 10.1016/j.tcb.2024.10.007
Ninon Very, Bart Staels, Jérôme Eeckhoute

Increased protein O-linked β-N-acetylglucosaminylation (O-GlcNAcylation) has emerged as a hallmark of mammalian cell activation, contributing to Warburg-like metabolic rewiring allowing the acquisition of new functionalities. Recent advances indicate that O-GlcNAcylation promotes the activity of transcriptional regulators driving gene expression reprogramming. This may offer new therapeutic opportunities in a broad spectrum of pathological conditions.

蛋白质 O-连环β-N-乙酰葡萄糖氨酰化(O-GlcNAcylation)的增加已成为哺乳动物细胞活化的标志,它有助于类似沃伯格的代谢重新布线,从而获得新的功能。最新研究进展表明,O-GlcNAcylation 可促进转录调节因子的活性,从而推动基因表达重编程。这可能会为多种病理情况提供新的治疗机会。
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引用次数: 0
Dynamic rRNA modifications as a source of ribosome heterogeneity. 动态 rRNA 修饰是核糖体异质性的来源。
IF 13 1区 生物学 Q1 CELL BIOLOGY Pub Date : 2024-11-04 DOI: 10.1016/j.tcb.2024.10.001
Ivan Milenkovic, Eva Maria Novoa

Ribosomal RNAs (rRNA) are the most abundant RNA molecules in almost all cell types. The general consensus in the field is that rRNA modifications are largely species-specific, with most previous works and databases solely stratifying modifications by the species of origin, without taking other levels of complexity into account. However, new evidence has emerged suggesting dynamic rRNA modifications may have additional layers of complexity and might play an important role in development and disease. In this review article, we summarize recent evidence supporting heterogeneity and dynamics in rRNA modifications in diverse biological contexts, challenging the simplistic view of 'one-species-one-rRNA-modification-pattern'. Moreover, we highlight how rRNA modification dynamics have been studied to date and how long-read sequencing methods can significantly improve our understanding of this largely unexplored yet highly abundant RNA family, across tissues, developmental stages, and diseases.

核糖体 RNA(rRNA)是几乎所有细胞类型中最丰富的 RNA 分子。该领域的普遍共识是,rRNA 的修饰在很大程度上是物种特异性的,以前的大多数研究工作和数据库都只是根据起源物种对修饰进行分层,而没有考虑其他层次的复杂性。然而,新的证据表明,动态 rRNA 修饰可能具有更多层次的复杂性,并可能在发育和疾病中发挥重要作用。在这篇综述文章中,我们总结了支持 rRNA 修饰在不同生物环境中的异质性和动态性的最新证据,对 "一种物种一种 rRNA 修饰模式 "的简单化观点提出了质疑。此外,我们还强调了迄今为止对 rRNA 修饰动态的研究情况,以及长读程测序方法如何能显著提高我们对这一在组织、发育阶段和疾病中基本未被探索但却非常丰富的 RNA 家族的认识。
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引用次数: 0
Timing is everything: advances in quantifying splicing kinetics. 时间就是一切:量化剪接动力学的进展。
IF 13 1区 生物学 Q1 CELL BIOLOGY Pub Date : 2024-11-01 Epub Date: 2024-05-21 DOI: 10.1016/j.tcb.2024.03.007
Hope E Merens, Karine Choquet, Autum R Baxter-Koenigs, L Stirling Churchman

Splicing is a highly regulated process critical for proper pre-mRNA maturation and the maintenance of a healthy cellular environment. Splicing events are impacted by ongoing transcription, neighboring splicing events, and cis and trans regulatory factors on the respective pre-mRNA transcript. Within this complex regulatory environment, splicing kinetics have the potential to influence splicing outcomes but have historically been challenging to study in vivo. In this review, we highlight recent technological advancements that have enabled measurements of global splicing kinetics and of the variability of splicing kinetics at single introns. We demonstrate how identifying features that are correlated with splicing kinetics has increased our ability to form potential models for how splicing kinetics may be regulated in vivo.

剪接是一个受到高度调控的过程,对于前核糖核酸的正常成熟和维持健康的细胞环境至关重要。剪接事件受到正在进行的转录、相邻剪接事件以及相应前 mRNA 转录本上顺式和反式调控因子的影响。在这种复杂的调控环境中,剪接动力学有可能影响剪接结果,但体内研究历来具有挑战性。在这篇综述中,我们将重点介绍最近的技术进步,这些技术进步使我们能够测量全局剪接动力学和单个内含子剪接动力学的变异性。我们展示了如何通过识别与剪接动力学相关的特征来提高我们建立潜在模型的能力,以了解剪接动力学在体内是如何被调控的。
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引用次数: 0
Cytoplasmic mtDNA clearance suppresses inflammatory immune responses. 细胞质 mtDNA 清除抑制炎症免疫反应。
IF 13 1区 生物学 Q1 CELL BIOLOGY Pub Date : 2024-11-01 Epub Date: 2024-10-07 DOI: 10.1016/j.tcb.2024.09.002
Chenghao Yan, Xu Liu, Haodong Xu, Liming Wang

Upon various stresses, mtDNA leaks from mitochondria into the cytoplasm, leading to cellular dysfunction and inflammation, thereby exacerbating disease progression. The autophagy-lysosome pathway has emerged as a pivotal quality control mechanism for eliminating abnormal cytoplasmic mtDNA. This article summarizes the mechanisms underlying mtDNA-triggered inflammation and how cytoplasmic mtDNA is eliminated.

在各种压力下,mtDNA 会从线粒体泄漏到细胞质中,导致细胞功能障碍和炎症,从而加剧疾病的发展。自噬-溶酶体途径已成为消除异常胞质 mtDNA 的关键质量控制机制。本文总结了mtDNA引发炎症的机制以及如何消除细胞质mtDNA。
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引用次数: 0
期刊
Trends in Cell Biology
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