Cell Research最新文献

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Perenniality: the tale of three MADS-box genes 常年性：三个 MADS 框基因的故事

IF 44.1 1区生物学 Q1 CELL BIOLOGY

Cell Research

Pub Date : 2024-07-11 DOI: 10.1038/s41422-024-01001-7

Zheng Li, Ruichen Ma, Rishikesh P. Bhalerao

引用次数: 0

Zero-shot prediction of mutation effects with multimodal deep representation learning guides protein engineering 利用多模态深度表征学习零点预测突变效应，为蛋白质工程提供指导。

IF 28.1 1区生物学 Q1 CELL BIOLOGY

Cell Research

Pub Date : 2024-07-05 DOI: 10.1038/s41422-024-00989-2

Peng Cheng, Cong Mao, Jin Tang, Sen Yang, Yu Cheng, Wuke Wang, Qiuxi Gu, Wei Han, Hao Chen, Sihan Li, Yaofeng Chen, Jianglin Zhou, Wuju Li, Aimin Pan, Suwen Zhao, Xingxu Huang, Shiqiang Zhu, Jun Zhang, Wenjie Shu, Shengqi Wang

Mutations in amino acid sequences can provoke changes in protein function. Accurate and unsupervised prediction of mutation effects is critical in biotechnology and biomedicine, but remains a fundamental challenge. To resolve this challenge, here we present Protein Mutational Effect Predictor (ProMEP), a general and multiple sequence alignment-free method that enables zero-shot prediction of mutation effects. A multimodal deep representation learning model embedded in ProMEP was developed to comprehensively learn both sequence and structure contexts from ~160 million proteins. ProMEP achieves state-of-the-art performance in mutational effect prediction and accomplishes a tremendous improvement in speed, enabling efficient and intelligent protein engineering. Specifically, ProMEP accurately forecasts mutational consequences on the gene-editing enzymes TnpB and TadA, and successfully guides the development of high-performance gene-editing tools with their engineered variants. The gene-editing efficiency of a 5-site mutant of TnpB reaches up to 74.04% (vs 24.66% for the wild type); and the base editing tool developed on the basis of a TadA 15-site mutant (in addition to the A106V/D108N double mutation that renders deoxyadenosine deaminase activity to TadA) exhibits an A-to-G conversion frequency of up to 77.27% (vs 69.80% for ABE8e, a previous TadA-based adenine base editor) with significantly reduced bystander and off-target effects compared to ABE8e. ProMEP not only showcases superior performance in predicting mutational effects on proteins but also demonstrates a great capability to guide protein engineering. Therefore, ProMEP enables efficient exploration of the gigantic protein space and facilitates practical design of proteins, thereby advancing studies in biomedicine and synthetic biology.

氨基酸序列的突变会引起蛋白质功能的改变。在生物技术和生物医学中，准确和无监督地预测突变效应至关重要，但这仍然是一个基本挑战。为了解决这一难题，我们在这里提出了蛋白质突变效应预测器（ProMEP），这是一种通用的、无需多序列比对的方法，可以实现突变效应的零次预测。我们开发了一个嵌入 ProMEP 的多模态深度表征学习模型，以从约 1.6 亿个蛋白质中全面学习序列和结构上下文。ProMEP 在突变效应预测方面达到了最先进的性能，并极大地提高了速度，从而实现了高效、智能的蛋白质工程。具体来说，ProMEP 准确预测了基因编辑酶 TnpB 和 TadA 的突变后果，并成功指导了高性能基因编辑工具及其工程变体的开发。TnpB 5 位点突变体的基因编辑效率高达 74.04%（野生型为 24.66%）；基于 TadA 15 位点突变体（除了 A106V/D108N 双突变使 TadA 失去脱氧腺苷脱氨酶活性外）开发的碱基编辑工具的 A-G 转换频率高达 77.27%（与之前基于 TadA 的腺嘌呤碱基编辑器 ABE8e 的 69.80% 相比），与 ABE8e 相比，旁观者和脱靶效应显著降低。ProMEP 不仅在预测突变对蛋白质的影响方面表现出卓越的性能，而且在指导蛋白质工程方面也显示出强大的能力。因此，ProMEP 能够有效探索巨大的蛋白质空间，促进蛋白质的实用设计，从而推动生物医学和合成生物学的研究。

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引用次数: 0

Bitter taste receptor TAS2R14 activation and G protein assembly by an intracellular agonist. 苦味受体 TAS2R14 被细胞内激动剂激活和 G 蛋白组装

IF 28.1 1区生物学 Q1 CELL BIOLOGY

Cell Research

Pub Date : 2024-07-05 DOI: 10.1038/s41422-024-00995-4

Lele Tao, Dongxue Wang, Qingning Yuan, Fenghui Zhao, Yu Zhang, Tianyuan Du, Shiyi Shen, H Eric Xu, Yi Li, Dehua Yang, Jia Duan

引用次数: 0

Molecular insights into the inhibition of proton-activated chloride channel by transfer RNA 转运核糖核酸抑制质子激活的氯离子通道的分子见解

IF 44.1 1区生物学 Q1 CELL BIOLOGY

Cell Research

Pub Date : 2024-06-28 DOI: 10.1038/s41422-024-00993-6

Pengliang Chi, Xiang Wang, Jialu Li, Hui Yang, Kaiju Li, Yuqi Zhang, Shiyi Lin, Leiye Yu, Shiqi Liu, Lu Chen, Ruobing Ren, Jianping Wu, Zhuo Huang, Jia Geng, Dong Deng

Dear Editor,

The proton-activated chloride (PAC) channel (also known as acid-sensitive outwardly rectifying anion channel, ASOR) plays critical roles in acid-induced cell death and endocytosis.^1,2 The structural investigations revealed that three protomers construct one PAC channel.^3,4,5 PAC’s three captured states (resting, activated, and desensitized) uncovered the gating and proton-sensing mechanism.^3,4,5 However, little is known about the regulatory factors of PAC.⁶

亲爱的编辑，质子激活的氯离子（PAC）通道（又称酸敏感外向整流阴离子通道，ASOR）在酸诱导的细胞死亡和内吞过程中发挥着关键作用。1,2 结构研究发现，三个原体构建了一个 PAC 通道。3,4,5 PAC 的三种捕获状态（静息、激活和脱敏）揭示了门控和质子感应机制。

引用次数: 0

Localized, highly efficient secretion of signaling proteins by migrasomes 迁移体局部高效分泌信号蛋白

IF 28.1 1区生物学 Q1 CELL BIOLOGY

Cell Research

Pub Date : 2024-06-25 DOI: 10.1038/s41422-024-00992-7

Haifeng Jiao, Xiaopeng Li, Ying Li, Yuting Guo, Xiaoyu Hu, Takami Sho, Yiqun Luo, Jinyu Wang, Huizhen Cao, Wanqing Du, Dong Li, Li Yu

Migrasomes, enriched with signaling molecules such as chemokines, cytokines and angiogenic factors, play a pivotal role in the spatially defined delivery of these molecules, influencing critical physiological processes including organ morphogenesis and angiogenesis. The mechanism governing the accumulation of signaling molecules in migrasomes has been elusive. In this study, we show that secretory proteins, including signaling proteins, are transported into migrasomes by secretory carriers via both the constitutive and regulated secretion pathways. During cell migration, a substantial portion of these carriers is redirected to the rear of the cell and actively transported into migrasomes, driven by the actin-dependent motor protein Myosin-5a. Once at the migrasomes, these carriers fuse with the migrasome membrane through SNARE-mediated mechanisms. Inhibiting migrasome formation significantly reduces secretion, suggesting migrasomes as a principal secretion route in migrating cells. Our findings reveal a specialized, highly localized secretion paradigm in migrating cells, conceptually paralleling the targeted neurotransmitter release observed in neuronal systems.

移行体富含趋化因子、细胞因子和血管生成因子等信号分子，在这些分子的空间传递中发挥着关键作用，影响着器官形态发生和血管生成等关键生理过程。信号分子在移行体中的积累机制一直难以捉摸。在这项研究中，我们发现分泌蛋白（包括信号蛋白）通过组成型分泌途径和调节型分泌途径被分泌载体运输到迁移体中。在细胞迁移过程中，这些载体的很大一部分被重新定向到细胞后部，并在肌动蛋白依赖性马达蛋白肌球蛋白-5a的驱动下被主动运输到迁移体中。一旦进入移行体，这些载体就会通过 SNARE 介导的机制与移行体膜融合。抑制迁移体的形成可显著减少分泌，这表明迁移体是迁移细胞的主要分泌途径。我们的研究结果揭示了迁移细胞中一种专门的、高度局部化的分泌模式，在概念上与神经元系统中观察到的定向神经递质释放相似。

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引用次数: 0

ANT2: the first mammalian mitochondrial RNA transport translocon ANT2：第一个哺乳动物线粒体 RNA 转运易位子

IF 28.1 1区生物学 Q1 CELL BIOLOGY

Cell Research

Pub Date : 2024-06-24 DOI: 10.1038/s41422-024-00994-5

Huanhuan Zhu, Weiqiang Lin, Aifu Lin

引用次数: 0

Combination therapy of KRAS G12V mRNA vaccine and pembrolizumab: clinical benefit in patients with advanced solid tumors KRAS G12V mRNA疫苗与pembrolizumab的联合疗法：晚期实体瘤患者的临床获益。

IF 28.1 1区生物学 Q1 CELL BIOLOGY

Cell Research

Pub Date : 2024-06-24 DOI: 10.1038/s41422-024-00990-9

Xinjing Wang, Wei Wang, Siyi Zou, Zhiwei Xu, Dan Cao, Shuai Zhang, Minzhi Wei, Qian Zhan, Chenlei Wen, Fanlu Li, Hao Chen, Da Fu, Lingxi Jiang, Ming Zhao, Baiyong Shen

引用次数: 0

AMPK targets PDZD8 to trigger carbon source shift from glucose to glutamine. AMPK 以 PDZD8 为靶标，触发碳源从葡萄糖向谷氨酰胺的转移。

IF 44.1 1区生物学 Q1 CELL BIOLOGY

Cell Research

Pub Date : 2024-06-19 DOI: 10.1038/s41422-024-00985-6

Mengqi Li, Yu Wang, Xiaoyan Wei, Wei-Feng Cai, Jianfeng Wu, Mingxia Zhu, Yongliang Wang, Yan-Hui Liu, Jinye Xiong, Qi Qu, Yan Chen, Xiao Tian, Luming Yao, Renxiang Xie, Xiaomin Li, Siwei Chen, Xi Huang, Cixiong Zhang, Changchuan Xie, Yaying Wu, Zheni Xu, Baoding Zhang, Bin Jiang, Zhi-Chao Wang, Qinxi Li, Gang Li, Shu-Yong Lin, Li Yu, Hai-Long Piao, Xianming Deng, Jiahuai Han, Chen-Song Zhang, Sheng-Cai Lin

The shift of carbon utilization from primarily glucose to other nutrients is a fundamental metabolic adaptation to cope with decreased blood glucose levels and the consequent decline in glucose oxidation. AMP-activated protein kinase (AMPK) plays crucial roles in this metabolic adaptation. However, the underlying mechanism is not fully understood. Here, we show that PDZ domain containing 8 (PDZD8), which we identify as a new substrate of AMPK activated in low glucose, is required for the low glucose-promoted glutaminolysis. AMPK phosphorylates PDZD8 at threonine 527 (T527) and promotes the interaction of PDZD8 with and activation of glutaminase 1 (GLS1), a rate-limiting enzyme of glutaminolysis. In vivo, the AMPK-PDZD8-GLS1 axis is required for the enhancement of glutaminolysis as tested in the skeletal muscle tissues, which occurs earlier than the increase in fatty acid utilization during fasting. The enhanced glutaminolysis is also observed in macrophages in low glucose or under acute lipopolysaccharide (LPS) treatment. Consistent with a requirement of heightened glutaminolysis, the PDZD8-T527A mutation dampens the secretion of pro-inflammatory cytokines in macrophages in mice treated with LPS. Together, we have revealed an AMPK-PDZD8-GLS1 axis that promotes glutaminolysis ahead of increased fatty acid utilization under glucose shortage.

碳的利用从主要利用葡萄糖转向利用其他营养物质，是应对血糖水平下降和随之而来的葡萄糖氧化下降的一种基本代谢适应。AMP 激活蛋白激酶（AMPK）在这种新陈代谢适应中起着至关重要的作用。然而，其潜在机制尚未完全明了。在这里，我们发现，PDZ 含域 8（PDZD8）是 AMPK 在低糖条件下激活的新底物，它是低糖促进谷氨酰胺溶解所必需的。AMPK 使 PDZD8 在苏氨酸 527 (T527) 处磷酸化，并促进 PDZD8 与谷氨酰胺酶 1 (GLS1) 的相互作用和激活，GLS1 是谷氨酰胺分解的限速酶。在体内，AMPK-PDZD8-GLS1 轴是增强谷氨酰胺酵解所必需的，骨骼肌组织的测试结果表明，谷氨酰胺酵解的增强早于禁食期间脂肪酸利用的增加。在低糖或急性脂多糖（LPS）处理下的巨噬细胞中也能观察到谷氨酰胺溶解的增强。PDZD8-T527A 突变抑制了经 LPS 处理的小鼠巨噬细胞中促炎细胞因子的分泌，这与谷氨酰胺分解增强的要求相一致。综上所述，我们揭示了 AMPK-PDZD8-GLS1 轴在葡萄糖不足的情况下促进谷氨酰胺酵解，而不是增加脂肪酸的利用。

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引用次数: 0

Pyroptosis: palmitoylation regulates GSDMD activation and pore formation 裂解：棕榈酰化调节 GSDMD 的激活和孔隙形成

IF 44.1 1区生物学 Q1 Biochemistry, Genetics and Molecular Biology

Cell Research

Pub Date : 2024-06-18 DOI: 10.1038/s41422-024-00988-3

Ella Hartenian, Petr Broz

引用次数: 0

AI accurately predicting the structure of biomolecular interactions 人工智能准确预测生物分子相互作用的结构。

IF 28.1 1区生物学 Q1 CELL BIOLOGY

Cell Research

Pub Date : 2024-06-14 DOI: 10.1038/s41422-024-00991-8

Zhenling Peng, Peilong Lu, Jianyi Yang

引用次数: 0

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