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Immunotherapy for atherosclerosis by targeting pro-inflammatory T cells 针对促炎 T 细胞的动脉粥样硬化免疫疗法。
IF 28.1 1区 生物学 Q1 CELL BIOLOGY Pub Date : 2024-04-02 DOI: 10.1038/s41422-024-00955-y
Amir Khan, Klaus Ley
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引用次数: 0
Substrate and drug recognition mechanisms of SLC19A3 SLC19A3 的底物和药物识别机制
IF 44.1 1区 生物学 Q1 Biochemistry, Genetics and Molecular Biology Pub Date : 2024-03-19 DOI: 10.1038/s41422-024-00951-2
Yu Dang, Tianyi Zhang, Shabareesh Pidathala, Guopeng Wang, Yijie Wang, Nanhao Chen, Chen Song, Chia-Hsueh Lee, Zhe Zhang
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引用次数: 0
Editorial Expression of Concern: HDAC2 phosphorylation-dependent Klf5 deacetylation and RARα acetylation induced by RAR agonist switch the transcription regulatory programs of p21 in VSMCs 社论表达的关注:RAR 激动剂诱导的 HDAC2 磷酸化依赖性 Klf5 去乙酰化和 RARα 乙酰化改变了 VSMCs 中 p21 的转录调控程序。
IF 44.1 1区 生物学 Q1 Biochemistry, Genetics and Molecular Biology Pub Date : 2024-03-15 DOI: 10.1038/s41422-024-00947-y
Bin Zheng, Mei Han, Ya-nan Shu, Ying-jie Li, Sui-bing Miao, Xin-hua Zhang, Hui-jing Shi, Tian Zhang, Jin-kun Wen
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引用次数: 0
Targeting pro-inflammatory T cells as a novel therapeutic approach to potentially resolve atherosclerosis in humans 以促炎性 T 细胞为靶点,将其作为一种新的治疗方法,有望解决人类动脉粥样硬化问题
IF 44.1 1区 生物学 Q1 Biochemistry, Genetics and Molecular Biology Pub Date : 2024-03-15 DOI: 10.1038/s41422-024-00945-0
Lin Fan, Junwei Liu, Wei Hu, Zexin Chen, Jie Lan, Tongtong Zhang, Yang Zhang, Xianpeng Wu, Zhiwei Zhong, Danyang Zhang, Jinlong Zhang, Rui Qin, Hui Chen, Yunfeng Zong, Jianmin Zhang, Bing Chen, Jun Jiang, Jifang Cheng, Jingyi Zhou, Zhiwei Gao, Zhenjie Liu, Ying Chai, Junqiang Fan, Pin Wu, Yinxuan Chen, Yuefeng Zhu, Kai Wang, Ying Yuan, Pintong Huang, Ying Zhang, Huiqin Feng, Kaichen Song, Xun Zeng, Wei Zhu, Xinyang Hu, Weiwei Yin, Wei Chen, Jian’an Wang
Atherosclerosis (AS), a leading cause of cardio-cerebrovascular disease worldwide, is driven by the accumulation of lipid contents and chronic inflammation. Traditional strategies primarily focus on lipid reduction to control AS progression, leaving residual inflammatory risks for major adverse cardiovascular events (MACEs). While anti-inflammatory therapies targeting innate immunity have reduced MACEs, many patients continue to face significant risks. Another key component in AS progression is adaptive immunity, but its potential role in preventing AS remains unclear. To investigate this, we conducted a retrospective cohort study on tumor patients with AS plaques. We found that anti-programmed cell death protein 1 (PD-1) monoclonal antibody (mAb) significantly reduces AS plaque size. With multi-omics single-cell analyses, we comprehensively characterized AS plaque-specific PD-1+ T cells, which are activated and pro-inflammatory. We demonstrated that anti-PD-1 mAb, when captured by myeloid-expressed Fc gamma receptors (FcγRs), interacts with PD-1 expressed on T cells. This interaction turns the anti-PD-1 mAb into a substitute PD-1 ligand, suppressing T-cell functions in the PD-1 ligands-deficient context of AS plaques. Further, we conducted a prospective cohort study on tumor patients treated with anti-PD-1 mAb with or without Fc-binding capability. Our analysis shows that anti-PD-1 mAb with Fc-binding capability effectively reduces AS plaque size, while anti-PD-1 mAb without Fc-binding capability does not. Our work suggests that T cell-targeting immunotherapy can be an effective strategy to resolve AS in humans.
动脉粥样硬化(AS)是导致全球心脑血管疾病的主要原因,其驱动因素是脂质含量的积累和慢性炎症。传统策略主要侧重于降低血脂,以控制动脉粥样硬化的发展,但残留的炎症风险会导致重大不良心血管事件(MACE)。虽然针对先天性免疫的抗炎疗法减少了 MACEs,但许多患者仍面临重大风险。强直性脊柱炎进展的另一个关键因素是适应性免疫,但其在预防强直性脊柱炎中的潜在作用仍不清楚。为了研究这个问题,我们对患有强直性脊柱炎斑块的肿瘤患者进行了一项回顾性队列研究。我们发现,抗程序性细胞死亡蛋白1(PD-1)单克隆抗体(mAb)能显著缩小强直性脊柱炎斑块的大小。通过多组学单细胞分析,我们全面描述了强直性脊柱炎斑块特异性PD-1+ T细胞的特征,这些细胞具有激活和促炎作用。我们证明,抗PD-1 mAb被骨髓表达的Fcγ受体(FcγRs)捕获后,会与T细胞上表达的PD-1相互作用。这种相互作用使抗PD-1 mAb成为PD-1配体的替代物,在PD-1配体缺乏的强直性脊柱炎斑块中抑制T细胞功能。此外,我们还对使用具有或不具有Fc结合能力的抗PD-1 mAb治疗的肿瘤患者进行了前瞻性队列研究。我们的分析表明,具有 Fc 结合能力的抗 PD-1 mAb 能有效缩小 AS 斑块,而不具有 Fc 结合能力的抗 PD-1 mAb 则不能。我们的研究表明,T细胞靶向免疫疗法是解决人类强直性脊柱炎的有效策略。
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引用次数: 0
Metabolic engineering of the paclitaxel anticancer drug 紫杉醇抗癌药物的代谢工程。
IF 28.1 1区 生物学 Q1 CELL BIOLOGY Pub Date : 2024-03-14 DOI: 10.1038/s41422-024-00950-3
Audrey Oudin, Nicolas Papon, Vincent Courdavault
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引用次数: 0
Multiple cancer cell types release LIF and Gal3 to hijack neural signals 多种癌细胞类型释放 LIF 和 Gal3,劫持神经信号。
IF 44.1 1区 生物学 Q1 Biochemistry, Genetics and Molecular Biology Pub Date : 2024-03-11 DOI: 10.1038/s41422-024-00946-z
Qun Xu, Ying Cao, Fanni Kong, Jiaqi Liu, Xin Chen, Yifei Zhao, Chin-Hui Lai, Xin Zhou, Hao Hu, Wei Fu, Jian Chen, Jing Yang
Neural signals can significantly influence cancer prognosis. However, how cancer cells may proactively modulate the nervous system to benefit their own survival is incompletely understood. In this study, we report an overlapping pattern of brain responses, including that in the paraventricular nucleus of the hypothalamus, in multiple mouse models of peripheral cancers. A multi-omic screening then identifies leukemia inhibitory factor (LIF) and galectin-3 (Gal3) as the key cytokines released by these cancer cell types to trigger brain activation. Importantly, increased plasma levels of these two cytokines are observed in patients with different cancers. We further demonstrate that pharmacologic or genetic blockage of cancer cell-derived LIF or Gal3 signaling abolishes the brain responses and strongly inhibits tumor growth. In addition, ablation of peripheral sympathetic actions can similarly restore antitumor immunity. These results have elucidated a novel, shared mechanism of multiple cancer cell types hijacking the nervous system to promote tumor progression.
神经信号可对癌症预后产生重大影响。然而,人们对癌细胞如何主动调节神经系统以利于自身生存尚不完全了解。在这项研究中,我们报告了多种外周癌症小鼠模型大脑反应的重叠模式,包括下丘脑室旁核的反应。通过多组学筛选,我们发现白血病抑制因子(LIF)和galectin-3(Gal3)是这些癌细胞类型释放的引发脑激活的关键细胞因子。重要的是,这两种细胞因子在不同癌症患者中的血浆水平都有所升高。我们进一步证明,药物或基因阻断癌细胞衍生的 LIF 或 Gal3 信号可消除脑部反应,并强烈抑制肿瘤生长。此外,消减外周交感神经的作用同样可以恢复抗肿瘤免疫力。这些结果阐明了多种癌细胞类型劫持神经系统以促进肿瘤进展的一种新的共享机制。
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引用次数: 0
Treating insomnia with 40 Hz light flicker 用 40 赫兹闪烁光治疗失眠症
IF 44.1 1区 生物学 Q1 Biochemistry, Genetics and Molecular Biology Pub Date : 2024-03-08 DOI: 10.1038/s41422-024-00948-x
P. Lorenzo Bozzelli, Li-Huei Tsai
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引用次数: 0
The rapid proximity labeling system PhastID identifies ATP6AP1 as an unconventional GEF for Rheb 快速接近标记系统 PhastID 将 ATP6AP1 鉴定为 Rheb 的非传统 GEF。
IF 44.1 1区 生物学 Q1 Biochemistry, Genetics and Molecular Biology Pub Date : 2024-03-06 DOI: 10.1038/s41422-024-00938-z
Ran Feng, Feng Liu, Ruofei Li, Zhifen Zhou, Zhuoheng Lin, Song Lin, Shengcheng Deng, Yingying Li, Baoting Nong, Ying Xia, Zhiyi Li, Xiaoqin Zhong, Shuhan Yang, Gang Wan, Wenbin Ma, Su Wu, Zhou Songyang
Rheb is a small G protein that functions as the direct activator of the mechanistic target of rapamycin complex 1 (mTORC1) to coordinate signaling cascades in response to nutrients and growth factors. Despite extensive studies, the guanine nucleotide exchange factor (GEF) that directly activates Rheb remains unclear, at least in part due to the dynamic and transient nature of protein–protein interactions (PPIs) that are the hallmarks of signal transduction. Here, we report the development of a rapid and robust proximity labeling system named Pyrococcus horikoshii biotin protein ligase (PhBPL)-assisted biotin identification (PhastID) and detail the insulin-stimulated changes in Rheb-proximity protein networks that were identified using PhastID. In particular, we found that the lysosomal V-ATPase subunit ATP6AP1 could dynamically interact with Rheb. ATP6AP1 could directly bind to Rheb through its last 12 amino acids and utilizes a tri-aspartate motif in its highly conserved C-tail to enhance Rheb GTP loading. In fact, targeting the ATP6AP1 C-tail could block Rheb activation and inhibit cancer cell proliferation and migration. Our findings highlight the versatility of PhastID in mapping transient PPIs in live cells, reveal ATP6AP1’s role as an unconventional GEF for Rheb, and underscore the importance of ATP6AP1 in integrating mTORC1 activation signals through Rheb, filling in the missing link in Rheb/mTORC1 activation.
Rheb 是一种小型 G 蛋白,它是雷帕霉素机理靶标复合体 1(mTORC1)的直接激活剂,可协调信号级联以响应营养物质和生长因子。尽管进行了大量研究,但直接激活 Rheb 的鸟嘌呤核苷酸交换因子(GEF)仍然不清楚,至少部分原因是作为信号转导标志的蛋白质-蛋白质相互作用(PPI)具有动态和瞬时的性质。在这里,我们报告了一种名为角越橘火球菌生物素蛋白连接酶(PhBPL)辅助生物素鉴定(PhastID)的快速、稳健的近距离标记系统的开发情况,并详细介绍了利用PhastID鉴定的Rheb-近距离蛋白网络在胰岛素刺激下发生的变化。我们特别发现溶酶体 V-ATPase 亚基 ATP6AP1 可与 Rheb 发生动态相互作用。ATP6AP1 可通过其最后 12 个氨基酸直接与 Rheb 结合,并利用其高度保守的 C 尾部的三天冬氨酸基团来增强 Rheb 的 GTP 负载。事实上,靶向 ATP6AP1 C 尾部可以阻断 Rheb 的活化,抑制癌细胞的增殖和迁移。我们的研究结果突显了 PhastID 在绘制活细胞中瞬时 PPIs 图谱方面的多功能性,揭示了 ATP6AP1 作为 Rheb 的非传统 GEF 的作用,并强调了 ATP6AP1 在通过 Rheb 整合 mTORC1 激活信号方面的重要性,填补了 Rheb/mTORC1 激活过程中缺失的环节。
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引用次数: 0
An all-in-one targeted protein degradation platform guided by degradation condensates-bridging bi-specific nanobodies 降解凝聚物桥接双特异性纳米抗体引导的一体化靶向蛋白质降解平台
IF 44.1 1区 生物学 Q1 Biochemistry, Genetics and Molecular Biology Pub Date : 2024-03-05 DOI: 10.1038/s41422-024-00942-3
Wen Jia, Weijie Li, Zengpeng Li, Pilong Li
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引用次数: 0
T follicular regulatory cells keep B cell-directed autoreactivity in check T 滤泡调节细胞控制 B 细胞导向的自反应性
IF 44.1 1区 生物学 Q1 Biochemistry, Genetics and Molecular Biology Pub Date : 2024-03-05 DOI: 10.1038/s41422-024-00941-4
Filipa Ribeiro, Luis Graca
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引用次数: 0
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Cell Research
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