• 文献检索
  • 文档翻译
  • 深度研究
  • 学术资讯
  • Suppr Zotero 插件Zotero 插件
  • 邀请有礼
  • 套餐&价格
  • 历史记录
应用&插件
Suppr Zotero 插件Zotero 插件浏览器插件Mac 客户端Windows 客户端微信小程序
定价
高级版会员购买积分包购买API积分包
服务
文献检索文档翻译深度研究API 文档MCP 服务
关于我们
关于 Suppr公司介绍联系我们用户协议隐私条款
关注我们

Suppr 超能文献

核心技术专利:CN118964589B侵权必究
粤ICP备2023148730 号-1Suppr @ 2026

文献检索

告别复杂PubMed语法,用中文像聊天一样搜索,搜遍4000万医学文献。AI智能推荐,让科研检索更轻松。

立即免费搜索

文件翻译

保留排版,准确专业,支持PDF/Word/PPT等文件格式,支持 12+语言互译。

免费翻译文档

深度研究

AI帮你快速写综述,25分钟生成高质量综述,智能提取关键信息,辅助科研写作。

立即免费体验

相似文献

1
When mitophagy dictates the outcome of cellular infection: the case of .当自噬决定细胞感染的结果时:以. 为例。
Autophagy. 2023 Nov;19(11):3022-3023. doi: 10.1080/15548627.2023.2246354. Epub 2023 Aug 17.
2
Host cell egress of Brucella abortus requires BNIP3L-mediated mitophagy.布鲁氏菌属 abortus 的宿主细胞外吐需要 BNIP3L 介导的线粒体自噬。
EMBO J. 2023 Jul 17;42(14):e112817. doi: 10.15252/embj.2022112817. Epub 2023 May 25.
3
To eat or not to eat mitochondria? How do host cells cope with mitophagy upon bacterial infection?吃还是不吃线粒体?宿主细胞在细菌感染时如何应对噬线粒体作用?
PLoS Pathog. 2023 Jul 6;19(7):e1011471. doi: 10.1371/journal.ppat.1011471. eCollection 2023 Jul.
4
Lipocalin 2 (Lcn2) interferes with iron uptake by Brucella abortus and dampens immunoregulation during infection of RAW 264.7 macrophages.脂钙素 2(Lcn2)干扰布鲁氏菌属流产生物型摄取铁,并在 RAW 264.7 巨噬细胞感染期间抑制免疫调节。
Cell Microbiol. 2018 Mar;20(3). doi: 10.1111/cmi.12813. Epub 2017 Dec 18.
5
Postreplication Roles of the Brucella VirB Type IV Secretion System Uncovered via Conditional Expression of the VirB11 ATPase.通过VirB11 ATP酶的条件表达揭示布鲁氏菌VirB IV型分泌系统的复制后作用。
mBio. 2016 Nov 29;7(6):e01730-16. doi: 10.1128/mBio.01730-16.
6
Is Brucella abortus a facultative intracellular pathogen with mitochondria-like activity?布鲁氏菌是一种具有类似线粒体活性的兼性细胞内病原体吗?
Med Hypotheses. 1998 Jul;51(1):41-5. doi: 10.1016/s0306-9877(98)90252-3.
7
A T4SS Effector Targets Host Cell Alpha-Enolase Contributing to Intracellular Lifestyle.一种IV型分泌系统效应蛋白靶向宿主细胞α-烯醇化酶,这有助于其胞内生存方式。
Front Cell Infect Microbiol. 2016 Nov 16;6:153. doi: 10.3389/fcimb.2016.00153. eCollection 2016.
8
Mitochondrial fragmentation affects neither the sensitivity to TNFα-induced apoptosis of Brucella-infected cells nor the intracellular replication of the bacteria.线粒体碎片化既不影响感染布鲁氏菌的细胞对 TNFα 诱导凋亡的敏感性,也不影响细菌的胞内复制。
Sci Rep. 2018 Mar 26;8(1):5173. doi: 10.1038/s41598-018-23483-3.
9
Critical role of ASC inflammasomes and bacterial type IV secretion system in caspase-1 activation and host innate resistance to Brucella abortus infection.ASC 炎性小体和细菌 IV 型分泌系统在 caspase-1 激活和宿主先天抵抗布鲁氏菌流产感染中的关键作用。
J Immunol. 2013 Apr 1;190(7):3629-38. doi: 10.4049/jimmunol.1202817. Epub 2013 Mar 4.
10
Brucella abortus Induces a Warburg Shift in Host Metabolism That Is Linked to Enhanced Intracellular Survival of the Pathogen.牛布鲁氏菌诱导宿主代谢发生瓦伯格效应转变,这与该病原体细胞内存活能力增强有关。
J Bacteriol. 2017 Jul 11;199(15). doi: 10.1128/JB.00227-17. Print 2017 Aug 1.

引用本文的文献

1
Natural flavonoids combat cytosolic MRSA by potentiating phagosome acidification.天然黄酮类化合物通过增强吞噬体酸化作用来对抗胞质型耐甲氧西林金黄色葡萄球菌。
Cell Commun Signal. 2025 Jun 2;23(1):259. doi: 10.1186/s12964-025-02252-6.
2
Roles of PANoptosis and related genes in acute liver failure: neoteric insight from bioinformatics analysis and animal experiment verification.PAN细胞焦亡及其相关基因在急性肝衰竭中的作用:来自生物信息学分析和动物实验验证的最新见解
J Zhejiang Univ Sci B. 2025 Apr 23;26(4):353-370. doi: 10.1631/jzus.B2300678.

本文引用的文献

1
Host cell egress of Brucella abortus requires BNIP3L-mediated mitophagy.布鲁氏菌属 abortus 的宿主细胞外吐需要 BNIP3L 介导的线粒体自噬。
EMBO J. 2023 Jul 17;42(14):e112817. doi: 10.15252/embj.2022112817. Epub 2023 May 25.

当自噬决定细胞感染的结果时:以. 为例。

When mitophagy dictates the outcome of cellular infection: the case of .

机构信息

Research Unit in Cell Biology (URBC) - Namur Research Institute for Life Sciences (NARILIS), University of Namur, Namur, Wallonia, Belgium.

Research Unit in Microorganisms Biology (URBM) - Namur Research Institute for Life Sciences (NARILIS), University of Namur, Namur, Wallonia, Belgium.

出版信息

Autophagy. 2023 Nov;19(11):3022-3023. doi: 10.1080/15548627.2023.2246354. Epub 2023 Aug 17.

DOI:10.1080/15548627.2023.2246354
PMID:37589593
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10549184/
Abstract

Mitochondria are at the basis of various cellular functions ranging from metabolism and redox homeostasis to inflammation and cell death regulation. Mitochondria therefore constitute an attractive target for invading pathogens to fulfil their infectious cycle. This involves the modulation to their advantage of mitochondrial metabolism and dynamics, including the controlled degradation of mitochondria through mitophagy. Mitophagy might for instance be beneficial for bacterial survival as it can clear bactericidal mitochondrial ROS produced by damaged organelle fragments from the intracellular niche. In the case of the bacterial pathogen , mitophagy induction has another role in the intracellular lifecycle of the bacteria. Indeed, in our study, we showed that triggers an iron-dependent BNIP3L-mediated mitophagy response required for proper bacterial egress and infection of neighboring cells. These results highlight the diversity of mitophagy processes that might be crucial for several stages of cellular infection.

摘要

线粒体是多种细胞功能的基础,从代谢和氧化还原平衡到炎症和细胞死亡调节。因此,线粒体成为入侵病原体完成其感染周期的一个有吸引力的目标。这涉及到对线粒体代谢和动力学的调节,包括通过自噬来控制线粒体的降解。自噬可能有利于细菌的存活,因为它可以清除受损细胞器碎片产生的杀菌性线粒体 ROS,从而清除细胞内龛位。对于细菌病原体来说,自噬的诱导在细菌的细胞内生命周期中还有另一个作用。事实上,在我们的研究中,我们表明 触发了一种铁依赖性 BNIP3L 介导的自噬反应,这对于细菌的适当排出和邻近细胞的感染是必需的。这些结果强调了自噬过程的多样性,这可能对细胞感染的几个阶段至关重要。