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The effects of ENDOG on lipid metabolism may be tissue-dependent and may not require its translocation from mitochondria.

作者信息

Llovera Marta, Gouveia Leonor, Zorzano Antonio, Sanchis Daniel

机构信息

Cell Signaling & Apoptosis Group, Universitat de Lleida/IRBLleida, Biomedicine-I Av. Rovira Roure 80, Lleida, 25198, Spain.

Endothelial Pathobiology and Microenvironment, Josep Carreras Leukaemia Research Institute, Barcelona, Spain.

出版信息

Nat Commun. 2024 Aug 21;15(1):7121. doi: 10.1038/s41467-024-51447-x.

DOI:10.1038/s41467-024-51447-x
PMID:39169002
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11339265/
Abstract
摘要
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3a8e/11339265/ae121669023c/41467_2024_51447_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3a8e/11339265/719b9a20dd8a/41467_2024_51447_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3a8e/11339265/0488cca325e3/41467_2024_51447_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3a8e/11339265/ae121669023c/41467_2024_51447_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3a8e/11339265/719b9a20dd8a/41467_2024_51447_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3a8e/11339265/0488cca325e3/41467_2024_51447_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3a8e/11339265/ae121669023c/41467_2024_51447_Fig3_HTML.jpg

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1
The effects of ENDOG on lipid metabolism may be tissue-dependent and may not require its translocation from mitochondria.内源性凋亡核酸酶(ENDOG)对脂质代谢的影响可能具有组织依赖性,且可能不需要其从线粒体易位。
Nat Commun. 2024 Aug 21;15(1):7121. doi: 10.1038/s41467-024-51447-x.
2
Reply to: The effects of ENDOG on lipid metabolism may be tissue-dependent and may not require its translocation from mitochondria.回复:内源性凋亡酶(ENDOG)对脂质代谢的影响可能具有组织依赖性,且可能不需要其从线粒体转位。
Nat Commun. 2024 Aug 21;15(1):7122. doi: 10.1038/s41467-024-51448-w.
3
Overexpression of SOD1 in transgenic rats attenuates nuclear translocation of endonuclease G and apoptosis after spinal cord injury.超氧化物歧化酶1在转基因大鼠中的过表达可减轻脊髓损伤后核酸内切酶G的核转位及细胞凋亡。
J Neurotrauma. 2006 May;23(5):595-603. doi: 10.1089/neu.2006.23.595.
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Mitochondrial BNIP3 upregulation precedes endonuclease G translocation in hippocampal neuronal death following oxygen-glucose deprivation.在氧糖剥夺后海马神经元死亡过程中,线粒体BNIP3的上调先于核酸内切酶G易位。
BMC Neurosci. 2009 Sep 8;10:113. doi: 10.1186/1471-2202-10-113.
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Reactive oxygen species-dependent EndoG release mediates cisplatin-induced caspase-independent apoptosis in human head and neck squamous carcinoma cells.活性氧依赖性的EndoG释放介导顺铂诱导的人头颈鳞状癌细胞中的非半胱天冬酶依赖性凋亡。
Int J Cancer. 2008 Feb 1;122(3):672-80. doi: 10.1002/ijc.23158.
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Endonuclease G is a novel determinant of cardiac hypertrophy and mitochondrial function.核酸内切酶 G 是心脏肥大和线粒体功能的一个新决定因素。
Nature. 2011 Oct 5;478(7367):114-8. doi: 10.1038/nature10490.
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The proapoptotic protein BNIP3 interacts with VDAC to induce mitochondrial release of endonuclease G.促凋亡蛋白BNIP3与电压依赖性阴离子通道相互作用,诱导核酸内切酶G从线粒体释放。
PLoS One. 2014 Dec 1;9(12):e113642. doi: 10.1371/journal.pone.0113642. eCollection 2014.
8
Early nuclear translocation of endonuclease G and subsequent DNA fragmentation after transient focal cerebral ischemia in mice.小鼠短暂性局灶性脑缺血后核酸内切酶G的早期核转位及随后的DNA片段化
Neurosci Lett. 2005 Sep 23;386(1):23-7. doi: 10.1016/j.neulet.2005.05.058.
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AIF and endoG translocation in noise exposure induced hair cell death.噪声暴露诱导毛细胞死亡过程中凋亡诱导因子(AIF)和内切核酸酶G(endoG)的转位
Hear Res. 2006 Jan;211(1-2):85-95. doi: 10.1016/j.heares.2005.10.004. Epub 2005 Nov 23.
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EndoG links Bnip3-induced mitochondrial damage and caspase-independent DNA fragmentation in ischemic cardiomyocytes.EndoG 介导 Bnip3 诱导的缺血性心肌细胞中线粒体损伤和 Caspase 非依赖性 DNA 片段化。
PLoS One. 2011 Mar 17;6(3):e17998. doi: 10.1371/journal.pone.0017998.

本文引用的文献

1
The biological function of cytoplasm-translocated ENDOG (endonuclease G).细胞质易位 ENDOG(核酸内切酶 G)的生物学功能。
Autophagy. 2024 Feb;20(2):445-447. doi: 10.1080/15548627.2023.2271750. Epub 2024 Jan 25.
2
Cytoplasmic Endonuclease G promotes nonalcoholic fatty liver disease via mTORC2-AKT-ACLY and endoplasmic reticulum stress.细胞质核酸内切酶 G 通过 mTORC2-AKT-ACLY 和内质网应激促进非酒精性脂肪性肝病。
Nat Commun. 2023 Oct 4;14(1):6201. doi: 10.1038/s41467-023-41757-x.
3
Disruption of mitochondrial dynamics triggers muscle inflammation through interorganellar contacts and mitochondrial DNA mislocation.
线粒体动力学的破坏通过细胞器间接触和线粒体 DNA 错位触发肌肉炎症。
Nat Commun. 2023 Jan 6;14(1):108. doi: 10.1038/s41467-022-35732-1.
4
Endonuclease G promotes autophagy by suppressing mTOR signaling and activating the DNA damage response.核酸内切酶 G 通过抑制 mTOR 信号通路和激活 DNA 损伤反应促进自噬。
Nat Commun. 2021 Jan 20;12(1):476. doi: 10.1038/s41467-020-20780-2.
5
Involvement of the mitochondrial nuclease EndoG in the regulation of cell proliferation through the control of reactive oxygen species.线粒体核酸内切酶 EndoG 通过控制活性氧参与细胞增殖的调控。
Redox Biol. 2020 Oct;37:101736. doi: 10.1016/j.redox.2020.101736. Epub 2020 Sep 24.
6
Cardiomyocyte hypertrophy induced by Endonuclease G deficiency requires reactive oxygen radicals accumulation and is inhibitable by the micropeptide humanin.Endonuclease G 缺乏诱导的心肌细胞肥大需要活性氧自由基的积累,并且可以被微肽人促胰岛素抑制。
Redox Biol. 2018 Jun;16:146-156. doi: 10.1016/j.redox.2018.02.021. Epub 2018 Mar 1.
7
EndoG Knockout Mice Show Increased Brown Adipocyte Recruitment in White Adipose Tissue and Improved Glucose Homeostasis.EndoG基因敲除小鼠白色脂肪组织中棕色脂肪细胞募集增加,葡萄糖稳态得到改善。
Endocrinology. 2016 Oct;157(10):3873-3887. doi: 10.1210/en.2015-1334. Epub 2016 Aug 22.
8
Mitochondrial DNA stress primes the antiviral innate immune response.线粒体DNA应激引发抗病毒先天性免疫反应。
Nature. 2015 Apr 23;520(7548):553-7. doi: 10.1038/nature14156. Epub 2015 Feb 2.
9
Endonuclease G is a novel determinant of cardiac hypertrophy and mitochondrial function.核酸内切酶 G 是心脏肥大和线粒体功能的一个新决定因素。
Nature. 2011 Oct 5;478(7367):114-8. doi: 10.1038/nature10490.
10
Switch from caspase-dependent to caspase-independent death during heart development: essential role of endonuclease G in ischemia-induced DNA processing of differentiated cardiomyocytes.心脏发育过程中从半胱天冬酶依赖性死亡向半胱天冬酶非依赖性死亡的转变:核酸内切酶G在缺血诱导的分化心肌细胞DNA处理中的重要作用。
J Biol Chem. 2006 Aug 11;281(32):22943-52. doi: 10.1074/jbc.M601025200. Epub 2006 Jun 5.