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

作者信息

Wang Wenjun, Zhou Qinghua

机构信息

The Sixth Affiliated Hospital of Jinan University (Dongguan Eastern Central Hospital), Jinan University, Dongguan, Guangdong, 523067, China.

The Biomedical Translational Research Institute, Health Science Center (School of Medicine), Jinan University, Guangzhou, Guangdong, 510632, China.

出版信息

Nat Commun. 2024 Aug 21;15(1):7122. doi: 10.1038/s41467-024-51448-w.

DOI:10.1038/s41467-024-51448-w
PMID:39168974
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11339254/
Abstract
摘要
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/04dd/11339254/ad04f2cd74e4/41467_2024_51448_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/04dd/11339254/58df61ec3263/41467_2024_51448_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/04dd/11339254/ad04f2cd74e4/41467_2024_51448_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/04dd/11339254/58df61ec3263/41467_2024_51448_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/04dd/11339254/ad04f2cd74e4/41467_2024_51448_Fig2_HTML.jpg

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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。
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2
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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。
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本文引用的文献

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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.
2
Autophagy restricts mitochondrial DNA damage-induced release of ENDOG (endonuclease G) to regulate genome stability.自噬限制线粒体 DNA 损伤诱导的 ENDOG(核酸内切酶 G)释放以调节基因组稳定性。
Autophagy. 2021 Nov;17(11):3444-3460. doi: 10.1080/15548627.2021.1874209. Epub 2021 Jan 19.
3
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.
4
Picroside II Exerts a Neuroprotective Effect by Inhibiting mPTP Permeability and EndoG Release after Cerebral Ischemia/Reperfusion Injury in Rats.毛兰素 II 通过抑制脑缺血/再灌注损伤后大鼠 mPTP 通透性和内源性核酸酶释放发挥神经保护作用。
J Mol Neurosci. 2018 Jan;64(1):144-155. doi: 10.1007/s12031-017-1012-z. Epub 2017 Dec 18.
5
AKT2 Blocks Nucleus Translocation of Apoptosis-Inducing Factor (AIF) and Endonuclease G (EndoG) While Promoting Caspase Activation during Cardiac Ischemia.AKT2在心肌缺血期间促进半胱天冬酶激活的同时,阻断凋亡诱导因子(AIF)和核酸内切酶G(EndoG)的核转位。
Int J Mol Sci. 2017 Mar 6;18(3):565. doi: 10.3390/ijms18030565.
6
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.
7
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.
8
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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EndoG is dispensable in embryogenesis and apoptosis.EndoG在胚胎发生和细胞凋亡过程中并非必需。
Cell Death Differ. 2006 Jul;13(7):1147-55. doi: 10.1038/sj.cdd.4401787. Epub 2005 Oct 21.
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Generation and characterization of endonuclease G null mice.核酸内切酶G基因敲除小鼠的产生与鉴定
Mol Cell Biol. 2005 Jan;25(1):294-302. doi: 10.1128/MCB.25.1.294-302.2005.