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相似文献

1
Expression of Concern to: Diet restriction inhibits apoptosis and HMGB1 oxidation and promotes inflammatory cell recruitment during acetaminophen hepatoxicity.致关注函:饮食限制在对乙酰氨基酚肝毒性期间抑制细胞凋亡和高迁移率族蛋白B1氧化,并促进炎症细胞募集。
Mol Med. 2020 Jan 30;26(1):13. doi: 10.1186/s10020-020-0140-z.
2
Expression of Concern to: The α7 nicotine acetylcholine receptor agonist GTS-21 improves bacterial clearance in mice by restoring hyperoxia-compromised macrophage function.关注内容:α7烟碱型乙酰胆碱受体激动剂GTS-21通过恢复高氧损伤的巨噬细胞功能改善小鼠细菌清除能力。
Mol Med. 2020 Feb 3;26(1):16. doi: 10.1186/s10020-020-0143-9.
3
Diet restriction inhibits apoptosis and HMGB1 oxidation and promotes inflammatory cell recruitment during acetaminophen hepatotoxicity.饮食限制可抑制细胞凋亡和高迁移率族蛋白 B1 的氧化,并促进对乙酰氨基酚肝毒性时炎症细胞的募集。
Mol Med. 2010 Nov-Dec;16(11-12):479-90. doi: 10.2119/molmed.2010.00126. Epub 2010 Aug 27.
4
Retraction Note: Diet restriction inhibits apoptosis and HMGB1 oxidation and promotes inflammatory cell recruitment during acetaminophen hepatotoxicity.撤稿说明:在对乙酰氨基酚肝毒性过程中,饮食限制可抑制细胞凋亡和高迁移率族蛋白B1(HMGB1)氧化,并促进炎性细胞募集。
Mol Med. 2020 Dec 30;26(1):130. doi: 10.1186/s10020-020-00262-3.
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RETRACTED: Molecular forms of HMGB1 and keratin-18 as mechanistic biomarkers for mode of cell death and prognosis during clinical acetaminophen hepatotoxicity.撤回:HMGB1 和角蛋白-18 的分子形式作为细胞死亡方式的机制生物标志物和临床对乙酰氨基酚肝毒性预后。
J Hepatol. 2012 May;56(5):1070-1079. doi: 10.1016/j.jhep.2011.12.019. Epub 2012 Jan 17.
6
Characterization and Quantification of Oxidized High Mobility Group Box 1 Proteoforms Secreted from Hepatocytes by Toxic Levels of Acetaminophen.乙酰氨基酚毒性水平诱导的肝细胞分泌的氧化高迁移率族蛋白 B1 蛋白形式的特征描述和定量。
Chem Res Toxicol. 2022 Oct 17;35(10):1893-1902. doi: 10.1021/acs.chemrestox.2c00161. Epub 2022 Aug 3.
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miR-30b-5p releases HMGB1 via UBE2D2/KAT2B/HMGB1 pathway to promote pro-inflammatory polarization and recruitment of macrophages.miR-30b-5p 通过 UBE2D2/KAT2B/HMGB1 通路释放 HMGB1,以促进促炎极化和巨噬细胞的募集。
Atherosclerosis. 2021 May;324:38-45. doi: 10.1016/j.atherosclerosis.2021.02.016. Epub 2021 Feb 26.
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Oxidation of HMGB1 Is a Dynamically Regulated Process in Physiological and Pathological Conditions.HMGB1 的氧化是生理和病理条件下一个动态调节的过程。
Front Immunol. 2020 Jun 24;11:1122. doi: 10.3389/fimmu.2020.01122. eCollection 2020.
9
High-mobility group box-1 protein and keratin-18, circulating serum proteins informative of acetaminophen-induced necrosis and apoptosis in vivo.高迁移率族蛋白 B1 与角蛋白 18:能反映体内对乙酰氨基酚诱导坏死和凋亡的循环血清蛋白。
Toxicol Sci. 2009 Dec;112(2):521-31. doi: 10.1093/toxsci/kfp235. Epub 2009 Sep 25.
10
Redox modification of cysteine residues regulates the cytokine activity of high mobility group box-1 (HMGB1).半胱氨酸残基的氧化还原修饰调节高迁移率族蛋白 B1(HMGB1)的细胞因子活性。
Mol Med. 2012 Mar 30;18(1):250-9. doi: 10.2119/molmed.2011.00389.

本文引用的文献

1
Diet restriction inhibits apoptosis and HMGB1 oxidation and promotes inflammatory cell recruitment during acetaminophen hepatotoxicity.饮食限制可抑制细胞凋亡和高迁移率族蛋白 B1 的氧化,并促进对乙酰氨基酚肝毒性时炎症细胞的募集。
Mol Med. 2010 Nov-Dec;16(11-12):479-90. doi: 10.2119/molmed.2010.00126. Epub 2010 Aug 27.

致关注函:饮食限制在对乙酰氨基酚肝毒性期间抑制细胞凋亡和高迁移率族蛋白B1氧化,并促进炎症细胞募集。

Expression of Concern to: Diet restriction inhibits apoptosis and HMGB1 oxidation and promotes inflammatory cell recruitment during acetaminophen hepatoxicity.

作者信息

Antoine Daniel James, Williams Dominic P, Kipar Anja, Laverty Hugh, Park B Kevin

机构信息

Medical Research Council Centre for Drug Safety Science, Liverpool, UK.

Department of Pharmacology and Therapeutics, Institute for Translational Medicine, Liverpool, UK.

出版信息

Mol Med. 2020 Jan 30;26(1):13. doi: 10.1186/s10020-020-0140-z.

DOI:10.1186/s10020-020-0140-z
PMID:32000658
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6993424/
Abstract

The Editors-in-Chief would like to alert readers that this article [1] is part of an investigation being conducted by the journal following the conclusions of an institutional enquiry at the University of Liverpool with respect to the quantitative mass spectrometry-generated results regarding acetylated and redox-modified HMGB1.

摘要

主编们特此提醒读者,本文[1]是该期刊在利物浦大学就定量质谱法生成的乙酰化和氧化还原修饰的高迁移率族蛋白B1(HMGB1)相关结果进行机构调查后所开展的一项调查的一部分。