SQOR

更新于：2025-05-07

基本信息

别名

CGI-44、SQOR、SQR

+ [4]

简介

Catalyzes the oxidation of hydrogen sulfide with the help of a quinone, such as ubiquinone-10, giving rise to thiosulfate and ultimately to sulfane (molecular sulfur) atoms. Requires an additional electron acceptor; can use sulfite, sulfide or cyanide (in vitro) (PubMed:22852582). It is believed the in vivo electron acceptor is glutathione (PubMed:25225291, PubMed:29715001).

关联

项与 SQOR 相关的药物

STI1

靶点

SQOR

作用机制

SQOR inhibitors

在研机构

Drexel University

原研机构

Drexel University

在研适应症

射血分数降低的心力衰竭

非在研适应症-

最高研发阶段临床前

首次获批国家/地区-

首次获批日期1800-01-20

100 项与 SQOR 相关的临床结果

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100 项与 SQOR 相关的转化医学

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0 项与 SQOR 相关的专利（医药）

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304

项与 SQOR 相关的文献（医药）

2025-04-23·Applied and Environmental Microbiology

Overexpression of sulfide:quinone reductase (SQR) in Acidithiobacillus ferrooxidans enhances sulfur, pyrite, and pyrrhotite oxidation

Article

作者: Jung, Heejung ; Banta, Scott ; Inaba, Yuta

ABSTRACT Hydrogen sulfide is produced during the dissolution of some sulfidic minerals and during the microbial metabolism of reduced sulfur compounds. The sulfide:quinone reductase (SQR) enzyme is able to oxidize H 2 S, and the bioleaching cells Acidithiobacillus ferrooxidans have two SQR genes, only one of which has been characterized. We cloned and overexpressed the two SQR genes in A. ferrooxidans and show that they both have SQR activity. Both AFE_0267 and AFE_1792 are active under anaerobic conditions, but only AFE_1792 is active under aerobic conditions. The effect of the SQR overexpression and the expression of related genes on sulfur metabolism was investigated. The overexpression of SQR improved cell growth and sulfur oxidation, suggesting enhanced SQR activity led to a reduction in H 2 S toxicity as well as providing additional energy through H 2 S oxidation. Additionally, the impact on the oxidation of pyrite and pyrrhotite was investigated. The rate of oxidation of pyrite by the engineered cells was enhanced, and, furthermore, the rate of pyrrhotite oxidation was more than doubled. IMPORTANCE H 2 S is a toxic sulfur intermediate, and the SQR enzyme has evolved to oxidize H 2 S in A. ferrooxidans . In addition to detoxification, H 2 S oxidation provides energy, and overexpression of SQR enhanced aerobic and anaerobic growth on sulfur. The SQR overexpression also enhanced pyrite and pyrrhotite oxidation, which may facilitate the pyrometallurgical processing of a number of critical materials including copper, nickel, and the platinum group metals.

2025-04-01·Advanced Science

Deletion of Pyruvate Carboxylase in Tubular Epithelial Cell Promotes Renal Fibrosis by Regulating SQOR/cGAS/STING‐Mediated Glycolysis

Article

作者: Yin, Hongling ; Yuan, Qiongjing ; Xie, Yanyun ; Zeng, Jianhua ; Peng, Zhangzhe ; Tao, Lijian ; Han, Yuanyuan ; Huang, Hao ; Xiong, Yiwei ; Zhang, Yan ; Huang, Ling ; Cheng, Jiawei ; Wang, Songkai ; Meng, Jie ; He, Xin

AbstractRenal fibrosis is a common pathway involved in the progression of various chronic kidney diseases to end‐stage renal disease. Recent studies show that mitochondrial injury of renal tubular epithelial cells (RTECs) is a crucial pathological foundation for renal fibrosis. However, the underlying regulatory mechanisms remain unclear. Pyruvate carboxylase (PC) is a catalytic enzyme located within the mitochondria that is intricately linked with mitochondrial damage and metabolism. In the present study, the downregulation of PC in various fibrotic animal and human kidney samples is demonstrated. Renal proximal tubule–specific Pcx gene knockout mice (PcxcKO) has significant interstitial fibrosis compared to control mice, with heightened expression of extracellular matrix molecules. This is further demonstrated in a stable PC knock‐out RTEC line. Mechanistically, PC deficiency reduces its interaction with sulfide:quinone oxidoreductase (SQOR), increasing the ubiquitination and degradation of SQOR. This leads to mitochondrial morphological and functional disruption, increased mtDNA release, activation of the cGAS‐STING pathway, and elevated glycolysis levels, and ultimately, promotes renal fibrosis. This study investigates the molecular mechanisms through which PC deficiency induces mitochondrial injury and metabolic reprogramming in RTECs. This study provides a novel theoretical foundation and potential therapeutic targets for the pathogenesis and treatment of renal fibrosis.

2025-02-01·Redox Biology

ASB1 engages with ELOB to facilitate SQOR ubiquitination and H2S homeostasis during spermiogenesis

Article

作者: Zheng, Bo ; Lv, Jinxing ; Gao, Wenxin ; Liu, Mingxi ; Wu, Tiantian ; Shen, Cong ; Xue, Jiajia ; Guo, Yueshuai ; Chen, Xia ; Yu, Jun ; Huang, Xiaoyan

Male infertility, frequently driven by oxidative stress, impacts half of infertile couples globally. Despite its significance, the precise mechanisms governing this process remain elusive. In this study, we demonstrate that ASB1, the substrate recognition subunit of a ubiquitin ligase, is highly expressed in the mouse testis. Mice lacking the Asb1 gene exhibit severe fertility impairment, characterized by oligoasthenoteratozoospermia. Subsequent investigations unveiled that Asb1 knockout (Asb1-KO) mice encountered excessive oxidative stress and decreased hydrogen sulfide (H₂S) levels in their testes, and severe sperm DNA damage. Notably, the compromised fertility and sperm quality in Asb1-KO mice was significantly ameliorated by administering NaHS, a H₂S donor. Mechanistically, ASB1 interacts with ELOB to induce the instability of sulfide-quinone oxidoreductase (SQOR) by enhancing its K48-linked ubiquitination on residues K207 and K344, consequently triggering proteasomal degradation. This process is crucial for preserving H₂S homeostasis and redox balance. Overall, our findings offer valuable insights into the role of ASB1 during spermiogenesis and propose H₂S supplementation as a promising therapeutic approach for oxidative stress-related male infertility.

项与 SQOR 相关的新闻（医药）

2022-09-28

·中国生物技术网

mLife | 深海硫酸盐还原菌可通过代谢硫代硫酸钠形成单质硫

中国科学院海洋研究所孙超岷研究员团队的文章“A deep‐sea sulfate‐reducing bacterium generates zero‐valent sulfur via metabolizing thiosulfate”于2022年9月23日在mLife 正式上线。该研究团队基于从南海冷泉中获得的硫酸盐还原菌及深海原位条件下该菌代谢不同硫源等开展了实验，发现了南海冷泉中硫酸盐还原菌能够通过代谢硫代硫酸钠形成单质硫，为研究我国南海冷泉广泛分布单质硫的成因提供了新思路。背景介绍单质硫是硫地球生物化学循环中的重要中间体。我国科研人员基于拉曼光谱检测到南海冷泉环境中单质硫含量丰富，但其形成原因尚不清晰。前期的研究成果表明，硫氧化菌是深海环境中单质硫形成的重要贡献者。然而，在深海冷泉环境中广泛分布的硫酸盐还原菌是否会介导单质硫的形成却鲜有报道。科学发现借助“科学号”科考船2018年南海冷泉航次获得的样品，孙超岷研究团队分离培养了一株典型硫酸盐还原菌Oceanidesulfovibrio marinus CS1。结合拉曼光谱及扫描电镜结果证实该硫酸盐还原菌能通过代谢硫代硫酸钠形成单质硫；结合蛋白组学及蛋白体外表达和功能分析等手段证实硫代硫酸盐还原酶(PhsA)及硫化:醌氧化还原酶(SQR)在驱动单质硫形成过程中起到关键作用。在这个过程中，硫代硫酸盐先被PhsA还原生成硫化物，然后硫化物被SQR氧化生成单质硫（图1）。图1 深海硫酸盐还原菌Oceanidesulfovibrio marinus CS1代谢硫代硫酸钠形成单质硫为了验证该硫酸盐还原菌在深海原位是否也能发挥类似的功能，科研人员借助“科学号”科考船2020年的南海冷泉航次，将该硫酸盐还原菌布放在深海冷泉喷口附近并培养了10 天。通过蛋白组学等实验证实：与实验室条件类似，PhsA和SQR的表达显著上调，提示该菌株极有可能在深海冷泉环境中也形成单质硫（图2）。图2 PhsA和SQR的表达在深海原位条件下显著上调值得注意的是，通过宏基因组分析，研究人员发现在南海冷泉不同深度沉积物中的硫酸盐还原菌基因组中phsA和sqr的同源基因广泛存在。考虑到硫酸盐还原菌是深海冷泉环境的一类高丰度微生物，因此，研究人员认为硫酸盐还原菌是介导深海冷泉环境单质硫形成的重要类群。总结展望前期大部分研究主要关注于硫氧化菌对深海环境单质硫形成的贡献，而忽略了硫酸盐还原菌在单质硫形成过程中的作用。本研究从新的视角折射了硫酸盐还原菌在深海环境硫元素循环中的重要地位，提示后期研究需要综合评估其在深海环境单质硫形成中的贡献，并揭示相应分子机制及其对深海硫元素循环的驱动作用。扫码或点击文章左下角查看英文原文https://onlinelibrary-wiley-com.libproxy1.nus.edu.sg/doi/full/10.1002/mlf2.12038引用本论文：Liu R, Shan Y, Xi S, Zhang X, Sun C. A deep‐sea sulfate‐reducing bacterium generates zero‐valent sulfur via metabolizing thiosulfate. mLife. 2022. https://doi-org.libproxy1.nus.edu.sg/10.1002/mlf2.12038

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