Affinage

SQOR

Sulfide:quinone oxidoreductase, mitochondrial · UniProt Q9Y6N5

Round 2 corrected
Length
450 aa
Mass
50.0 kDa
Annotated
2026-04-28
63 papers in source corpus 16 papers cited in narrative 16 extracted findings

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

SQOR is a mitochondrial inner-membrane FAD-containing flavoenzyme that catalyzes the two-electron oxidation of hydrogen sulfide to a persulfide intermediate, transferring electrons to the ubiquinone pool; glutathione and sulfite serve as physiological persulfide acceptors, channeling sulfane sulfur toward thiosulfate production through a conserved three-enzyme mitochondrial sulfide oxidation pathway (PMID:22852582, PMID:25225291, PMID:18494801). By feeding electrons into coenzyme Q, SQOR drives reverse electron transport at complex I to activate AMPK-dependent signaling and elevates ubiquinol levels that suppress ferroptosis independently of GPX4 (PMID:32923620, PMID:41759595). SQOR protein turnover is regulated by ASB1–ELOB-mediated K48-linked ubiquitination at K207 and K344 and is stabilized by physical interaction with pyruvate carboxylase; loss of SQOR causes toxic H2S accumulation, complex IV inhibition, mtDNA release with cGAS–STING activation, and is the basis of a Leigh disease caused by biallelic SQOR variants (PMID:39733518, PMID:39836535, PMID:32160317). SQOR deficiency in colorectal cancer cells disrupts polysulfide homeostasis, impairs proliferation, and reduces tumor growth in xenograft models (PMID:40305883).

Mechanistic history

Synthesis pass · year-by-year structured walk · 8 steps
  1. 1999 High

    Identification of a eukaryotic sulfide:quinone oxidoreductase (HMT2 in fission yeast) established that mitochondria harbor a dedicated FAD-dependent enzyme for H₂S oxidation coupled to quinone reduction, resolving the long-open question of how eukaryotic cells detoxify sulfide.

    Evidence Purified HMT2 protein characterized by cell fractionation, immunocytochemistry, and in vitro enzymatic assay in S. pombe

    PMID:10224084

    Open questions at the time
    • Human ortholog not yet characterized
    • Physiological persulfide acceptor unknown
    • Tissue distribution of activity undefined
  2. 2008 High

    Reconstitution of a complete three-step mitochondrial sulfide oxidation pathway (SQR → sulfur dioxygenase → rhodanese) and kinetic characterization of eukaryotic SQR with site-directed mutagenesis defined the catalytic requirements and pathway topology for sulfide catabolism to thiosulfate.

    Evidence Heterologous expression in yeast, mutagenesis of conserved catalytic residues, and pathway reconstitution in rat liver mitochondria

    PMID:18248458 PMID:18494801

    Open questions at the time
    • Human enzyme kinetics not yet measured
    • Electron acceptor specificity in mammalian membranes unresolved
  3. 2010 High

    Demonstration that SQR activity is tissue-specific in mammals (present in kidney, liver, heart; absent in brain) and that SQR-driven sulfide oxidation produces the first evidence of reverse electron transfer in living cells resolved why neural tissue is uniquely sensitive to sulfide toxicity.

    Evidence Mitochondrial isolation from mouse tissues, SQR activity assay, oxygen consumption and cellular sulfide measurements in HT-29 colonocytes

    PMID:20398623

    Open questions at the time
    • Molecular basis of tissue-specific expression unknown
    • In vivo physiological significance of reverse electron transfer not yet established
  4. 2012 High

    Kinetic and spectroscopic characterization of purified recombinant human SQOR revealed noncovalently bound FAD, a long-wavelength charge-transfer intermediate, and high catalytic efficiency (kcat/Km ~2.9 × 10⁷ M⁻¹ s⁻¹), establishing the molecular properties of the human enzyme and identifying sulfite as a candidate physiological persulfide acceptor.

    Evidence Recombinant human SQOR expressed in E. coli, UV-vis spectroscopy, pre-steady-state kinetics

    PMID:22852582

    Open questions at the time
    • Glutathione not yet tested as persulfide acceptor
    • No structural model of human SQOR available
  5. 2014 High

    Discovery that glutathione serves as the primary persulfide acceptor for human SQOR, generating GSSH, reframed the pathway: the dominant route is H₂S → GSSH → thiosulfate rather than direct sulfite acceptance, and rhodanese functions biosynthetically in thiosulfate formation.

    Evidence In vitro reconstitution with purified enzymes at physiological metabolite concentrations, kinetic modeling

    PMID:25225291

    Open questions at the time
    • Relative contributions of GSH vs sulfite in vivo unresolved
    • Structural basis of persulfide acceptor selectivity unknown
  6. 2020 High

    Genetic epistasis experiments showed SQR-driven electron flow into the Q-pool powers reverse electron transport at complex I to generate superoxide and activate AMPK, establishing a signaling function for sulfide oxidation beyond simple detoxification, and biallelic SQOR mutations were identified as the cause of Leigh disease through toxic H₂S accumulation and complex IV inhibition.

    Evidence SQR, complex I, and AMPK knockouts with mitochondrial membrane potential and superoxide readouts in vivo (ICH model); exome sequencing, spectrophotometric enzyme assay, and western blot in patient tissue

    PMID:32160317 PMID:32923620

    Open questions at the time
    • Whether AMPK activation is direct or secondary to energy stress unclear
    • Full spectrum of SQOR loss-of-function clinical phenotypes not delineated
    • Structural impact of pathogenic variants modeled only in silico
  7. 2024 High

    Identification of ASB1–ELOB as the E3 ligase complex that K48-ubiquitinates SQOR at K207 and K344 for proteasomal degradation defined the first post-translational turnover mechanism for SQOR, linking ubiquitin-mediated SQOR degradation to H₂S homeostasis and male fertility.

    Evidence Reciprocal Co-IP, ubiquitination site mutagenesis, ASB1 knockout mice with NaHS rescue

    PMID:39733518

    Open questions at the time
    • Whether other E3 ligases also target SQOR unknown
    • Signals triggering ASB1-mediated degradation not defined
  8. 2025 High

    Multiple studies converged to show that SQOR loss has broad downstream consequences: pyruvate carboxylase stabilizes SQOR protein and its absence triggers ubiquitination, mtDNA release, cGAS–STING activation and renal fibrosis; SQOR-generated ubiquinol suppresses ferroptosis independently of GPX4 via the ATF4/CTH/SQOR axis; and SQOR deficiency in colorectal cancer cells disrupts polysulfide balance, impairs proliferation, and reduces xenograft tumor growth.

    Evidence PC–SQOR Co-IP and PC-KO mice; SQOR KD/OE with CoQ10H2, lipid peroxidation, and genetic epistasis; SQOR-KO HCT116 xenografts with metabolomics

    PMID:39836535 PMID:40305883 PMID:41759595

    Open questions at the time
    • Whether PC–SQOR interaction is direct or complex-mediated not fully resolved
    • ALDOA downregulation mechanism upon SQOR loss requires independent confirmation
    • Relative importance of ubiquinol production vs H₂S clearance in ferroptosis protection unclear

Open questions

Synthesis pass · forward-looking unresolved questions
  • A high-resolution structure of human SQOR, the regulatory signals controlling SQOR expression across tissues, the in vivo contribution of microbial H₂S to SQOR-dependent host bioenergetics, and the full clinical spectrum of SQOR deficiency remain to be established.
  • No crystal or cryo-EM structure of human SQOR
  • Transcriptional and epigenetic regulation largely uncharacterized
  • Tissue-specific conditional knockouts beyond intestine not fully explored

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0016491 oxidoreductase activity 7
Localization
GO:0005739 mitochondrion 7
Pathway
R-HSA-1430728 Metabolism 4 R-HSA-5357801 Programmed Cell Death 2 R-HSA-1643685 Disease 1
Partners
ASB1ELOBPC

Evidence

Reading pass · 16 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
1999 The fission yeast ortholog of SQOR, HMT2, was identified as a mitochondrial sulfide:quinone oxidoreductase. HMT2 protein localizes to mitochondria (cell fractionation and immunocytochemistry), binds FAD, and catalyzes quinone (CoQ2) reduction by sulfide in vitro. Loss of hmt2+ causes abnormal sulfide accumulation and cadmium hypersensitivity. Genetic complementation, cell fractionation, immunocytochemistry, in vitro enzymatic assay with purified protein The Journal of biological chemistry High 10224084
2008 Arenicola marina SQR expressed in Saccharomyces cerevisiae mitochondria catalyzes sulfide oxidation using decyl-ubiquinone as electron acceptor (Km H2S = 23 µM, Km DUQ = 6.4 µM) and requires an S0 acceptor (cyanide, producing thiocyanate; or thioredoxin + sulfite). Site-directed mutagenesis of six conserved amino acids (essential in bacterial SQR) abolished activity, implicating them in the eukaryotic catalytic mechanism. Heterologous expression in yeast, affinity purification, in vitro enzymatic assay, site-directed mutagenesis The FEBS journal High 18248458
2008 A mitochondrial pathway for sulfide oxidation to thiosulfate was defined in rat liver and Arenicola marina: (1) membrane-bound SQR converts sulfide to persulfides and transfers electrons to the ubiquinone pool; (2) a sulfur dioxygenase oxidizes one persulfide to sulfite; (3) rhodanese transfers a second persulfide to sulfite, yielding thiosulfate. Rhodanese thus functions as a sulfurtransferase in this pathway. Mitochondrial fractionation, enzymatic assays for each step, reconstitution of pathway The FEBS journal High 18494801
2010 SQR activity is present in mitochondria from mouse kidney, liver, and heart but absent from brain mitochondria and neuroblastoma cells, explaining neural tissue's greater sulfide sensitivity. SQR oxidation of sulfide takes precedence over complex I (demonstrated by competition assays). In colonocyte HT-29 cells, sulfide oxidation via SQR provides the first demonstrated example of reverse electron transfer in living cells. Mitochondrial isolation, SQR activity assay, oxygen consumption measurements, cellular sulfide concentration monitoring Biochimica et biophysica acta High 20398623
2012 Human SQOR expressed in E. coli contains noncovalently bound FAD and catalyzes two-electron oxidation of H2S to sulfane sulfur (S0) using CoQ1 as electron acceptor. FAD is reduced via a long-wavelength-absorbing intermediate (λmax = 673 nm). Sulfite, cyanide, or sulfide can serve as S0 acceptors, producing thiosulfate, thiocyanate, or H2S2, respectively. Sulfite is proposed as the physiological acceptor (kcat/Km,H2S = 2.9 × 10^7 M−1 s−1 at pH 7.5). Recombinant protein expression, in vitro enzymatic assay, UV-visible spectroscopy, pre-steady-state kinetics Biochemistry High 22852582
2014 Human SQR uses glutathione (in addition to sulfite) as a persulfide acceptor, generating glutathione persulfide (GSSH) as the primary intermediate. Rhodanese preferentially synthesizes rather than utilizes thiosulfate. Kinetic data and simulations at physiological metabolite concentrations support pathway organization: H2S → SQR → GSSH → thiosulfate or sulfite. In vitro enzymatic assays, kinetic measurements, mathematical modeling/simulation The Journal of biological chemistry High 25225291
2014 Acidithiobacillus ferrooxidans SQR contains a non-covalent FAD cofactor. Cys160, Cys356, and His198 are critical for catalytic activity (variants show greatly reduced DUQ reduction), while Cys128 and His132 are not essential for the reductive half-reaction. EPR reveals a neutral flavin semiquinone; the Cys160Ala variant accumulates a semiquinone consistent with a Cys356–S(γ)–S–C(4A)–FAD adduct intermediate. FAD Em = −139 mV at pH 7.0. Site-directed mutagenesis, steady-state and pre-steady-state kinetics, EPR spectroscopy, potentiometric titration Archives of biochemistry and biophysics High 25303790
2016 S. aureus SQR (type I flavoprotein) catalyzes two-electron oxidation of Na2S to sulfane sulfur using FAD and a quinone acceptor. The reaction requires a C167–C344 disulfide in the resting enzyme, with a C344 persulfide intermediate confirmed by mass spectrometry of sulfide-reacted enzyme. Cyanide, sulfite, or CoA serve as S0 acceptors in vitro; with CstB (a persulfide dioxygenase), CoASSH and thiosulfate are produced from sulfide. Δsqr strains show elevated CoASSH and inorganic tetrasulfide. In vitro enzymatic assay, mass spectrometry of reaction intermediates, genetic deletion, sulfur metabolite profiling Biochemistry High 27806570
2020 SQR-mediated H2S oxidation drives reverse electron transport (RET) at mitochondrial complex I, repurposing complex I toward superoxide production. This superoxide-dependent mitochondrial uncoupling activates AMPK downstream. Deletion of SQR, complex I, or AMPK abolishes therapeutic effects of H2S after intracerebral hemorrhage. SQR-induced uncoupling is mechanistically separable from complex IV inhibition by H2S. Genetic deletion (SQR KO, complex I KO, AMPK KO), mitochondrial membrane potential measurements, superoxide detection, AMPK activity assays, in vivo intracerebral hemorrhage model Science advances High 32923620
2020 Pathogenic variants in SQOR (p.Glu213Lys and c.446delT frameshift) cause Leigh disease with complex IV inhibition. p.Glu213Lys disrupts hydrogen bonding with neighboring residues, resulting in severely reduced SQOR protein and enzyme activity measured spectrophotometrically. Sulfide-generating enzyme levels were unchanged, indicating the mechanism is H2S accumulation due to loss of SQOR catabolism, which inhibits complex IV. Exome sequencing, spectrophotometric enzyme activity assay, western blotting, mitochondrial function assay in patient muscle and liver tissue Journal of inherited metabolic disease High 32160317
2024 ASB1 (substrate recognition subunit of a ubiquitin E3 ligase) interacts with ELOB to promote K48-linked ubiquitination of SQOR at residues K207 and K344, leading to proteasomal degradation of SQOR. ASB1 knockout in mice causes elevated H2S, oxidative stress, and sperm DNA damage; fertility defects are rescued by NaHS (H2S donor), establishing SQOR degradation as the mechanism linking ASB1 to H2S homeostasis. Co-immunoprecipitation, ubiquitination assay, site-directed mutagenesis of ubiquitination sites, ASB1 knockout mice, NaHS rescue experiment, western blotting Redox biology High 39733518
2025 Pyruvate carboxylase (PC) physically interacts with SQOR; PC deficiency reduces this interaction, increasing ubiquitination and proteasomal degradation of SQOR. Loss of SQOR leads to mitochondrial morphological and functional disruption, increased mtDNA release, activation of the cGAS-STING pathway, elevated glycolysis, and renal fibrosis. Co-immunoprecipitation (PC-SQOR interaction), ubiquitination assay, PC knockout mice (PcxcKO) and stable KO cell line, cGAS-STING pathway assays, mitochondrial morphology imaging Advanced science High 39836535
2025 SQOR knockdown in HCT116 colorectal cancer cells disrupts polysulfide homeostasis, diminishes mitochondrial function, impairs proliferation, and triggers early apoptosis. SQR KO reduces tumor growth in xenograft mice. Metabolomic analysis reveals reprogramming of glycolysis at the fructose-1,6-bisphosphate degradation step; western blot and enzymatic assays confirm decreased ALDOA levels and activity as the downstream effector. SQOR knockout, tumor xenograft model, metabolomics, western blotting, enzymatic activity assay for ALDOA Redox biology Medium 40305883
2025 SQOR mediates ferroptosis resistance by using hydrogen selenide to reduce ubiquinone, thereby elevating ubiquinol levels and suppressing lipid peroxidation independently of GPX4. In the ATF4/CTH/SQOR axis, ATF4 drives CTH expression to generate H2S, which SQOR converts to CoQ10H2 (ubiquinol); SQOR-deficient cells cannot rescue CoQ10H2 or prevent ferroptosis even with elevated H2S or CTH overexpression. SQOR knockdown/overexpression, CoQ10H2 measurement, lipid peroxidation assay (MDA), ATF4/CTH/SQOR genetic epistasis, alternative oxidase overexpression Biochemical pharmacology Medium 41759595
2023 SQOR interacts with the C9-ALS dipeptide repeat protein GA50 (identified by yeast two-hybrid). SQOR knockdown in HMC3 microglia activates the NLRP3 inflammasome by upregulating intracellular ROS and promoting cytoplasmic escape of mitochondrial DNA. The small molecule irisflorentin blocks the SQOR–GA50 interaction and inhibits NLRP3 inflammasome activity. Yeast two-hybrid, SQOR knockdown, ROS measurement, mtDNA cytoplasmic escape assay, NLRP3 inflammasome activity assay, small-molecule inhibitor competition Antioxidants Medium 37891975
2025 SQOR deficiency confined to murine intestinal epithelial cells perturbs colon bioenergetics in a manner reversed by antibiotics, establishing that microbial H2S is a significant local contributor to host mitochondrial energy metabolism via SQOR. Combined intestinal SQOR deficiency and high dietary methionine disrupts colon architecture, alters microbiome composition, increases systemic thiosulfate (H2S oxidation biomarker), raises ketone bodies, reduces locomotor activity, and decreases ventricular volume associated with lower aquaporin 1. Intestinal epithelial cell-specific SQOR knockout mice, antibiotic treatment, brain MRI, aquaporin 1 western blot, serum metabolomics bioRxivpreprint Medium bio_10.1101_2025.04.09.647962

Source papers

Stage 0 corpus · 63 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2002 Generation and initial analysis of more than 15,000 full-length human and mouse cDNA sequences. Proceedings of the National Academy of Sciences of the United States of America 1479 12477932
2017 Architecture of the human interactome defines protein communities and disease networks. Nature 1085 28514442
2015 A human interactome in three quantitative dimensions organized by stoichiometries and abundances. Cell 1015 26496610
2021 Dual proteome-scale networks reveal cell-specific remodeling of the human interactome. Cell 705 33961781
2012 A census of human soluble protein complexes. Cell 689 22939629
2011 Phylogenetic-based propagation of functional annotations within the Gene Ontology consortium. Briefings in bioinformatics 656 21873635
2006 Hsp90 cochaperone Aha1 downregulation rescues misfolding of CFTR in cystic fibrosis. Cell 517 17110338
2011 Mapping the NPHP-JBTS-MKS protein network reveals ciliopathy disease genes and pathways. Cell 507 21565611
1994 Oligo-capping: a simple method to replace the cap structure of eukaryotic mRNAs with oligoribonucleotides. Gene 492 8125298
2004 The status, quality, and expansion of the NIH full-length cDNA project: the Mammalian Gene Collection (MGC). Genome research 438 15489334
2008 Three enzymatic activities catalyze the oxidation of sulfide to thiosulfate in mammalian and invertebrate mitochondria. The FEBS journal 415 18494801
2005 Diversification of transcriptional modulation: large-scale identification and characterization of putative alternative promoters of human genes. Genome research 409 16344560
2000 Identification of novel human genes evolutionarily conserved in Caenorhabditis elegans by comparative proteomics. Genome research 392 10810093
2012 Interpreting cancer genomes using systematic host network perturbations by tumour virus proteins. Nature 319 22810586
2012 Novel genetic loci identified for the pathophysiology of childhood obesity in the Hispanic population. PloS one 312 23251661
2021 Quantitative high-confidence human mitochondrial proteome and its dynamics in cellular context. Cell metabolism 239 34800366
2012 Human sulfide:quinone oxidoreductase catalyzes the first step in hydrogen sulfide metabolism and produces a sulfane sulfur metabolite. Biochemistry 237 22852582
2016 Mitochondrial Protein Interaction Mapping Identifies Regulators of Respiratory Chain Function. Molecular cell 220 27499296
2010 Oxidation of hydrogen sulfide remains a priority in mammalian cells and causes reverse electron transfer in colonocytes. Biochimica et biophysica acta 219 20398623
2014 Organization of the human mitochondrial hydrogen sulfide oxidation pathway. The Journal of biological chemistry 215 25225291
2019 H4K20me0 recognition by BRCA1-BARD1 directs homologous recombination to sister chromatids. Nature cell biology 162 30804502
2018 Identification of phagocytosis regulators using magnetic genome-wide CRISPR screens. Nature genetics 146 30397336
2022 PHGDH Inhibits Ferroptosis and Promotes Malignant Progression by Upregulating SLC7A11 in Bladder Cancer. International journal of biological sciences 143 36147463
2007 Large-scale identification of c-MYC-associated proteins using a combined TAP/MudPIT approach. Cell cycle (Georgetown, Tex.) 127 17314511
2016 Response of tomato wilt pathogen Ralstonia solanacearum to the volatile organic compounds produced by a biocontrol strain Bacillus amyloliquefaciens SQR-9. Scientific reports 123 27103342
2007 Toward a confocal subcellular atlas of the human proteome. Molecular & cellular proteomics : MCP 114 18029348
2021 A protein interaction landscape of breast cancer. Science (New York, N.Y.) 111 34591612
2019 Systematic bromodomain protein screens identify homologous recombination and R-loop suppression pathways involved in genome integrity. Genes & development 110 31753913
2021 FBW7 suppresses ovarian cancer development by targeting the N6-methyladenosine binding protein YTHDF2. Molecular cancer 106 33658012
1999 A fission yeast gene for mitochondrial sulfide oxidation. The Journal of biological chemistry 82 10224084
2011 Beta-HPV 5 and 8 E6 promote p300 degradation by blocking AKT/p300 association. PLoS pathogens 81 21901101
2020 SQR mediates therapeutic effects of H2S by targeting mitochondrial electron transport to induce mitochondrial uncoupling. Science advances 77 32923620
2008 Sulfide : quinone oxidoreductase (SQR) from the lugworm Arenicola marina shows cyanide- and thioredoxin-dependent activity. The FEBS journal 68 18248458
2011 Biocontrol of Rhizoctonia solani damping-off disease in cucumber with Bacillus pumilus SQR-N43. Microbiological research 67 21775112
2020 Pathogenic variants in SQOR encoding sulfide:quinone oxidoreductase are a potentially treatable cause of Leigh disease. Journal of inherited metabolic disease 52 32160317
2016 Staphylococcus aureus sqr Encodes a Type II Sulfide:Quinone Oxidoreductase and Impacts Reactive Sulfur Speciation in Cells. Biochemistry 42 27806570
2018 Taxonomic distribution, structure/function relationship and metabolic context of the two families of sulfide dehydrogenases: SQR and FCSD. Biochimica et biophysica acta. Bioenergetics 39 29684324
2008 Molecular analysis of the diversity of the sulfide : quinone reductase (sqr) gene in sediment environments. Microbiology (Reading, England) 34 18832317
2010 Growth, Fe3+ reductase activity, and siderophore production by Paenibacillus polymyxa SQR-21 under differential iron conditions. Current microbiology 30 20358373
2024 ASB1 engages with ELOB to facilitate SQOR ubiquitination and H2S homeostasis during spermiogenesis. Redox biology 18 39733518
2014 Complete Genome Sequence of Paenibacillus polymyxa SQR-21, a Plant Growth-Promoting Rhizobacterium with Antifungal Activity and Rhizosphere Colonization Ability. Genome announcements 17 24723719
2013 Promoter analysis and transcription regulation of fus gene cluster responsible for fusaricidin synthesis of Paenibacillus polymyxa SQR-21. Applied microbiology and biotechnology 16 24072159
2025 Deletion of Pyruvate Carboxylase in Tubular Epithelial Cell Promotes Renal Fibrosis by Regulating SQOR/cGAS/STING-Mediated Glycolysis. Advanced science (Weinheim, Baden-Wurttemberg, Germany) 15 39836535
2015 Association of the I264T variant in the sulfide quinone reductase-like (SQRDL) gene with osteoporosis in Korean postmenopausal women. PloS one 14 26258864
2015 Sulfide exposure results in enhanced sqr transcription through upregulating the expression and activation of HSF1 in echiuran worm Urechis unicinctus. Aquatic toxicology (Amsterdam, Netherlands) 13 26675369
2014 Characterization of the kinetics and electron paramagnetic resonance spectroscopic properties of Acidithiobacillus ferrooxidans sulfide:quinone oxidoreductase (SQR). Archives of biochemistry and biophysics 13 25303790
2023 Glycine-Alanine Dipeptide Repeat Protein from C9-ALS Interacts with Sulfide Quinone Oxidoreductase (SQOR) to Induce the Activity of the NLRP3 Inflammasome in HMC3 Microglia: Irisflorentin Reverses This Interaction. Antioxidants (Basel, Switzerland) 12 37891975
2018 A novel transcription factor Rwdd1 and its SUMOylation inhibit the expression of sqr, a key gene of mitochondrial sulfide metabolism in Urechis unicinctus. Aquatic toxicology (Amsterdam, Netherlands) 10 30278355
2021 A novel transcription factor MRPS27 up-regulates the expression of sqr, a key gene of mitochondrial sulfide metabolism in echiuran worm Urechis unicinctus. Comparative biochemistry and physiology. Toxicology & pharmacology : CBP 5 33549829
2016 NF1, Sp1 and HSF1 are synergistically involved in sulfide-induced sqr activation in echiuran worm Urechis unicinctus. Aquatic toxicology (Amsterdam, Netherlands) 5 27070384
2025 SQOR as a metabolic rheostat of H2S: structure, redox homeostasis, and disease therapy. Frontiers in cell and developmental biology 4 41210256
2025 Comprehensive analysis of SQOR involvement in ferroptosis resistance of pancreatic ductal adenocarcinoma in hypoxic environments. Frontiers in immunology 3 40375994
2024 Hydrogen sulfide maintains mitochondrial homeostasis and regulates ganoderic acids biosynthesis by SQR under heat stress in Ganoderma lucidum. Redox biology 3 38865903
2017 Changes in transcription pattern lead to a marked decrease in COX, CS and SQR activity after the developmental point of the 22(nd) gestational week. Physiological research 3 29137472
2013 The supernatant of Bacillus pumilus SQR-N43 has antifungal activity towards Rhizoctonia solani. Journal of basic microbiology 3 23417338
2025 Overexpression of sulfide:quinone reductase (SQR) in Acidithiobacillus ferrooxidans enhances sulfur, pyrite, and pyrrhotite oxidation. Applied and environmental microbiology 1 40130842
2025 Knockout of the sulfide: quinone oxidoreductase SQR reduces growth of HCT116 tumor xenograft. Redox biology 1 40305883
2025 Promiscuous enzyme SQOR in cellular metabolism and ferroptosis regulation. BMB reports 1 40495478
2007 A scanning tunneling microscopy study of distyrylbenzene on Ag/Ge(111)-(sqr rt of 3 x sqr rt of 3)R30 degrees. Langmuir : the ACS journal of surfaces and colloids 1 17973407
2026 Sodium aescinate induces renal cell ferroptosis through the ATF4/CTH/SQOR axis. Biochemical pharmacology 0 41759595
2025 Comprehensive analysis of bioinformatics identification TST, SQOR and NRDC is mitochondria-related biomarkers of ischemic cerebral apoplexy. Scientific reports 0 40087350
2024 Heterologous expression of sulfur: quinone oxidoreductase (Sqr) to improve Thioalkalivibrio versutus D301 desulfurization performance. Journal of applied microbiology 0 39264044
2001 Efficient removal of sulfide following integration of multiple copies of the sulfide-quinone oxidoreductase gene (sqr) into the Escherichia coli chromosome. Journal of bioscience and bioengineering 0 16233028