Affinage

GSR

Glutathione reductase, mitochondrial · UniProt P00390

Round 2 corrected
Length
522 aa
Mass
56.3 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

GSR (glutathione reductase) is a homodimeric FAD-dependent oxidoreductase that catalyzes the NADPH-dependent reduction of oxidized glutathione (GSSG) to GSH, maintaining cellular glutathione redox homeostasis critical for antioxidant defense, genomic integrity, and suppression of fibrotic and tumorigenic signaling. Electrons flow from NADPH through the FAD prosthetic group to a redox-active disulfide (Cys-58/Cys-63), with His-467' facilitating disulfide exchange with GSSG; the active-site Cys-63 can be irreversibly oxidized to sulfenic or sulfinic acid by nitric oxide carriers, inactivating the enzyme (PMID:7334521, PMID:6822532, PMID:9546215). GSR cooperates non-redundantly with the thioredoxin reductase system to suppress oxidative DNA damage and cancer malignancy, with GSR specifically required for tumor initiation in murine lung cancer models, while its loss can be partially compensated by upregulation of thioredoxin reductase or the transsulfuration pathway depending on tissue context (PMID:31097586, PMID:28686716, PMID:27117030). GSR deficiency reduces intracellular GSH, elevates ROS, and activates TGF-β/Smad2 signaling to promote epithelial-to-mesenchymal transition, fibroblast activation, and cellular senescence, linking glutathione redox imbalance to pulmonary fibrosis (PMID:40723921).

Mechanistic history

Synthesis pass · year-by-year structured walk · 10 steps
  1. 1981 High

    Determination of the three-dimensional structure of human GSR established it as a homodimeric FAD-containing enzyme with a redox-active disulfide at the active site, providing the structural framework for all subsequent mechanistic studies.

    Evidence X-ray crystallography at 2 Å resolution of human erythrocyte glutathione reductase

    PMID:7334521

    Open questions at the time
    • No reaction intermediates captured at this stage
    • Catalytic mechanism inferred but not demonstrated structurally
  2. 1983 High

    Crystallographic trapping of reaction intermediates resolved the full catalytic cycle — NADPH→FAD→Cys-58/Cys-63 disulfide→GSSG — and identified His-467' as essential for disulfide exchange, answering how electrons traverse the enzyme.

    Evidence X-ray crystallography of multiple reaction intermediates combined with active-site iodoacetamide alkylation

    PMID:6822532

    Open questions at the time
    • Kinetic validation of individual electron-transfer steps not performed in this study
    • Role of conformational dynamics in catalysis not addressed
  3. 1987 High

    Refinement to 1.54 Å resolution revealed that the FAD cofactor and entire active center are exceptionally well-ordered, with the flavin N5 positioned for proton transfer, providing atomic-level detail of cofactor geometry relevant to the reductive half-reaction.

    Evidence X-ray crystallography with restrained least-squares refinement (R-factor 18.6%, 77,690 reflections)

    PMID:3656429

    Open questions at the time
    • No dynamic or solution-state measurements to complement the crystal data
  4. 1998 High

    Crystal structures of GSR complexed with NO-carriers revealed that irreversible oxidation of active-site Cys-63 to sulfenic or sulfinic acid constitutes the mechanism of NO-mediated inactivation, identifying a physiologically relevant mode of enzyme regulation.

    Evidence X-ray crystallography at 1.7 Å of GSNO- and DNIC-[GSH]₂-treated GSR

    PMID:9546215

    Open questions at the time
    • In vivo relevance of NO-mediated GSR inactivation not demonstrated
    • Reversibility or cellular repair of sulfinic acid modification not explored
  5. 2011 High

    Genetic and biochemical work in C. elegans demonstrated that GSR-1 and thioredoxin reductase TRXR-1 function cooperatively to reduce cuticle disulfides during molting, establishing the first in vivo developmental role for glutathione reductase beyond generic antioxidant defense.

    Evidence RNAi knockdown, genetic mutants, exogenous GSH rescue, cuticle disulfide redox measurement in C. elegans

    PMID:21199936

    Open questions at the time
    • Vertebrate developmental role of GSR not addressed
    • Specific cuticle substrates of GSR-1-generated GSH not identified
  6. 2016 High

    Identification of cytoplasmic and mitochondrial GSR-1 isoforms in C. elegans, with only cytoplasmic GSR-1 rescuing embryonic lethality, demonstrated that cytoplasmic glutathione redox homeostasis is the essential compartment-specific function, while mitochondrial GSR-1 contributes to organelle integrity and stress resistance.

    Evidence GFP reporters, isoform-specific rescue, mitochondrial imaging, stress assays in gsr-1 null C. elegans

    PMID:27117030

    Open questions at the time
    • Whether compartment-specific essentiality is conserved in mammals not tested
    • Molecular targets of cytoplasmic GSH that mediate embryonic viability not identified
  7. 2017 Medium

    Gsr knockout mice revealed that the thioredoxin system compensates for GSR loss in the cochlea under basal conditions, demonstrating functional redundancy between the two major disulfide reductase systems in vivo in mammals.

    Evidence Gsr homozygous knockout mouse, ABR, enzyme activity assays for GSR/TrxR/Trx, oxidative damage markers

    PMID:28686716

    Open questions at the time
    • Compensation tested only in cochlea; generalizability to other tissues unknown
    • Whether compensation holds under stress not tested in this study
  8. 2019 High

    Simultaneous deletion of TrxR1 and Gsr in mouse liver caused a ~100-fold increase in DNA damage and dramatically enhanced cancer malignancy, demonstrating that the two antioxidant systems are non-redundant guardians of genomic integrity and tumor suppression.

    Evidence Conditional double knockout in mouse liver, DNA damage quantification, DEN-induced hepatocellular carcinoma model, metabolomics

    PMID:31097586

    Open questions at the time
    • Specific DNA lesion types caused by combined loss not characterized
    • Whether increased malignancy reflects increased initiation, progression, or both not resolved
  9. 2017 Medium

    GSR overexpression conferred chemotherapy resistance in glioblastoma cells by maintaining redox homeostasis, while GSR silencing re-sensitized resistant cells, identifying GSR-mediated GSH maintenance as a druggable determinant of temozolomide and cisplatin resistance.

    Evidence Reciprocal siRNA knockdown and overexpression in glioblastoma cell lines, drug sensitivity, ROS, and GSH quantification

    PMID:29105080

    Open questions at the time
    • No in vivo tumor model validation
    • Downstream effectors of GSR-dependent chemoresistance beyond ROS not identified
  10. 2025 Medium

    GSR deficiency was shown to activate TGF-β/Smad2 signaling through elevated ROS, promoting EMT, fibroblast activation, senescence, and migration — linking glutathione redox imbalance mechanistically to pulmonary fibrosis pathogenesis.

    Evidence GSR siRNA knockdown in A549 and MRC5 cells, GSH/ROS measurements, EMT markers, TGF-β/Smad2 pathway analysis, bleomycin mouse model

    PMID:40723921

    Open questions at the time
    • Whether GSR loss directly activates TGF-β ligand production or sensitizes receptor signaling not distinguished
    • Rescue by GSH supplementation of the fibrotic phenotype not fully demonstrated

Open questions

Synthesis pass · forward-looking unresolved questions
  • Key unresolved questions include whether the compartment-specific essentiality of cytoplasmic versus mitochondrial GSR is conserved in mammals, the precise molecular targets of GSR-maintained GSH that mediate embryonic viability and tumor suppression, and whether NO-mediated inactivation of GSR Cys-63 is a regulated signaling event in vivo.
  • No mammalian isoform-specific rescue experiment reported
  • In vivo physiological relevance of NO-mediated GSR inactivation untested
  • Structural basis for GSR vs TrxR1 non-redundancy in cancer not defined

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0016491 oxidoreductase activity 4 GO:0140657 ATP-dependent activity 1
Localization
GO:0005829 cytosol 2 GO:0005739 mitochondrion 1
Pathway
R-HSA-1430728 Metabolism 4 R-HSA-8953897 Cellular responses to stimuli 4 R-HSA-1643685 Disease 2
Partners
TRXR-1TXNRD1

Evidence

Reading pass · 16 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
1981 The three-dimensional crystal structure of human glutathione reductase (GSR) was determined at 2 Å resolution, establishing the enzyme as a homodimer with FAD as a prosthetic group and revealing a redox-active disulfide at the active site. X-ray crystallography Journal of molecular biology High 7334521
1982 Sequence analysis of the NADPH domain (residues 158–293) and interface domain (residues 365–478) of human erythrocyte glutathione reductase established the complete amino acid sequence (478 residues per chain, Mr ~51,600 per subunit for FAD-free apoenzyme); Tyr-197 was identified as the residue involved in an induced-fit mechanism for NADPH binding. CNBr fragment isolation, automated solid-phase Edman degradation, trypsin/chymotrypsin digestion of peptides European journal of biochemistry High 7060551
1983 X-ray crystallographic analysis of reaction intermediates established the catalytic mechanism of GSR: NADPH binds with its nicotinamide ring stacking onto the re-face of FAD; electron transfer from NADPH reduces the FAD, which then reduces the redox-active disulfide (Cys-58/Cys-63); Cys-58 attacks the substrate GSSG to form a mixed protein-glutathione disulfide; His-467' is essential for catalysis by facilitating disulfide exchange; and electrons flow NADPH → FAD → protein disulfide → GSSG. X-ray crystallography of reaction intermediates, active-site alkylation with iodoacetamide The Journal of biological chemistry High 6822532
1987 Refinement of the human GSR crystal structure to 1.54 Šresolution revealed that: FAD is tightly bound with the flavin ring most rigid (mean B ~8.7 Ų); the entire active center is particularly well ordered; the dimer interface contains a rigid conserved contact area and a flexible region not conserved in E. coli GR; N5 of the flavin can accommodate a proton consistent with its role in proton transfer during catalysis; and no buried cations compensate the pyrophosphate charge of FAD. X-ray crystallography, restrained least-squares refinement (R-factor 18.6%, 77,690 reflections) Journal of molecular biology High 3656429
1998 Crystal structures at 1.7 Å resolution showed that human GSR (hGR) is irreversibly inactivated by NO-carriers: S-nitrosoglutathione (GSNO) oxidizes the active-site Cys-63 to a cysteine sulfenic acid (R-SOH), while diglutathionyl-dinitroso-iron (DNIC-[GSH]2) oxidizes Cys-63 to a cysteine sulfinic acid (R-SO2H), establishing sulfhydryl oxidation of the active-site cysteine as the mechanism of NO-mediated enzyme inactivation. X-ray crystallography of inhibitor-enzyme complexes at 1.7 Å resolution Nature structural biology High 9546215
2011 In C. elegans, GSR-1 (glutathione reductase, ortholog of mammalian GSR) functions together with the selenoprotein TRXR-1 thioredoxin reductase to reduce disulfide bonds in the cuticle during molting; loss of both enzymes leaves cuticle disulfides oxidized and blocks removal of the old cuticle. Exogenously supplied reduced glutathione (GSH) was sufficient to reduce cuticle disulfides and induce apolysis, demonstrating that the GSR-1/TRXR-1 axis drives regulated cuticle reduction. RNAi knockdown, genetic mutant analysis, exogenous GSH rescue experiment, biochemical measurement of cuticle disulfide redox state Proceedings of the National Academy of Sciences of the United States of America High 21199936
2013 In C. elegans, GSR-1 (sole glutathione reductase, ortholog of mammalian GSR) is essential for survival under juglone (redox cycling agent) stress but not arsenite stress; its loss impairs GSSG recycling, which in turn induces compensatory GSH synthesis (but not vice versa); overexpression of GSR-1 increases stress tolerance; and GSR-1 expression, regulated by transcription factor SKN-1, also affects lifespan, establishing the GSH redox state as a determinant of longevity. RNAi screen, genetic knockdown and overexpression, glutathione level measurement (GSH/GSSG ratio), survival assays under multiple stressors PloS one Medium 23593298
2016 In C. elegans, gsr-1 encodes two GSR-1 isoforms: one cytoplasmic and one mitochondrial (demonstrated by GFP reporters). Complete loss of gsr-1 causes fully penetrant embryonic lethality characterized by cell division delay and aberrant chromatin distribution at the nuclear periphery. Cytoplasmic but not mitochondrial GSR-1 is sufficient to rescue embryonic lethality, indicating that cytoplasmic glutathione redox homeostasis is the critical function. Maternally supplied GSR-1 supports development but animals are short-lived, sensitive to stress, and show increased mitochondrial fragmentation and reduced mitochondrial DNA content. GFP reporter localization, loss-of-function mutant analysis, isoform-specific rescue experiments, mitochondrial imaging, stress assays Free radical biology & medicine High 27117030
2017 In Gsr knockout mice, loss of GSR activity and reduced GSH/GSSG ratio in cochlear cytosol did not impair cochlear antioxidant defense under normal conditions; instead, Gsr deficiency was compensated by increased activities of cytosolic thioredoxin (Trx) and thioredoxin reductase (TrxR) in the inner ear, identifying the thioredoxin system as a functional backup capable of supporting GSSG reduction in the peripheral auditory system. Gsr homozygous knockout mouse (backcrossed to CBA/CaJ), auditory brainstem response (ABR), histology, enzyme activity assays (GSR, GPX, GCL, TrxR, Trx), oxidative damage markers PloS one Medium 28686716
2017 GSR expression is elevated in temozolomide (TMZ)-resistant glioblastoma cells compared to sensitive cells; GSR silencing re-sensitized resistant cells to TMZ and cisplatin, while GSR overexpression in sensitive cells conferred chemotherapy resistance. GSR-mediated drug resistance operates through maintenance of redox homeostasis (lower ROS, higher GSH and antioxidant capacity), and modulation of the redox state by L-buthionine sulfoximine or exogenous GSH regulated GSR-dependent resistance. siRNA silencing and overexpression of GSR in glioblastoma cell lines, drug sensitivity assays, ROS measurement, antioxidant capacity and GSH quantification Journal of neurochemistry Medium 29105080
2019 In mouse liver, simultaneous deletion of TrxR1 and Gsr (double-null) caused ~100-fold higher DNA damage indices compared to single nulls or wild-type, demonstrating that TrxR1 and Gsr together maintain genomic integrity and that their combined loss creates extreme oxidative stress. Elevated oxidative stress (in TrxR1/Gsr-null livers) correlated with significantly increased malignancy of DEN-induced liver cancers, establishing these two antioxidant systems as cooperative determinants of cancer malignancy. Conditional and germline knockout mouse genetics, DNA damage quantification, DEN-induced hepatocellular carcinoma model, metabolomics, Nrf2 expression analysis Proceedings of the National Academy of Sciences of the United States of America High 31097586
2013 1,25(OH)₂ vitamin D upregulates glutathione reductase (GR) activity and protein expression, as well as glutamate cysteine ligase (GCLC), in U937 monocytes, leading to increased GSH formation and decreased ROS, MCP-1, and IL-8 secretion under high-glucose conditions, establishing a direct regulatory link between vitamin D signaling and the GSR/glutathione antioxidant pathway. Cell culture with vitamin D treatment, GR activity assay (NADPH oxidation), GCLC protein ELISA, GSH HPLC, ROS measurement, cytokine ELISA Biochemical and biophysical research communications Medium 23770363
2025 GSR deficiency in lung epithelial (A549) and fibroblast (MRC5) cells reduces intracellular GSH levels and elevates ROS, which activates the TGF-β/Smad2 signaling pathway, promoting epithelial-to-mesenchymal transition (EMT), fibroblast activation, and cellular senescence. GSR knockdown also promotes cell migration. Together, these data mechanistically link GSR-mediated glutathione redox homeostasis to TGF-β/Smad2-driven pulmonary fibrosis. GSR siRNA knockdown in A549 and MRC5 cells, GSH measurement, ROS assay, EMT marker analysis, TGF-β/Smad2 pathway activity, migration and senescence assays, bleomycin mouse model Biomolecules Medium 40723921
2025 In C. elegans, inactivation of the nonsense-mediated mRNA decay (NMD) pathway suppresses the embryonic lethality of gsr-1 (glutathione reductase) mutants via upregulation of cth-1 and cth-2 (cystathionine-γ-lyase isoforms of the transsulfuration pathway), which generate cysteine for alternative GSH synthesis. The thioredoxin system (which can also provide cysteine via cystine reduction) is not required for this suppression, establishing the transsulfuration pathway as a specific compensatory route for GSR-1 loss. Genetic suppressor screen, NMD pathway mutants, RNAi of cth-1/cth-2, epistasis analysis, embryonic lethality quantification bioRxiv (preprint)preprint Medium bio_10.1101_2025.01.09.632117
2024 In a murine lung tumor model (Kras G12D/Nrf2 D29H), deletion of GSR (but not TXNRD1) suppressed tumor initiation regardless of Nrf2 status, while TXNRD1 (but not GSR) was required for progression of Nrf2-activated tumors. Simultaneous deletion of GSR and TXNRD1 further reduced both initiation and progression, demonstrating that the glutathione and thioredoxin antioxidant systems play distinct, non-redundant roles in lung tumorigenesis. Conditional knockout of GSR and TXNRD1 alone or combined in KrasG12D/Nrf2D29H lung tumor mouse model, tumor initiation and progression quantification bioRxiv (preprint)preprint Medium bio_10.1101_2024.08.20.608800
2025 Structural comparison of human GSR with AIF, DLD, and TrxR reveals a conserved overall fold (pairwise RMSD <3.2 Å across all four enzymes) with spatially aligned FAD and NAD(P)H cofactor-binding pockets, consistent with a conserved FAD/NAD(P)H-dependent catalytic mechanism involving electron transfer via the flavin cofactor. Comparative structural analysis using available crystallographic data, RMSD-based superposition International journal of biological macromolecules Low 40451368

Source papers

Stage 0 corpus · 63 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2005 A human protein-protein interaction network: a resource for annotating the proteome. Cell 1704 16169070
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
2004 Immunoaffinity profiling of tyrosine phosphorylation in cancer cells. Nature biotechnology 916 15592455
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
2008 Large-scale proteomics and phosphoproteomics of urinary exosomes. Journal of the American Society of Nephrology : JASN 607 19056867
1987 Refined structure of glutathione reductase at 1.54 A resolution. Journal of molecular biology 465 3656429
2004 The status, quality, and expansion of the NIH full-length cDNA project: the Mammalian Gene Collection (MGC). Genome research 438 15489334
2015 Panorama of ancient metazoan macromolecular complexes. Nature 407 26344197
1996 Normalization and subtraction: two approaches to facilitate gene discovery. Genome research 401 8889548
2005 Human ISG15 conjugation targets both IFN-induced and constitutively expressed proteins functioning in diverse cellular pathways. Proceedings of the National Academy of Sciences of the United States of America 383 16009940
2004 14-3-3-affinity purification of over 200 human phosphoproteins reveals new links to regulation of cellular metabolism, proliferation and trafficking. The Biochemical journal 372 14744259
1983 The catalytic mechanism of glutathione reductase as derived from x-ray diffraction analyses of reaction intermediates. The Journal of biological chemistry 285 6822532
2012 A high-throughput approach for measuring temporal changes in the interactome. Nature methods 273 22863883
2021 Quantitative high-confidence human mitochondrial proteome and its dynamics in cellular context. Cell metabolism 239 34800366
1981 Three-dimensional structure of glutathione reductase at 2 A resolution. Journal of molecular biology 226 7334521
2011 Toward an understanding of the protein interaction network of the human liver. Molecular systems biology 207 21988832
1982 Glutathione reductase from human erythrocytes. The sequences of the NADPH domain and of the interface domain. European journal of biochemistry 193 7060551
2013 Vitamin D upregulates glutamate cysteine ligase and glutathione reductase, and GSH formation, and decreases ROS and MCP-1 and IL-8 secretion in high-glucose exposed U937 monocytes. Biochemical and biophysical research communications 184 23770363
2020 UFMylation maintains tumour suppressor p53 stability by antagonizing its ubiquitination. Nature cell biology 168 32807901
2009 Gene-centric association signals for lipids and apolipoproteins identified via the HumanCVD BeadChip. American journal of human genetics 164 19913121
2001 Aging- and photoaging-dependent changes of enzymic and nonenzymic antioxidants in the epidermis and dermis of human skin in vivo. The Journal of investigative dermatology 164 11710935
2009 Antioxidative enzymes and increased oxidative stress in depressive women. Clinical biochemistry 151 19527700
2020 Comparative Application of BioID and TurboID for Protein-Proximity Biotinylation. Cells 146 32344865
1998 Enzyme inactivation through sulfhydryl oxidation by physiologic NO-carriers. Nature structural biology 144 9546215
2009 Ubiquitin-mediated proteolysis of HuR by heat shock. The EMBO journal 142 19322201
2013 In-depth proteomic analyses of exosomes isolated from expressed prostatic secretions in urine. Proteomics 138 23533145
1977 Glutathione reductase from human erythrocytes. Isolation of the enzyme and sequence analysis of the redox-active peptide. European journal of biochemistry 136 923580
2017 Glutathione reductase mediates drug resistance in glioblastoma cells by regulating redox homeostasis. Journal of neurochemistry 131 29105080
2013 Proteomic analysis of podocyte exosome-enriched fraction from normal human urine. Journal of proteomics 126 23376485
2019 TrxR1, Gsr, and oxidative stress determine hepatocellular carcinoma malignancy. Proceedings of the National Academy of Sciences of the United States of America 70 31097586
2011 Selenoprotein TRXR-1 and GSR-1 are essential for removal of old cuticle during molting in Caenorhabditis elegans. Proceedings of the National Academy of Sciences of the United States of America 63 21199936
2021 Ammonium Ferric Citrate induced Ferroptosis in Non-Small-Cell Lung Carcinoma through the inhibition of GPX4-GSS/GSR-GGT axis activity. International journal of medical sciences 58 33746607
2013 The glutathione reductase GSR-1 determines stress tolerance and longevity in Caenorhabditis elegans. PloS one 51 23593298
2019 Activities of antioxidant seminal plasma enzymes (SOD, CAT, GPX and GSR) are higher in jackasses than in stallions and are correlated with sperm motility in jackasses. Theriogenology 47 31479834
2012 Antioxidant enzymes GSR, SOD1, SOD2, and CAT gene variants and bone mineral density values in postmenopausal women: a genetic association analysis. Menopause (New York, N.Y.) 34 22089180
1982 Phosphotransferase-mediated regulation of carbohydrate utilisation in Escherichia coli K12: identification of the products of genes on the specialised transducing phages lambda iex (crr) and lambda gsr (tgs). The EMBO journal 25 6234165
1983 Phosphotransferase-mediated regulation of carbohydrate utilization in Escherichia coli K12: location of the gsr (tgs) and iex (crr) genes by specialized transduction. Journal of general microbiology 24 6302202
2024 GSR-DB: a manually curated and optimized taxonomical database for 16S rRNA amplicon analysis. mSystems 19 38189256
2017 GSR is not essential for the maintenance of antioxidant defenses in mouse cochlea: Possible role of the thioredoxin system as a functional backup for GSR. PloS one 19 28686716
1986 Chromosomal mapping of enzyme loci in the domestic cat: GSR to C2, ADA and ITPA to A3, and LDHA-ACP2 to D1. Cytogenetics and cell genetics 19 3007037
2002 Salt-tolerant mutants in glycophytic salinity response (GSR) genes in Catharanthus roseus. TAG. Theoretical and applied genetics. Theoretische und angewandte Genetik 17 12582847
2016 Glutathione reductase gsr-1 is an essential gene required for Caenorhabditis elegans early embryonic development. Free radical biology & medicine 13 27117030
1983 Phosphotransferase-mediated regulation of carbohydrate utilization in Escherichia coli K12: the nature of the iex (crr) and gsr (tgs) mutations. Journal of general microbiology 11 6302201
2022 Identification, analysis of deleterious SNPs of the human GSR gene and their effects on the structure and functions of associated proteins and other diseases. Scientific reports 10 35361806
2019 Glutathione reductase (GSR) gene deletion and chromosome 8 aneuploidy in primary lung cancers detected by fluorescence in situ hybridization. American journal of cancer research 10 31285952
1996 Epidermal cells on stubs used for detection of GSR with SEM-EDX: analysis of DNA polymorphisms. Journal of forensic sciences 9 8754577
2010 Genetic study of gutter-shaped root (GSR) in AKXL RI mouse strains using QTL analysis. Journal of oral science 6 20587944
1996 Chromosome localization of the loci for PEPA, PEPB, PEPS, IDH1, GSR, MPI, PGM1, NP, SOD1, and ME1 in the common shrew (Sorex araneus). Mammalian genome : official journal of the International Mammalian Genome Society 6 8661695
2000 Molecular genetic study of the gutter shaped root (GSR) on mouse chromosome 17. Journal of oral science 5 10808271
2025 Structural impact of GSR and LRP8 gene polymorphisms on protein function and their role in racing performance of homing pigeons. International journal of biological macromolecules 2 40246119
1996 Sequence analysis of a 14.2 kb fragment of Saccharomyces cerevisiae chromosome XIV that includes the ypt53, tRNALeu and gsr m2 genes and four new open reading frames. Yeast (Chichester, England) 2 8771715
1991 Mapping of the silver fox genes: assignments of the genes for ME1, ADK, PP, PEPA, GSR, MPI, and GOT1. Cytogenetics and cell genetics 2 2013231
2023 Genetic Variants of the Gsr Gene (rs2978663) and the Progression of Osteoporosis. Acta informatica medica : AIM : journal of the Society for Medical Informatics of Bosnia & Herzegovina : casopis Drustva za medicinsku informatiku BiH 1 37038483
2026 GSR-ST: A generalized spatial-temporal framework for genomic signals and regions prediction using multi-scale feature fusion. Computational biology and chemistry 0 41558219
2026 Deep Learning as a Compass for Industrial Biocatalysis: The Grase Framework Rewrites the Rules for Polyurethane Recycling. Biotechnology journal 0 41934218
2025 Apoptosis-inducing factor (AIF), dihydrolipoamide dehydrogenase (DLD), glutathione disulfide reductase (GSR), and thioredoxin reductase (TrxR) in cancer and neurological disorders: Structural insights, redox regulation, and therapeutic potential. International journal of biological macromolecules 0 40451368
2025 GSR Deficiency Exacerbates Oxidative Stress and Promotes Pulmonary Fibrosis. Biomolecules 0 40723921
2025 Circular RNA Gsr-0002 promotes schistosomiasis-induced liver fibrosis by regulating the DNMT3A/PTEN pathway. International journal of biological macromolecules 0 41203147
2025 Identification of GSR and CBR1 as biomarkers in HIV-associated emphysema through transcriptomic analysis. HIV medicine 0 41313200
2025 Endometrial Cell Senescence and Recurrent Spontaneous Abortion: Biomarker Potential of UCP2 and GSR. Reproductive sciences (Thousand Oaks, Calif.) 0 41387654
2022 Experiences in successive forensic analysis of GSR and DNA traces collected on a single tape lift stub. Journal of forensic sciences 0 36089843
1990 [Cloning of grisin resistance gene gsr and the study of its functioning in Streptomyces griseus Kr. strain]. Antibiotiki i khimioterapiia = Antibiotics and chemoterapy [sic] 0 2127665