Affinage

GLRX3

Glutaredoxin-3 · UniProt O76003

Length
335 aa
Mass
37.4 kDa
Annotated
2026-04-28
58 papers in source corpus 18 papers cited in narrative 18 extracted findings

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

GLRX3 (PICOT) is a multidomain monothiol glutaredoxin that functions as a [2Fe-2S] cluster chaperone central to cytosolic iron-sulfur protein biogenesis and cellular iron homeostasis, while also modulating cardiac contractility, chromatin regulation, and redox-dependent signaling. Its two Grx domains and bound glutathione coordinate bridging [2Fe-2S] clusters in a homodimeric complex; these clusters are transferred to the CIA machinery component NUBP1—where they undergo reductive coupling to [4Fe-4S] clusters—and to anamorsin via a BOLA2–GLRX3 heterotrimeric intermediate, and the Trx–GrxA module is the minimal unit required for cellular iron metabolism (PMID:20226171, PMID:32429669, PMID:26613676, PMID:40400140). In cardiomyocytes, GLRX3 inhibits calcineurin-NFAT–driven hypertrophy by disrupting the MLP–calcineurin interaction at the Z-disc and enhances contractility by directly inhibiting PKCζ kinase activity, thereby increasing phospholamban and troponin phosphorylation (PMID:18258855, PMID:22449794, PMID:18929570). GLRX3 additionally interacts with the PRC2 subunit EED in the nucleus to sustain H3K27me3 at target gene promoters such as CCND2, and in satellite glial cells it deglutathionylates HMGB1 at Cys106 to generate a TLR4 agonist that drives neuropathic pain signaling (PMID:31527584, PMID:42007893).

Mechanistic history

Synthesis pass · year-by-year structured walk · 13 steps
  1. 2000 Medium

    Identifying GLRX3 as a PKCθ-interacting protein established it as a thioredoxin-fold protein with signaling-modulatory capacity in T cells, opening the question of its endogenous function.

    Evidence Yeast two-hybrid screen with PKCθ bait, overexpression/reporter assays in Jurkat T cells

    PMID:10636891

    Open questions at the time
    • Interaction not confirmed by reciprocal co-immunoprecipitation
    • Endogenous function and physiological relevance of PKCθ interaction undefined
    • No assessment of redox or Fe-S cluster biology
  2. 2006 High

    Demonstration that GLRX3 overexpression suppresses cardiac hypertrophy and enhances contractility in vivo established a cardioprotective function but left the molecular target unresolved.

    Evidence Adenoviral and transgenic mouse overexpression with pressure-overload model, cardiomyocyte contractility and Ca²⁺ handling assays

    PMID:16809552

    Open questions at the time
    • Direct molecular target mediating anti-hypertrophic effect unknown
    • Mechanism of enhanced Ca²⁺ responsiveness not identified
  3. 2008 High

    Identification of the MLP–calcineurin axis as the direct target of GLRX3's anti-hypertrophic action, combined with loss-of-function confirmation in heterozygous mice, resolved the signaling mechanism in cardiomyocytes.

    Evidence GST pull-down, mass spectrometry, co-IP, NFAT translocation assay, transgenic overexpression and gene-trap knockout mouse models

    PMID:18258855 PMID:18929570

    Open questions at the time
    • Whether GLRX3's Fe-S cluster status affects its cardiac signaling functions unknown
    • SERCA/phospholamban regulation mechanism not fully dissected
  4. 2010 High

    Biochemical demonstration that GLRX3 homodimer coordinates two bridging [2Fe-2S] clusters via its Grx active-site cysteines and glutathione reframed the protein as an iron-sulfur cluster scaffold rather than a classical oxidoreductase.

    Evidence UV-visible/CD spectroscopy, ⁵⁵Fe co-IP from Jurkat cells, oxidant/RNS sensitivity assays

    PMID:20226171

    Open questions at the time
    • Physiological recipients of the Fe-S clusters not identified
    • Whether cluster binding is required for signaling functions untested
  5. 2011 High

    Knockout lethality at E12.5 and cell-cycle arrest at G2/M in GLRX3-null cells demonstrated that GLRX3 is essential for vertebrate development and mitotic progression.

    Evidence Grx3 knockout mouse, FACS cell-cycle analysis of MEFs and siRNA-treated HeLa cells, live-cell imaging

    PMID:21575136

    Open questions at the time
    • Whether cell-cycle defect is secondary to impaired Fe-S cluster delivery or a separate function unclear
    • Mechanism of mitotic exit failure unresolved
  6. 2012 High

    Direct inhibition of PKCζ kinase activity by the GLRX3 Trx domain provided a second molecular mechanism for enhanced cardiac contractility, downstream of which PKCα and PP2A activities are reduced.

    Evidence Domain-mapped pull-down, in vitro kinase assay, AAV-mediated gene transfer, cardiomyocyte contractility assays

    PMID:22449794

    Open questions at the time
    • In vivo relevance of PKCζ inhibition not tested independently of MLP-calcineurin pathway
    • Structural basis of Trx-domain–PKCζ interaction unknown
  7. 2013 High

    Zebrafish and human cell studies showing impaired hemoglobin maturation and defective cytosolic Fe/S enzyme activity upon GLRX3 depletion established its essential role in intracellular iron utilization and Fe-S protein biogenesis.

    Evidence Zebrafish morpholino knockdown, HeLa siRNA, IRP1 activity assay, ferritin/TfR1 Western blot

    PMID:23615448

    Open questions at the time
    • Direct Fe-S cluster transfer to specific acceptors not demonstrated in cells
    • Relationship to CIA pathway components unknown
  8. 2015 High

    Structural and biochemical reconstitution of the BOLA2–GLRX3 heterotrimeric complex and demonstration of [2Fe-2S] cluster transfer to anamorsin identified the first physiological Fe-S cluster delivery pathway from GLRX3.

    Evidence NMR spectroscopy, UV-visible/CD spectroscopy, in vitro cluster transfer to apo-anamorsin

    PMID:26613676

    Open questions at the time
    • Cellular confirmation of this transfer route not provided
    • Whether BOLA2 is required for all GLRX3-mediated cluster transfers unclear
  9. 2018 High

    Crystal structures of yeast Grx3 domains and identification of EED (PRC2) as a nuclear interaction partner expanded GLRX3's roles to include GST activity via inter-domain disulfide and chromatin regulation via H3K27me3 modulation.

    Evidence X-ray crystallography, NMR, SPR for yeast Grx3 domains; yeast two-hybrid, reciprocal co-IP, ChIP for EED interaction in Jurkat cells

    PMID:29524511 PMID:30595380

    Open questions at the time
    • Whether Fe-S cluster occupancy modulates EED binding unknown
    • Genome-wide scope of GLRX3–PRC2 regulation not defined
  10. 2019 Medium

    GLRX3 knockdown was shown to reduce EED/EZH2 occupancy and H3K27me3 at the CCND2 promoter, derepressing cyclin D2 expression, and separately to impair ATR-dependent DNA-damage signaling, broadening its nuclear functions.

    Evidence Nuclear co-IP, ChIP, siRNA knockdown with RT-PCR/Western blot for CCND2; genotoxic stress with phospho-ATR/Chk1/γH2AX analysis

    PMID:31176019 PMID:31527584

    Open questions at the time
    • Direct versus indirect role in ATR pathway not resolved
    • Single-lab studies for both EED and ATR functions
    • Whether PRC2 and DNA-damage roles depend on GLRX3 redox or Fe-S activity untested
  11. 2020 High

    In vitro reconstitution showed GLRX3 transfers [2Fe-2S] clusters to NUBP1 (CIA scaffold), where glutathione-dependent reductive coupling generates [4Fe-4S] clusters, placing GLRX3 upstream of the cytosolic iron-sulfur assembly pathway.

    Evidence Cluster transfer assay with UV-visible/CD spectroscopy and size-exclusion chromatography

    PMID:32429669

    Open questions at the time
    • Cellular validation of GLRX3-to-NUBP1 transfer not performed
    • Order of GLRX3 delivery to NUBP1 versus anamorsin in vivo unknown
  12. 2025 High

    CRISPR knockout and domain-rescue experiments established that the Trx–GrxA module is the minimal functional unit required for cellular iron homeostasis, resolving which domains are necessary for Fe-S cluster delivery in human cells.

    Evidence HeLa GLRX3 CRISPR/Cas9 knockout, IRP1 activity assay, domain-truncation rescue transfection

    PMID:40400140

    Open questions at the time
    • Role of the second Grx domain (GrxB) in cellular physiology unresolved
    • Whether Trx-GrxA sufficiency extends to all GLRX3-dependent pathways unknown
  13. 2026 Medium

    Identification of GLRX3-catalyzed deglutathionylation of HMGB1 at Cys106 in satellite glial cells as a driver of TLR4-mediated neuropathic pain revealed a cell-type-specific enzymatic function with direct disease relevance.

    Evidence Single-nucleus RNA-seq, redox proteomics, satellite glia-targeted GLRX3 knockdown, HMGB1 glutathionylation assay, mouse pain behavior

    PMID:42007893

    Open questions at the time
    • Single study; independent replication needed
    • Whether this deglutathionylation activity is relevant outside the neuropathic pain context untested
    • Catalytic mechanism details beyond Cys148 identification lacking

Open questions

Synthesis pass · forward-looking unresolved questions
  • A unified model explaining how GLRX3's Fe-S cluster chaperone function, redox enzymatic activity, and signaling-inhibitory roles are coordinated or segregated across cell types and subcellular compartments remains to be established.
  • Whether Fe-S cluster occupancy regulates GLRX3's nuclear (PRC2, DDR) or cardiac (MLP, PKCζ) functions is unknown
  • No structural model of full-length human GLRX3 exists
  • In vivo flux through GLRX3-to-NUBP1 versus GLRX3-BOLA2-to-anamorsin pathways not quantified

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0140104 molecular carrier activity 3 GO:0098772 molecular function regulator activity 2 GO:0016491 oxidoreductase activity 1 GO:0016740 transferase activity 1 GO:0140096 catalytic activity, acting on a protein 1
Localization
GO:0005829 cytosol 3 GO:0005634 nucleus 2 GO:0005856 cytoskeleton 1
Pathway
R-HSA-1430728 Metabolism 4 R-HSA-162582 Signal Transduction 2 R-HSA-4839726 Chromatin organization 2 R-HSA-1640170 Cell Cycle 1
Partners
BOLA2CSRP3CYBC1EEDHMGB1NUBP1PRKCQPRKCZ
Complex memberships
BOLA2-GLRX3 heterotrimerGLRX3 [2Fe-2S]-bridged homodimer

Evidence

Reading pass · 18 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
2000 PICOT (GLRX3) was identified as a PKCθ-interacting protein via yeast two-hybrid; its N-terminal thioredoxin-like domain mediates interaction with PKC, and overexpression of full-length PICOT inhibits JNK activation and AP-1/NF-κB transcription in T cells. Yeast two-hybrid, co-localization, transient overexpression with reporter assays The Journal of biological chemistry Medium 10636891
2006 PICOT/GLRX3 overexpression inhibits cardiac hypertrophy induced by endothelin-1, phenylephrine, and pressure overload; overexpression increases ventricular function and cardiomyocyte contractility associated with increased myofilament Ca2+ responsiveness and faster SR Ca2+ reuptake. Adenovirus-mediated gene transfer, transgenic mouse model, cardiomyocyte contractility assays, Ca2+ handling analysis Circulation research High 16809552
2008 PICOT directly interacts with muscle LIM protein (MLP) via its C-terminal half (PICOT-C), co-localizes with MLP at the Z-disc, and disrupts the MLP-calcineurin interaction, thereby inhibiting calcineurin-NFAT signaling and blocking cardiac hypertrophy. GST pull-down, mass spectrometry, co-immunoprecipitation, confocal microscopy, calcineurin phosphatase activity assay, NFAT translocation assay, transgenic mouse model Circulation research High 18258855
2008 PICOT-deficient (heterozygous) mice exhibit exacerbated pressure overload-induced cardiac hypertrophy with enhanced calcineurin-NFAT signaling, and isolated cardiomyocytes show reduced contractility with hypophosphorylation of phospholamban and reduced SERCA activity. Gene-trap knockout mouse, pressure overload model, calcineurin-NFAT signaling assays, SERCA activity measurement, phospholamban phosphorylation Journal of molecular and cellular cardiology High 18929570
2010 Human GLRX3/PICOT binds two bridging [2Fe-2S] clusters in a homodimeric complex, with cluster ligation provided by active-site cysteinyl residues of its two monothiol glutaredoxin (Grx) domains and non-covalently bound glutathione; [2Fe-2S] clusters are not redox-active but are released upon treatment with ferricyanide or S-nitrosoglutathione. UV-visible absorption, CD spectroscopy, 55Fe co-immunoprecipitation from Jurkat cells, treatment with oxidants/RNS Biochemical and biophysical research communications High 20226171
2011 Mammalian Grx3/PICOT is essential for embryonic development (Grx3-/- mice die at E12.5), and Grx3-deficient mouse embryonic fibroblasts and HeLa cells show impaired cell cycle progression at G2/M with increased binucleated cells, indicating a role in mitotic exit. Grx3 knockout mouse, mouse embryonic fibroblast cell cycle analysis (FACS), siRNA knockdown in HeLa cells, live cell imaging The FEBS journal High 21575136
2012 PICOT directly binds the catalytic domain of PKCζ via its N-terminal thioredoxin-like domain and inhibits PKCζ kinase activity in vitro; this inhibition decreases PKCα and PP2A activities, leading to increased phosphorylation of phospholamban and troponin I/T and enhanced cardiac contractility. Protein pull-down, in vitro kinase assay, PKCζ pseudosubstrate inhibitor, AAV-mediated gene transfer, cardiomyocyte contractility assays Journal of molecular and cellular cardiology High 22449794
2013 Depletion of vertebrate Grx3 (PICOT) in zebrafish severely impairs hemoglobin maturation; silencing in HeLa cells decreases activity of cytosolic Fe/S proteins (including iron-regulatory protein 1), reduces ferritin, and increases transferrin receptor levels, indicating impaired intracellular iron utilization despite normal iron uptake. Zebrafish morpholino knockdown, siRNA knockdown in HeLa cells, IRP1 activity assay, ferritin and transferrin receptor Western blot Molecular biology of the cell High 23615448
2013 PICOT is cleaved by caspase-3 at two sites (DRLD101/G and EELD226/T) during apoptosis; PICOT wild-type and the D101A/D226A double mutant both accelerate etoposide-induced caspase-3 activation, whereas PICOT knockdown blocks this. In vitro caspase-3 cleavage assay, site-directed mutagenesis, staurosporine/etoposide treatment, pan-caspase inhibitor, siRNA knockdown Biochemical and biophysical research communications Medium 23415866
2015 Human BOLA2 and GLRX3 form a heterotrimeric complex (two BOLA2 molecules per one GLRX3 molecule) that binds two [2Fe-2S]2+ clusters bridged between each BOLA2 and one Grx domain of GLRX3, and this complex transfers both clusters to apo-anamorsin producing its mature holo state. NMR spectroscopy, UV-visible and CD spectroscopy, in vitro reconstitution, cluster transfer assay Journal of the American Chemical Society High 26613676
2018 Crystal structures of the Trx domain and Grx domain of yeast Grx3 were solved; the Trx domain contributes to glutathione S-transferase activity via an inter-domain disulfide bond between Cys37 and Cys176; NMR and pull-down assays show Fra2 forms a noncovalent heterodimer with Grx3 via its helix-turn-helix motif interacting with the C-terminal segment of Grx3's Grx domain. X-ray crystallography, NMR spectroscopy, pull-down assay, surface plasmon resonance, GST activity assay Journal of molecular biology High 29524511
2018 PICOT interacts with EED (a core component of PRC2) via each of its two C-terminal PICOT/Grx domains; PICOT and EED co-localize predominantly in the nucleus of Jurkat T cells, and PICOT knockdown reduces H3K27me3 at the MYT1 PRC2 target gene. Yeast two-hybrid, GST pull-down, reciprocal Co-IP, immunofluorescence, ChIP analysis Biochemical and biophysical research communications Medium 30595380
2019 PICOT knockdown in Jurkat T cells impairs ATR-dependent DNA-damage signaling: PICOT-deficient cells show reduced and delayed phosphorylation of ATR, Chk1, Chk2, and γH2AX in response to genotoxic stress and radiation; PICOT partially localizes to γH2AX foci at DNA double-strand breaks. siRNA knockdown, genotoxic drug treatment, radiation, Western blot for phospho-ATR/Chk1/Chk2/γH2AX, immunofluorescence/confocal microscopy, caspase-3 activity assay Cellular signalling Medium 31176019
2019 PICOT interacts with chromatin-associated EED and PICOT knockdown reduces H3K27me3 and EED/EZH2 occupancy at the CCND2 gene promoter, leading to increased cyclin D2 (CCND2) mRNA and protein expression in T cells. Co-IP from nuclear fractions, ChIP, siRNA knockdown, RT-PCR, Western blot Cell death & disease Medium 31527584
2020 Dimeric cluster-bridged GLRX3 transfers its [2Fe-2S]2+ clusters to monomeric apo-NUBP1 (an early CIA machinery component); in the presence of glutathione as reductant, the transferred clusters are reductively coupled to form [4Fe-4S]2+ clusters on both N-terminal (CX13CX2CX5C) and C-terminal (CPXC) motifs of NUBP1, with C-terminal cluster binding promoting NUBP1 dimerization. In vitro reconstitution, UV-visible and CD spectroscopy, size exclusion chromatography, cluster transfer assay with glutathione Journal of the American Chemical Society High 32429669
2020 Human GLRX3 and GMP synthase (hGMPs) physically interact through conserved residues that bridge iron/sulfur clusters and glutathione; together they downregulate the Gcn2/integrated stress response pathway under nutritional stress in yeast complementation assays. Yeast humanization complementation assay, two-hybrid interaction, mouse cDNA library screen Applied and environmental microbiology Medium 32414791
2025 In HeLa GLRX3 knockout cells (generated by CRISPR/Cas), loss of GLRX3 activates iron-regulatory protein 1 (IRP1), indicating iron starvation; rescue experiments show that only the Trx-GrxA construct (not individual domains alone) can restore the phenotype, demonstrating that the Trx domain together with the first Grx domain is the functionally critical module for cellular iron metabolism. CRISPR/Cas9 knockout, IRP1 activity assay, domain-rescue transfection, Western blot FEBS letters High 40400140
2026 In satellite glial cells, GLRX3 catalyzes deglutathionylation of HMGB1 at Cys106 via its catalytic Cys148 residue; this converts HMGB1 into a TLR4-MD2 agonist, activating neuronal NF-κB and upregulating TRPA1/TRPV2 in nociceptors to sustain neuropathic pain in aged mice. Single-nucleus RNA sequencing, redox proteomics, satellite glial cell-targeted GLRX3 knockdown, HMGB1 glutathionylation assay, TLR4 signaling assays, mouse pain behavior assays Brain : a journal of neurology Medium 42007893

Source papers

Stage 0 corpus · 58 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2009 The yeast iron regulatory proteins Grx3/4 and Fra2 form heterodimeric complexes containing a [2Fe-2S] cluster with cysteinyl and histidyl ligation. Biochemistry 168 19715344
2006 Glutaredoxins Grx3 and Grx4 regulate nuclear localisation of Aft1 and the oxidative stress response in Saccharomyces cerevisiae. Journal of cell science 156 17074835
2000 Inhibition of the c-Jun N-terminal kinase/AP-1 and NF-kappaB pathways by PICOT, a novel protein kinase C-interacting protein with a thioredoxin homology domain. The Journal of biological chemistry 154 10636891
2005 A novel monothiol glutaredoxin (Grx4) from Escherichia coli can serve as a substrate for thioredoxin reductase. The Journal of biological chemistry 120 15833738
2013 Crucial function of vertebrate glutaredoxin 3 (PICOT) in iron homeostasis and hemoglobin maturation. Molecular biology of the cell 84 23615448
2001 Plasmodium falciparum possesses a classical glutaredoxin and a second, glutaredoxin-like protein with a PICOT homology domain. The Journal of biological chemistry 83 11479312
2010 Characterization of the human monothiol glutaredoxin 3 (PICOT) as iron-sulfur protein. Biochemical and biophysical research communications 79 20226171
2006 PICOT inhibits cardiac hypertrophy and enhances ventricular function and cardiomyocyte contractility. Circulation research 73 16809552
2008 PICOT attenuates cardiac hypertrophy by disrupting calcineurin-NFAT signaling. Circulation research 70 18258855
2009 Both Php4 function and subcellular localization are regulated by iron via a multistep mechanism involving the glutaredoxin Grx4 and the exportin Crm1. The Journal of biological chemistry 68 19502236
2023 A Redox Homeostasis Modulatory Hydrogel with GLRX3+ Extracellular Vesicles Attenuates Disc Degeneration by Suppressing Nucleus Pulposus Cell Senescence. ACS nano 62 37432866
2004 Analysis of the interaction between piD261/Bud32, an evolutionarily conserved protein kinase of Saccharomyces cerevisiae, and the Grx4 glutaredoxin. The Biochemical journal 61 14519092
2008 PICOT is a critical regulator of cardiac hypertrophy and cardiomyocyte contractility. Journal of molecular and cellular cardiology 59 18929570
2015 Elucidating the Molecular Function of Human BOLA2 in GRX3-Dependent Anamorsin Maturation Pathway. Journal of the American Chemical Society 58 26613676
2002 Cloning and characterization of CXIP1, a novel PICOT domain-containing Arabidopsis protein that associates with CAX1. The Journal of biological chemistry 55 12480930
2005 Molecular mapping of functionalities in the solution structure of reduced Grx4, a monothiol glutaredoxin from Escherichia coli. The Journal of biological chemistry 52 15840565
2011 Grx4 monothiol glutaredoxin is required for iron limitation-dependent inhibition of Fep1. Eukaryotic cell 51 21421748
2011 A mammalian monothiol glutaredoxin, Grx3, is critical for cell cycle progression during embryogenesis. The FEBS journal 51 21575136
2018 The Monothiol Glutaredoxin Grx4 Regulates Iron Homeostasis and Virulence in Cryptococcus neoformans. mBio 50 30514787
2011 Investigation of in vivo diferric tyrosyl radical formation in Saccharomyces cerevisiae Rnr2 protein: requirement of Rnr4 and contribution of Grx3/4 AND Dre2 proteins. The Journal of biological chemistry 46 21931161
2011 Multi-domain CGFS-type glutaredoxin Grx4 regulates iron homeostasis via direct interaction with a repressor Fep1 in fission yeast. Biochemical and biophysical research communications 33 21531205
2010 Glutaredoxins Grx4 and Grx3 of Saccharomyces cerevisiae play a role in actin dynamics through their Trx domains, which contributes to oxidative stress resistance. Applied and environmental microbiology 32 20889785
2017 Schizosaccharomyces pombe Grx4 regulates the transcriptional repressor Php4 via [2Fe-2S] cluster binding. Metallomics : integrated biometal science 27 28725905
2011 PICOT is a molecule which binds to anamorsin. Biochemical and biophysical research communications 27 21513700
2012 PICOT increases cardiac contractility by inhibiting PKCζ activity. Journal of molecular and cellular cardiology 23 22449794
2019 The conserved CDC motif in the yeast iron regulator Aft2 mediates iron-sulfur cluster exchange and protein-protein interactions with Grx3 and Bol2. Journal of biological inorganic chemistry : JBIC : a publication of the Society of Biological Inorganic Chemistry 20 31493153
2017 PICOT alleviates myocardial ischemia-reperfusion injury by reducing intracellular levels of reactive oxygen species. Biochemical and biophysical research communications 20 28257842
2016 The Escherichia coli BolA Protein IbaG Forms a Histidine-Ligated [2Fe-2S]-Bridged Complex with Grx4. Biochemistry 19 27951647
2020 GLRX3 Acts as a [2Fe-2S] Cluster Chaperone in the Cytosolic Iron-Sulfur Assembly Machinery Transferring [2Fe-2S] Clusters to NUBP1. Journal of the American Chemical Society 18 32429669
2020 TRIM16 protects human periodontal ligament stem cells from oxidative stress-induced damage via activation of PICOT. Experimental cell research 18 33091421
2008 PICOT, protein kinase C theta-interacting protein, is a novel regulator of FcepsilonRI-mediated mast cell activation. Cellular immunology 17 18479680
2020 Proteomic profiling of the monothiol glutaredoxin Grx3 reveals its global role in the regulation of iron dependent processes. PLoS genetics 16 32525871
2021 The monothiol glutaredoxin Grx4 influences thermotolerance, cell wall integrity, and Mpk1 signaling in Cryptococcus neoformans. G3 (Bethesda, Md.) 15 34542604
2013 Caspase-3-mediated cleavage of PICOT in apoptosis. Biochemical and biophysical research communications 15 23415866
2018 Structural and Biochemical Insights into the Multiple Functions of Yeast Grx3. Journal of molecular biology 14 29524511
2016 Reversible glutathionylation of Sir2 by monothiol glutaredoxins Grx3/4 regulates stress resistance. Free radical biology & medicine 14 27085841
2016 Physical interaction between the MAPK Slt2 of the PKC1-MAPK pathway and Grx3/Grx4 glutaredoxins is required for the oxidative stress response in budding yeast. Free radical biology & medicine 14 28007574
2019 Novel interactions of Selenium Binding Protein family with the PICOT containing proteins AtGRXS14 and AtGRXS16 in Arabidopsis thaliana. Plant science : an international journal of experimental plant biology 13 30824043
2019 PICOT (GLRX3) is a positive regulator of stress-induced DNA-damage response. Cellular signalling 13 31176019
2017 Function of glutaredoxin 3 (Grx3) in oxidative stress response caused by iron homeostasis disorder in Candida albicans. Future microbiology 13 29039220
2010 Determinants of activity in glutaredoxins: an in vitro evolved Grx1-like variant of Escherichia coli Grx3. The Biochemical journal 11 20604742
2022 LncRNA FGF7-5 and lncRNA GLRX3 together inhibits the formation of carotid plaque via regulating the miR-2681-5p/ERCC4 axis in atherosclerosis. Cell cycle (Georgetown, Tex.) 10 36071684
2021 GLRX3, a novel cancer stem cell-related secretory biomarker of pancreatic ductal adenocarcinoma. BMC cancer 9 34794402
2020 Interactions of GMP with Human Glrx3 and with Saccharomyces cerevisiae Grx3 and Grx4 Converge in the Regulation of the Gcn2 Pathway. Applied and environmental microbiology 9 32414791
2010 Widespread expression of PICOT in mouse and human tissues with predominant localization to epithelium. The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society 8 20498481
2019 PICOT binding to chromatin-associated EED negatively regulates cyclin D2 expression by increasing H3K27me3 at the CCND2 gene promoter. Cell death & disease 7 31527584
2018 PICOT binding to the polycomb group protein, EED, alters H3K27 methylation at the MYT1 PRC2 target gene. Biochemical and biophysical research communications 7 30595380
2023 Iron homeostasis proteins Grx4 and Fra2 control activity of the Schizosaccharomyces pombe iron repressor Fep1 by facilitating [2Fe-2S] cluster removal. The Journal of biological chemistry 5 37923140
2023 Structural conservation in the glutathione binding in Sphingomonas sp. glutaredoxin Grx3 and variations for cold adaptation. Biochimica et biophysica acta. Proteins and proteomics 4 37935252
2024 Integrating multi-omics techniques and in vitro experiments reveals that GLRX3 regulates the immune microenvironment and promotes hepatocellular carcinoma cell proliferation and invasion through iron metabolism pathways. Frontiers in immunology 3 39654899
2023 The Monothiol Glutaredoxin Grx4 Influences Iron Homeostasis and Virulence in Ustilago maydis. Journal of fungi (Basel, Switzerland) 2 37998917
2022 Schizosaccharomyces pombe Grx4, Fep1, and Php4: In silico analysis and expression response to different iron concentrations. Frontiers in genetics 2 36568394
2025 The thioredoxin-like and one glutaredoxin domain are required to rescue the iron-starvation phenotype of HeLa GLRX3 knock out cells. FEBS letters 1 40400140
2024 Schizosaccharomyces pombe Grx4 is subject to autophagic degradation under nitrogen- and iron- starvation and ER-stress. Archives of biochemistry and biophysics 1 39603377
2020 Yeast glutaredoxin, GRX4, functions as a glutathione S-transferase required for red ade pigment formation in Saccharomyces cerevisiae. Journal of biosciences 1 32098918
2026 Functional significance of highly conserved residues in dithiol glutaredoxin (Grx3) of cyanobacterium Synechococcus elongatus PCC 7942. Computational biology and chemistry 0 41935503
2026 Satellite glial GLRX3 drives ageing-biased neuropathic pain via HMGB1. Brain : a journal of neurology 0 42007893
2025 Structural Adaptations of Bacterial Grx3 to Temperature: Pro29 Is Essential for Cold Adaptation in Sphingomonas sp. Grx3. ACS omega 0 40521461