Affinage

G6PC3

Glucose-6-phosphatase 3 · UniProt Q9BUM1

Length
346 aa
Mass
38.7 kDa
Annotated
2026-06-09
54 papers in source corpus 15 papers cited in narrative 15 extracted findings
Cross-family judge vs UniProt: Affinage preferred faithfulness: 5/5 claims corpus-supported (100%)

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

G6PC3 is an endoplasmic reticulum glucose-6-phosphatase that performs a metabolite-repair function essential for neutrophil and cellular viability (PMID:19118303, PMID:30626647). Acting together with the G6P transporter G6PT/SLC37A4, it hydrolyzes 1,5-anhydroglucitol-6-phosphate (1,5-AG6P), a toxic inhibitor of low-KM hexokinases; loss of G6PC3 lets 1,5-AG6P accumulate to millimolar levels, blocking glycolysis and causing glycolytic failure and cell death, a mechanism validated in patient cells and reversed in mice and patients by lowering circulating 1,5-anhydroglucitol with SGLT2 inhibitors (PMID:30626647, PMID:35506446). Loss-of-function mutations abolish enzymatic activity and produce severe congenital neutropenia, with downstream ER stress, PERK activation, intrinsic mitochondrial apoptosis, and elevated GSK-3β activity in neutrophils and fibroblasts (PMID:19118303, PMID:21292774, PMID:23686134). The metabolic deficit impairs early glycolysis and the hexose monophosphate shunt, compromising NADPH generation, superoxide production, migration, and bacterial killing, and is accompanied by hypoglycosylation of the NADPH oxidase component gp91(phox) and elevated neutrophil CXCR4 driving bone marrow retention (PMID:21385794, PMID:20616219, PMID:33259599). Beyond myeloid metabolism, G6PC3 supports homologous-recombination DNA repair by promoting BRCA1 expression and recruitment to double-strand breaks (PMID:40261702), and is required in pachytene spermatocytes for XY body formation and meiotic sex chromosome inactivation (PMID:39420835).

Mechanistic history

Synthesis pass · year-by-year structured walk · 10 steps
  1. 2006 Medium

    Established that G6PC3 is a bona fide glucose-6-phosphate hydrolase in vivo and distinguished its physiology from the hepatic G6PC isoform, framing it as a non-gluconeogenic phosphatase.

    Evidence G6PC3/UGRP knockout mouse phenotyping with enzymatic assay in brain homogenates and plasma metabolite profiling

    PMID:17023421

    Open questions at the time
    • The physiological substrate beyond generic G6P was not identified
    • No mechanistic link to neutrophil biology established at this stage
  2. 2009 High

    Answered why G6PC3 mutations cause disease by showing they abolish phosphatase activity and trigger ER stress and apoptosis in neutrophils and fibroblasts, defining a loss-of-function mechanism for congenital neutropenia.

    Evidence Enzymatic assays with reconstitution and patient cell apoptosis/ER stress studies across multiple families

    PMID:19118303

    Open questions at the time
    • The metabolite whose accumulation drives toxicity was unknown
    • Connection between enzymatic loss and ER stress was correlative
  3. 2010 Medium

    Linked G6PC3 deficiency to neutrophil trafficking by showing elevated CXCR4 drives bone marrow retention, explaining the myelokathexis component of neutropenia.

    Evidence Flow cytometry of CXCR4 and pharmacological rescue with AMD3100 in G6pc3-/- mice

    PMID:20616219

    Open questions at the time
    • Mechanism connecting metabolic defect to CXCR4 upregulation not resolved
    • Single-lab mouse and patient data
  4. 2011 Medium

    Characterized the apoptotic and signaling pathways downstream of metabolic failure (PERK, PI3K/Akt, intrinsic mitochondrial apoptosis) and showed N-/O-glycan defects on the NADPH oxidase subunit gp91(phox), and defined glucose-responsive transcriptional control of the G6PC3 promoter.

    Evidence Western blotting and apoptosis assays in G6pc3-/- mice; mass spectrometric glycomics of patient neutrophils; promoter-luciferase reporter with deletion mutagenesis

    PMID:21292774 PMID:21385794 PMID:21474354

    Open questions at the time
    • Causal chain from glycolytic deficit to hypoglycosylation not directly demonstrated
    • Promoter regulation studied in cell lines without in vivo confirmation
  5. 2013 Medium

    Resolved whether neutropenia is a survival or differentiation defect by genetic epistasis, showing both contribute and implicating Bim/Bax-dependent apoptosis at differentiation onset.

    Evidence Hoxb8 progenitor model with Bcl-XL transgenic rescue, Bim knockdown, and bone marrow transplantation

    PMID:23686134

    Open questions at the time
    • Bcl-XL rescued survival but not functional defects, leaving the functional deficit mechanism open
    • Single-lab model system
  6. 2019 High

    Identified the toxic substrate by showing G6PC3 and G6PT hydrolyze 1,5-AG6P, whose accumulation inhibits hexokinases and causes glycolytic failure, and demonstrated in vivo rescue by lowering blood 1,5-anhydroglucitol.

    Evidence Enzymology, metabolomics, and SGLT2 inhibitor treatment of G6pc3-/- mice

    PMID:30626647

    Open questions at the time
    • Did not establish whether 1,5-AG6P repair explains the DNA repair or meiotic roles
    • Human therapeutic validation not yet performed at this stage
  7. 2020 Medium

    Quantified the downstream metabolic and functional consequences, tracing impaired glycolysis and hexose monophosphate shunt flux to defective NADPH-dependent respiratory burst, migration, and bacterial killing.

    Evidence Stable isotope tracing metabolomics with neutrophil functional assays; flow cytometry and glucose supplementation rescue

    PMID:32930428 PMID:33259599

    Open questions at the time
    • Patient-cell studies from limited donors
    • Glucose rescue was only partial
  8. 2022 Medium

    Translated the 1,5-AG6P mechanism to humans by showing empagliflozin lowers neutrophil 1,5-AG6P and normalizes counts, confirming the metabolite-repair model clinically.

    Evidence Clinical SGLT2 inhibitor treatment with metabolite measurement and neutrophil counts in patients

    PMID:35506446

    Open questions at the time
    • Only two patients
    • Long-term efficacy and effects on non-myeloid functions not assessed
  9. 2024 Medium

    Extended G6PC3 function beyond metabolism by demonstrating an essential meiotic role in XY body formation and meiotic sex chromosome inactivation in spermatocytes.

    Evidence CRISPR-Cas9 knockout mouse with immunofluorescence localization, meiotic staging, and MSCI assessment

    PMID:39420835

    Open questions at the time
    • Molecular mechanism linking phosphatase activity to MSCI unknown
    • Whether a metabolic substrate underlies the meiotic role is unresolved
  10. 2025 Medium

    Revealed a genome-stability role by showing G6PC3 promotes HR-repair gene expression and BRCA1 recruitment to double-strand breaks, with deficiency accelerating tumorigenesis.

    Evidence RNAi screen, gammaH2AX/micronuclei assays, HR repair and BRCA1 recruitment assays, RNA-seq, and Trp53-null mouse mammary tumor model

    PMID:40261702

    Open questions at the time
    • Whether DNA-repair role is a direct enzymatic function or a downstream metabolic consequence is unresolved
    • Single-lab finding

Open questions

Synthesis pass · forward-looking unresolved questions
  • How a single ER glucose-6-phosphatase mechanistically connects its metabolite-repair activity to homologous recombination and meiotic sex chromosome inactivation remains unknown.
  • No demonstrated substrate or metabolite mediating the DNA repair role
  • No mechanism connecting phosphatase activity to BRCA1 expression or MSCI

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0016787 hydrolase activity 3
Localization
GO:0005783 endoplasmic reticulum 2
Pathway
R-HSA-1430728 Metabolism 3 R-HSA-168256 Immune System 3 R-HSA-73894 DNA Repair 1
Partners
SLC37A4

Evidence

Reading pass · 15 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
2009 Homozygous missense mutations in G6PC3 abolish glucose-6-phosphatase enzymatic activity, leading to increased ER stress, increased GSK-3β activity, and enhanced apoptosis in neutrophils and fibroblasts; reconstitution experiments confirmed the enzymatic defect. Functional enzymatic assay, reconstitution experiments, patient cell studies (neutrophils/fibroblasts), apoptosis assays The New England journal of medicine High 19118303
2019 G6PC3 and the glucose-6-phosphate transporter G6PT/SLC37A4 collaborate to hydrolyze 1,5-anhydroglucitol-6-phosphate (1,5-AG6P), a potent inhibitor of low-KM hexokinases; G6PC3-deficient neutrophils accumulate 1,5-AG6P to ~3 mM, inhibiting hexokinase activity and causing glycolytic failure and cell death. Treating G6PC3-deficient mice with an SGLT2 inhibitor to lower blood 1,5-anhydroglucitol restored normal neutrophil counts. Enzymological assays, cell culture, metabolomics, in vivo mouse model (G6pc3-/- mice), SGLT2 inhibitor treatment Proceedings of the National Academy of Sciences of the United States of America High 30626647
2011 G6PC3 deficiency causes hypoglycosylation of gp91(phox), the electron-transporting component of the NADPH oxidase, in neutrophils; mass spectrometric glycomic profiling showed severely truncated complex-type N-glycan antennae and truncated O-glycan core 2 antennae in patient neutrophils. SDS-PAGE, mass spectrometric glycomic profiling of patient neutrophils Glycobiology Medium 21385794
2010 G6PC3 deficiency (G260R loss-of-function mutation) leads to markedly increased CXCR4 expression on neutrophils, contributing to bone marrow retention (myelokathexis) and neutropenia; the CXCR4 antagonist AMD3100 rapidly reversed neutropenia in G6pc3-/- mice, and G-CSF normalized CXCR4 expression and neutrophil counts. Flow cytometry (CXCR4 expression), G6pc3-/- mouse model, pharmacological rescue with AMD3100 Blood Medium 20616219
2011 G6pc3-/- neutrophils undergoing ER stress activate PERK (protein kinase-like ER kinase) and PI3K/Akt signaling; neutrophil apoptosis is mediated in part via the intrinsic mitochondrial pathway. G-CSF in vivo therapy corrects neutropenia, normalizes p-Akt and active caspase-3 levels, increases glucose uptake, and elevates intracellular G6P, lactate, and ATP. Western blotting (signaling pathway analysis), flow cytometry (apoptosis), glucose uptake assay, metabolite measurement in G6pc3-/- mice with/without G-CSF Blood Medium 21292774
2006 UGRP/G6PC3 knockout mice show ~50% reduction in G6P hydrolytic activity in brain homogenates, confirming G6PC3 can hydrolyze G6P in vivo; female knockout mice exhibit growth retardation, elevated plasma glucagon (~60%), and reduced plasma cholesterol (~20%), but no hypoglycemia, hepatic glycogen accumulation, or hypertriglyceridemia (in contrast to G6PC1 knockout). G6PC3/UGRP knockout mouse phenotyping, enzymatic activity assay in brain homogenates, plasma metabolite measurements The Journal of biological chemistry Medium 17023421
2013 In a G6PC3-/- mouse differentiation model, progenitor cells showed substantial apoptosis upon differentiation initiation; impaired glucose utilization was associated with ER stress, upregulation of Bim and Bax, and reduced neutrophil elastase expression/secretion. Bcl-XL overexpression rescued survival but not functional deficiencies; Bim knockdown also protected against apoptosis. Both survival and differentiation defects contribute to neutropenia. Hoxb8-conditional progenitor cell model, Bcl-XL transgenic rescue, Bim knockdown, bone marrow transplantation, MAP kinase signaling assays, cytokine secretion measurement Cell death and differentiation Medium 23686134
2020 G6PC3-deficient human neutrophils exhibit dramatic impairments in early glycolysis (reduced hexose phosphate levels), hexose monophosphate shunt (required for NADPH generation), and total adenylate pool, as measured by stable isotope tracing; these metabolic defects are associated with defective CD11b expression, F-actin assembly, migration, bacterial killing, and superoxide generation (<25% of control). Metabolomics with stable isotope-labeled tracers (U-13C-glucose, 13C,15N-glutamine, U-13C-fructose), functional neutrophil assays (migration, bactericidal activity, respiratory burst, CD11b/F-actin) Blood advances Medium 33259599
2022 Treatment of G6PC3-deficient children with the SGLT2 inhibitor empagliflozin decreased blood 1,5-anhydroglucitol and neutrophil 1,5-AG6P levels and improved/normalized neutrophil counts, directly validating the 1,5-AG6P accumulation mechanism in human patients. Clinical treatment study with metabolite measurement (blood 1,5-AG and neutrophil 1,5-AG6P), neutrophil counts before and after empagliflozin Journal of inherited metabolic disease Medium 35506446
2011 G6PC3 promoter activity is regulated by glucose concentration (responsive between 1–5.5 mM), pyruvate, and AMP kinase (AICAR reduces activity); two adjacent E-boxes (-274 to -279 and -299 to -304) function as a glucose response element. The G6PC3 promoter is unresponsive to glucostatic hormones, unlike the hepatic G6PC isoform. Transient transfection with G6PC3 promoter-luciferase reporter, dual luciferase assay, deletion mutagenesis, pharmacological inhibitors Molecular genetics and metabolism Medium 21474354
2017 G6PC3-deficient monocytes have reduced glycolytic reserve; upon LPS stimulation, they show significantly increased NLRP3 inflammasome-dependent production of IL-1β and IL-18, and enhanced IL-6 and TNF production, linking G6PC3-dependent glycolysis to inflammasome regulation. Extracellular flux assay (glycolytic reserve), cytokine measurement (ELISA), NLRP3 inflammasome inhibition assay, whole blood assay Frontiers in immunology Low 29163546
2020 G6PC3-deficient neutrophils display higher activation markers (CD11b, CD66b, CD14), excessive IL-8 and reactive oxygen species production, increased apoptosis and secondary necrosis; secondary necrosis after E. coli stimulation was partially rescued with supplemental exogenous glucose, implicating glucose deficit in inflammatory dysregulation. Flow cytometry, cytokine measurement, ROS assay, glucose supplementation rescue experiment in patient neutrophils Journal of leukocyte biology Low 32930428
2025 G6PC3-deficient cells exhibit increased γH2AX foci and micronuclei formation, and defects in homologous recombination (HR) repair including impaired BRCA1 recruitment to DNA double-strand breaks; RNA-seq showed G6PC3 promotes expression of multiple HR repair genes including BRCA1. G6pc3 deficiency accelerates mammary tumor formation in Trp53-null mice. RNAi screen, γH2AX immunofluorescence, micronuclei assay, HR repair assay, BRCA1 recruitment to DSBs, RNA-seq, CRISPR-Select functional analysis, mouse mammary tumor model JCI insight Medium 40261702
2024 G6PC3 is predominantly expressed in pachytene spermatocytes and concentrated in the XY body; CRISPR-Cas9 knockout of G6pc3 in mice causes complete meiotic arrest at the pachytene stage, complete sterility, abnormal XY body formation, and impaired meiotic sex chromosome inactivation (MSCI). CRISPR-Cas9 knockout mouse, immunofluorescence localization, meiotic staging, XY body analysis, MSCI assessment Acta biochimica et biophysica Sinica Medium 39420835
2024 The G6PC3 c.210delC frameshift mutation leads to complete loss of G6PC3 protein expression; patient-derived cells treated with 1,5-anhydroglucitol (1,5-AG) exhibit markedly reduced engagement of glycolysis as measured by extracellular flux assay, confirming that 1,5-AG6P accumulation inhibits glycolysis in G6PC3-deficient cells. Protein expression analysis, extracellular flux assay (glycolysis measurement), treatment with 1,5-AG in patient-derived EBV-B cells Journal of clinical immunology Low 39630167

Source papers

Stage 0 corpus · 54 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2009 A syndrome with congenital neutropenia and mutations in G6PC3. The New England journal of medicine 265 19118303
2019 Failure to eliminate a phosphorylated glucose analog leads to neutropenia in patients with G6PT and G6PC3 deficiency. Proceedings of the National Academy of Sciences of the United States of America 136 30626647
2009 Prevalence of mutations in ELANE, GFI1, HAX1, SBDS, WAS and G6PC3 in patients with severe congenital neutropenia. British journal of haematology 131 19775295
2011 G6PC3 mutations are associated with a major defect of glycosylation: a novel mechanism for neutrophil dysfunction. Glycobiology 75 21385794
2010 Severe congenital neutropenia resulting from G6PC3 deficiency with increased neutrophil CXCR4 expression and myelokathexis. Blood 69 20616219
2013 A clinical and molecular review of ubiquitous glucose-6-phosphatase deficiency caused by G6PC3 mutations. Orphanet journal of rare diseases 66 23758768
2011 Homozygosity mapping and whole-exome sequencing to detect SLC45A2 and G6PC3 mutations in a single patient with oculocutaneous albinism and neutropenia. The Journal of investigative dermatology 57 21677667
2014 Clinical spectrum and long-term follow-up of 14 cases with G6PC3 mutations from the French Severe Congenital Neutropenia Registry. Orphanet journal of rare diseases 48 25491320
2011 G-CSF improves murine G6PC3-deficient neutrophil function by modulating apoptosis and energy homeostasis. Blood 44 21292774
2012 Inflammatory bowel disease and T cell lymphopenia in G6PC3 deficiency. Journal of clinical immunology 39 23180359
2010 Further delineation of the phenotype of severe congenital neutropenia type 4 due to mutations in G6PC3. European journal of human genetics : EJHG 36 20717171
2002 Expression of high in normal-1 (HIN-1) and uteroglobin related protein-1 (UGRP-1) in adult and developing tissues. Mechanisms of development 35 12175512
2022 Successful use of empagliflozin to treat neutropenia in two G6PC3-deficient children: Impact of a mutation in SGLT5. Journal of inherited metabolic disease 34 35506446
2005 Interleukin-5 reduces the expression of uteroglobin-related protein (UGRP) 1 gene in allergic airway inflammation. Immunology letters 33 15626484
2023 Treatment of the Neutropenia Associated with GSD1b and G6PC3 Deficiency with SGLT2 Inhibitors. Diagnostics (Basel, Switzerland) 32 37238286
2016 G6PC3, ALDOA and CS induction accompanies mir-122 down-regulation in the mechanical asphyxia and can serve as hypoxia biomarkers. Oncotarget 31 27793029
2010 Mutations in the G6PC3 gene cause Dursun syndrome. American journal of medical genetics. Part A 31 20799326
2006 Deletion of the gene encoding the ubiquitously expressed glucose-6-phosphatase catalytic subunit-related protein (UGRP)/glucose-6-phosphatase catalytic subunit-beta results in lowered plasma cholesterol and elevated glucagon. The Journal of biological chemistry 22 17023421
2012 Adult siblings with homozygous G6PC3 mutations expand our understanding of the severe congenital neutropenia type 4 (SCN4) phenotype. BMC medical genetics 20 23171239
2020 Metabolic abnormalities in G6PC3-deficient human neutrophils result in severe functional defects. Blood advances 18 33259599
2011 Two cases of syndromic neutropenia with a report of novel mutation in G6PC3. Iranian journal of allergy, asthma, and immunology 18 21891829
2020 Neutrophil dysfunction triggers inflammatory bowel disease in G6PC3 deficiency. Journal of leukocyte biology 16 32930428
2012 G6PC3 mutations cause non-syndromic severe congenital neutropenia. Molecular genetics and metabolism 16 23298686
2013 Survival and differentiation defects contribute to neutropenia in glucose-6-phosphatase-β (G6PC3) deficiency in a model of mouse neutrophil granulocyte differentiation. Cell death and differentiation 15 23686134
2013 A novel homozygous mutation in G6PC3 presenting as cyclic neutropenia and severe congenital neutropenia in the same family. Journal of clinical immunology 15 24105461
2017 Glucose-6-Phosphatase Catalytic Subunit 3 (G6PC3) Deficiency Associated With Autoinflammatory Complications. Frontiers in immunology 14 29163546
2011 A case of syndromic neutropenia and mutation in G6PC3. Journal of pediatric hematology/oncology 13 21285905
2016 Phenotypic Heterogeneity of Neutropenia and Gastrointestinal Illness Associated with G6PC3 Founder Mutation. Journal of pediatric hematology/oncology 12 27571123
2013 A novel G6PC3 gene mutation in a patient with severe congenital neutropenia. Journal of pediatric hematology/oncology 12 23018568
2022 SLGT2 Inhibitor Rescues Myelopoiesis in G6PC3 Deficiency. Journal of clinical immunology 10 35838821
2020 Lentiviral gene therapy and vitamin B3 treatment enable granulocytic differentiation of G6PC3-deficient induced pluripotent stem cells. Gene therapy 10 32051561
2020 Hypothesis: A Novel Neuroprotective Role for Glucose-6-phosphatase (G6PC3) in Brain-To Maintain Energy-Dependent Functions Including Cognitive Processes. Neurochemical research 9 32815045
2014 Severe congenital neutropenia due to G6PC3 deficiency: early and delayed phenotype in two patients with two novel mutations. Italian journal of pediatrics 9 25391451
2021 Altered Functions of Neutrophils in Two Chinese Patients With Severe Congenital Neutropenia Type 4 Caused by G6PC3 Mutations. Frontiers in immunology 8 34305938
2022 Severe congenital neutropenia due to G6PC3 deficiency: Case series of five patients and literature review. Scandinavian journal of immunology 7 34964150
2021 Comprehensive multi-omics analysis of G6PC3 deficiency-related congenital neutropenia with inflammatory bowel disease. iScience 7 33748703
2023 A molecular signature for the G6PC3/SLC37A2/SLC37A4 interactors in glioblastoma disease progression and in the acquisition of a brain cancer stem cell phenotype. Frontiers in endocrinology 6 38034009
2022 Severe Congenital Neutropenia Type 4: A Rare Disease Harboring a G6pc3 Gene Pathogenic Variant Particular to the Mexican Population. Revista de investigacion clinica; organo del Hospital de Enfermedades de la Nutricion 6 36546889
2021 Novel G6PC3 Mutations in Patients with Congenital Neutropenia: Case Reports and Review of the Literature. Endocrine, metabolic & immune disorders drug targets 5 34137364
2014 A novel G6PC3 gene mutation in severe congenital neutropenia: pancytopenia and variable bone marrow phenotype can also be part of this syndrome. European journal of haematology 5 24750412
2024 Identifying G6PC3 as a Potential Key Molecule in Hypoxic Glucose Metabolism of Glioblastoma Derived from the Depiction of 18F-Fluoromisonidazole and 18F-Fluorodeoxyglucose Positron Emission Tomography. BioMed research international 4 38449509
2023 Severe congenital neutropenia due to G6PC3 deficiency: early and delayed phenotype of a patient. Allergy, asthma, and clinical immunology : official journal of the Canadian Society of Allergy and Clinical Immunology 4 37296469
2022 Amyloidosis in a Patient With Congenital Neutropenia Because of G6PC3 Deficiency. Journal of pediatric hematology/oncology 4 34224517
2017 Coronin 3 negatively regulates G6PC3 in HepG2 cells, as identified by label‑free mass‑spectrometry. Molecular medicine reports 4 28713988
2013 A novel phenotype variant of severe congenital neutropenia caused by G6PC3 deficiency. Pediatric blood & cancer 4 23441086
2016 A Severe Congenital Neutropenia Type 4 Case (G6PC3 Mutation) Presented With Large Platelets in the Peripheral Smear. Journal of pediatric hematology/oncology 3 26808373
2014 Testicular failure in a patient with G6PC3 deficiency. Pediatric research 3 24796372
2011 Functional analysis of the 5' flanking region of the human G6PC3 gene: regulation of promoter activity by glucose, pyruvate, AMP kinase and the pentose phosphate pathway. Molecular genetics and metabolism 2 21474354
2024 Molecular and clinical characterization of a founder mutation causing G6PC3 deficiency. medRxiv : the preprint server for health sciences 1 38798393
2024 Molecular and Clinical Characterization of a Founder Mutation Causing G6PC3 Deficiency. Journal of clinical immunology 1 39630167
2025 G6PC3 promotes genome maintenance and is a candidate mammary tumor suppressor. JCI insight 0 40261702
2024 Molecular and clinical characterization of a founder mutation causing G6PC3 deficiency. Research square 0 39041036
2024 G6PC3 is involved in spermatogenesis by maintaining meiotic sex chromosome inactivation. Acta biochimica et biophysica Sinica 0 39420835
2023 [Correction of the pathogenic mutation in the G6PC3 gene by adenine base editing in mutant embryos]. Zhonghua xue ye xue za zhi = Zhonghua xueyexue zazhi 0 37357000

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