Affinage

G6PC1

Glucose-6-phosphatase catalytic subunit 1 · UniProt P35575

Length
357 aa
Mass
40.5 kDa
Annotated
2026-06-09
45 papers in source corpus 16 papers cited in narrative 17 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

G6PC1 (glucose-6-phosphatase-alpha) is an integral ER membrane glycoprotein that catalyzes the terminal, rate-limiting step of hepatic gluconeogenesis and glycogenolysis — hydrolysis of glucose-6-phosphate to glucose and phosphate — with its active center facing the ER lumen (PMID:18449899). Cryo-EM structures resolve a nine-transmembrane-helix architecture with a large lumen-facing catalytic pocket, and show that substrate binding drives substantial conformational rearrangement of that pocket via an induced-fit mechanism, with phosphatidylserine implicated in regulating activity (PMID:40664655, PMID:39847333). Extensive mutagenesis across the protein distinguishes residues required for catalysis from those required for protein stability and proper glycosylation/localization, and loss-of-function mutations that abolish enzymatic activity cause glycogen storage disease type Ia (PMID:10738525, PMID:18449899, PMID:30890478). The enzyme's contribution to hepatic glucose production is dose-sensitive: restoring ≥3% of normal hepatic activity in G6pc-deficient mice prevents hepatocellular adenoma/carcinoma, linking G6Pase-alpha deficiency to impaired autophagy and hepatocarcinogenesis (PMID:32430177). G6PC1 expression is controlled at multiple levels — transcriptionally through ChREBP and FOXO1 acting at the promoter, with the Mediator kinase subunit MED13 required for fructose-driven ChREBP-dependent activation, and antagonistically through RXRα at DR1 elements (PMID:33812059, PMID:37719384); and post-transcriptionally through METTL14/METTL3-installed m6A marks read by YTHDF1/3 to enhance mRNA stability and translation, and through 3'-UTR AU-rich elements and miRNAs including miR-494 (PMID:40278833, PMID:28502559, PMID:37301960). A CAV1-dependent vesicular pathway traffics G6PC1 to the plasma membrane to support hepatic glucose production.

Mechanistic history

Synthesis pass · year-by-year structured walk · 15 steps
  1. 1999 High

    Established that specific G6PC residues are catalytically essential by showing defined missense mutations abolish enzymatic activity, moving GSD-Ia genotypes toward functional interpretation.

    Evidence Site-directed mutagenesis of four missense variants expressed in COS-7 cells with glucose-6-phosphatase activity assays

    PMID:10738525

    Open questions at the time
    • Did not distinguish loss of catalysis from loss of folding/stability
    • No structural basis for residue importance
  2. 2008 High

    Consolidated the structure-function map of G6PC, defining it as an ER-membrane glycoprotein with a lumen-facing active center and classifying many mutations by their effect on activity versus stability.

    Evidence Compiled heterologous expression, enzymatic assays, and biochemical topology analysis across many mutations

    PMID:18449899

    Open questions at the time
    • Topology and active-site geometry inferred biochemically, not from a structure
    • Regulatory inputs not addressed
  3. 2009 Medium

    Challenged the dogma that elevated G6PC transcription drives fasting hyperglycemia, showing hepatic G6PC mRNA is not increased in T2DM, reframing where dysregulation occurs.

    Evidence Human liver biopsies and rodent fasting-hyperglycemia models with mRNA quantification and isotope-tracer glucose production measurement

    PMID:19587243

    Open questions at the time
    • Negative finding does not exclude post-transcriptional or trafficking-level regulation
    • Does not identify the actual driver of increased gluconeogenesis
  4. 2019 Medium

    Demonstrated in vivo dose-dependence of G6Pase-alpha activity by engineering a hyperactive variant, showing a threshold (≥3% activity) sufficient to prevent tumor development and linking deficiency to autophagy impairment.

    Evidence rAAV delivery of G6PC-S298C in G6pc-/- mice with hepatic activity assays and 66-week phenotyping

    PMID:32430177

    Open questions at the time
    • Mechanism linking deficiency to autophagy impairment not fully defined
    • Single engineered variant in a mouse model
  5. 2019 Medium

    Provided a genetic tool and confirmed essentiality of G6pc Exon 3 in vivo, showing its deletion recapitulates human GSD-Ia.

    Evidence Conditional loxP/Cre knockout mouse with phenotypic characterization

    PMID:19548314

    Open questions at the time
    • Phenotype establishes necessity but not tissue-specific regulatory detail
  6. 2019 Medium

    Identified substrate-level transcriptional feedback, showing glycerol — the preferred fasting gluconeogenic substrate — induces G6pc expression.

    Evidence Primary mouse hepatocyte glucose production assays, 13C isotope tracing, and qPCR

    PMID:31645433

    Open questions at the time
    • Transcription factors mediating glycerol induction not identified
    • Physiological magnitude of feedback unclear
  7. 2021 High

    Placed G6pc transcription within the Mediator kinase module, showing MED13 is required for fructose-driven, ChREBP-dependent activation while FOXO1 promoter binding is independent of it.

    Evidence Liver-specific MED13 knockout mice with ChIP at the G6pc promoter, transcriptional activity assays, and glycogen measurements

    PMID:33812059

    Open questions at the time
    • How MED13 couples to ChREBP at the promoter not resolved
    • Relative contribution of ChREBP vs FOXO1 not quantified
  8. 2021 Medium

    Refined variant pathogenicity interpretation by showing some VUS act through reduced protein levels, altered glycosylation, and mislocalization rather than catalysis alone.

    Evidence Heterologous fusion-protein expression of 29 variants with Western blot, glycosylation analysis, and immunofluorescence

    PMID:34258141

    Open questions at the time
    • Enzymatic activity of all variants not directly measured
    • Single hepatocyte-derived cell line
  9. 2017 Medium

    Established post-transcriptional control of G6PC1 through the 3'-UTR, showing an ARE-dependent SNP destabilizes mRNA and sensitizes it to miRNA repression.

    Evidence Luciferase 3'-UTR reporter and miRNA reporter assays in HepG2 cells with deletion constructs

    PMID:28502559

    Open questions at the time
    • Endogenous mRNA stability effect not measured
    • Specific trans-acting ARE-binding factors not identified
  10. 2023 Medium

    Identified RXRα-DR1 antagonism as a transcriptional brake, with retinaldehyde suppressing G6PC expression and glucose production.

    Evidence DR1 luciferase reporter assays, molecular docking, and mRNA/protein quantification in primary human hepatocytes and HepG2 cells

    PMID:37719384

    Open questions at the time
    • In vivo physiological relevance not established
    • Endogenous occupancy of the DR1 element not directly shown
  11. 2023 Medium

    Linked G6pc repression to cancer metabolic rewiring, showing miR-494 represses G6pc to drive a glycolytic, glycogen/lipid-accumulating survival phenotype in hepatocellular carcinoma.

    Evidence Metabolic assays, live-imaging, and qPCR in HCC cells, patients, and preclinical models

    PMID:37301960

    Open questions at the time
    • Direct miR-494/G6pc binding versus indirect effect not fully dissected
    • Mechanism connecting G6pc loss to HIF-1A activation incomplete
  12. 2023 Medium

    Clarified the functional scope of G6PC1/G6PC2 by showing they modulate intraluminal G6P flux and glucose-stimulated signaling but do not significantly drive HSD11B1-dependent glucocorticoid conversion.

    Evidence Transcriptional fusion gene assay and overexpression in 832/13 and HepG2 cells plus G6pc2 knockout mice

    PMID:37855366

    Open questions at the time
    • Negative result for HSD11B1 coupling in specific systems only
    • G6PC1-specific (vs G6PC2) contribution to islet signaling not isolated
  13. 2025 High

    Defined the m6A regulatory layer, showing METTL14/METTL3 mark G6pc mRNA and YTHDF1/3 readers enhance its stability and translation to control hepatic glucose production.

    Evidence In vitro methylation, METTL14 KO/OE in hepatocytes and mice, five-site m6A mutagenesis (G6pcΔ5A), YTHDF RIP, mRNA stability and glucose production assays, and genetic rescue

    PMID:40278833

    Open questions at the time
    • Upstream signals controlling METTL14 deposition on G6pc not defined
    • Why YTHDF2 does not bind not explained mechanistically
  14. 2025 High

    Resolved the long-inferred topology and catalytic mechanism at atomic resolution, showing nine TM helices, a lumen-facing pocket, an induced-fit substrate engagement, and a possible phosphatidylserine regulatory site.

    Evidence Cryo-EM of apo, fully-open, substrate (G6P/F6P)-bound, product-bound, and catalytic-mutant (H176A) states with functional analysis

    PMID:39847333 PMID:40664655

    Open questions at the time
    • Catalytic chemistry of the phosphohydrolase step not fully detailed
    • Structural basis of phosphatidylserine regulation only partially defined
  15. 2025 Medium

    Extended G6PC1 function beyond the ER lumen, showing a CAV1-dependent vesicular pathway delivers it to the plasma membrane to contribute to hepatic glucose production.

    Evidence Liver-specific CAV1 knockout mice with glucose tolerance tests and fasting glucose/insulin measurements (preprint)

    Open questions at the time
    • Preprint, not peer-reviewed
    • Functional role of plasma-membrane-localized G6PC1 versus ER-localized enzyme not resolved

Open questions

Synthesis pass · forward-looking unresolved questions
  • How the transcriptional (ChREBP/FOXO1/MED13/RXRα), m6A, 3'-UTR/miRNA, and CAV1-trafficking regulatory layers are integrated to set hepatic G6PC1 output under physiological fasting versus disease states remains unresolved.
  • No unified model linking transcriptional, post-transcriptional, and trafficking control
  • Relative quantitative contribution of each regulatory layer in vivo unknown

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0016787 hydrolase activity 5 GO:0016740 transferase activity 2
Localization
GO:0005783 endoplasmic reticulum 3 GO:0005886 plasma membrane 1
Pathway
R-HSA-1430728 Metabolism 3
Partners
CAV1

Evidence

Reading pass · 17 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
2025 Cryo-EM structures of human G6PC1 were solved in apo (partially open) and fully open states, and in complex with substrates G6P or F6P and product phosphate. G6PC1 comprises nine transmembrane helices with a large catalytic pocket facing the ER lumen. Substrate binding induces substantial conformational rearrangements (induced-fit mechanism) in the catalytic pocket that facilitate sugar moiety binding. The structures also reveal a potential mechanism by which phosphatidylserine regulates G6PC1 activity. Cryo-EM structure determination with functional analysis; substrate-bound and apo forms resolved Cell discovery High 40664655
2025 Cryo-EM structures of wild-type human G6PC1 (apo) and a catalytic mutant G6PC1-H176A bound to G6P were solved, revealing nine transmembrane helices, a large catalytic pocket facing the ER lumen, and that G6P binding induces substantial conformational rearrangements in the catalytic pocket facilitating sugar moiety binding. Cryo-EM structure determination of wild-type apo and H176A mutant + G6P complex, with functional analyses Proceedings of the National Academy of Sciences of the United States of America High 39847333
1999 Four missense mutations in G6PC (W77R, A124T, G184E, L211P) were individually introduced by site-directed mutagenesis and expressed in COS-7 cells; all four mutations completely abolished G6PC enzymatic (glucose-6-phosphatase) activity, establishing these residues as functionally critical. In vitro expression system (COS-7 cells), site-directed mutagenesis, enzymatic activity assay Annals of human genetics High 10738525
2008 G6PC encodes glucose-6-phosphatase-alpha, a highly hydrophobic glycoprotein anchored in the ER membrane with its active center facing the ER lumen, catalyzing hydrolysis of glucose-6-phosphate to glucose and phosphate. Functional characterization of 50 missense, 2 nonsense, and 2 insertion/deletion mutations confirmed their effects on enzymatic activity and protein stability, establishing structure-function relationships across the protein. Compiled functional characterization from heterologous expression and enzymatic assays across multiple studies; topology established by biochemical analysis Human mutation High 18449899
2021 A panel of 29 G6PC coding variants was heterologously expressed as fusion proteins in a hepatocyte-derived cell line. The screen revealed variant effects on steady-state protein levels, N-linked glycosylation status, and intracellular distribution. The VUS p.Cys109Tyr exhibited significantly reduced protein levels, altered glycosylation, and abnormally diffuse localization, consistent with pathogenicity. Heterologous expression of fusion proteins, Western blot for protein levels and glycosylation, immunofluorescence for intracellular distribution JIMD reports Medium 34258141
2019 A single amino acid substitution S298C in human G6PC (rAAV-G6PC-S298C) increased enzymatic efficacy approximately 3-fold compared to native G6PC in G6pc-/- mice, demonstrating that position 298 influences G6PC activity level in vivo. Restoring ≥3% of normal hepatic G6Pase-alpha activity prevented hepatocellular adenoma/carcinoma development, and G6Pase-alpha deficiency leads to hepatic autophagy impairment that can contribute to hepatocarcinogenesis. In vivo gene transfer in G6pc-/- mice, hepatic G6Pase activity assay, long-term (66-week) phenotypic characterization Biochemical and biophysical research communications Medium 32430177
2021 The Mediator complex kinase module subunit MED13 is required for transcriptional activation of G6pc by fructose in the liver. In liver-specific MED13 knockout mice, ChREBP binding to the G6pc promoter was dramatically reduced and ChREBP-beta and FOXO1 transcriptional activities were suppressed, while FOXO1 binding to the G6pc promoter was unaffected. This establishes that MED13/Mediator kinase module is necessary for ChREBP-dependent G6pc transcription and consequent regulation of liver glycogen levels. Liver-specific MED13 knockout mice, G6PC enzymatic activity assay, ChIP assay at G6pc promoter, transcriptional activity assays in hepatocytes, glycogen measurements Molecular metabolism High 33812059
2025 METTL14, in complex with METTL3, installs N6-methyladenosine (m6A) on G6pc mRNA at five sites. m6A readers YTHDF1 and YTHDF3 (but not YTHDF2) bind to m6A-marked G6pc mRNA to increase both its stability and translation, thereby increasing G6PC protein levels and hepatic glucose production. Deletion of five m6A sites (G6pcΔ5A) blocked METTL14-induced effects. Liver-specific Mettl14 knockout decreased G6pc expression and gluconeogenesis; hepatocyte-specific G6pc restoration reversed defective hepatic glucose production in Mettl14 KO mice. In vitro m6A methylation, METTL14 KO and OE in hepatocytes and mice, m6A site mutagenesis (G6pcΔ5A), RIP assays, mRNA stability assay, glucose production assay, genetic rescue experiment Advanced science (Weinheim, Baden-Wurttemberg, Germany) High 40278833
2017 A 3'-UTR SNP rs2229611 in G6PC1 reduces mRNA stability and decreases expression. In HepG2 cells, luciferase constructs bearing the rs2229611 allele showed significantly decreased expression compared to wild-type 3'-UTR, due to reduced mRNA stability mediated by AU-rich elements (AREs). miRNAs also showed more distinct inhibition of reporter function with rs2229611. This demonstrates a post-transcriptional regulatory mechanism for G6PC1 expression. Luciferase reporter assay in HepG2 cells, 3'-UTR deletion constructs, pmirGLO-UTR constructs for miRNA effects Clinica chimica acta; international journal of clinical chemistry Medium 28502559
2023 Retinaldehyde (Rald) downregulates G6PC expression by antagonizing retinoid X receptor alpha (RXRα) at direct repeat 1 (DR1) response elements in the G6PC/PCK1 promoters. This was confirmed by luciferase reporter assays and molecular docking. In primary human hepatocytes and HepG2 cells, Rald treatment decreased G6PC mRNA and protein expression and reduced glucose production. Luciferase reporter assays (DR1 elements), molecular docking, primary human hepatocyte experiments, mRNA/protein quantification Acta pharmaceutica Sinica. B Medium 37719384
2023 miR-494 targets G6pc mRNA in hepatocellular carcinoma cells, inducing a metabolic shift toward glycolytic phenotype through G6pc repression and HIF-1A pathway activation. The miR-494/G6pc axis drives glycogen and lipid droplet accumulation that favors cell survival under harsh conditions. Functional analysis, metabolic assays, live-imaging of HCC cells, qPCR in HCC patients and preclinical models Journal of experimental & clinical cancer research : CR Medium 37301960
2019 Glycerol can induce G6pc expression (a rate-limiting enzyme of gluconeogenesis) in primary mouse hepatocytes, demonstrating a substrate-level regulatory feedback on G6PC transcription. Glycerol is the preferred gluconeogenic substrate over pyruvate/lactate at physiological fasting concentrations both in vitro and in vivo. Primary mouse hepatocyte glucose production assays, 13C isotope tracing, real-time PCR for G6pc expression The Journal of biological chemistry Medium 31645433
2025 G6PC1 traffics to the plasma membrane via a CAV1 (Caveolin-1)-dependent vesicular pathway in hepatocytes. Liver-specific CAV1 knockout (L.Cav1-/- mice) reduced G6PC1 plasma membrane localization, decreased fasting hyperglycemia and hyperinsulinemia, and improved insulin sensitivity in mice on high-fat/high-sucrose diet, establishing that CAV1-mediated G6PC1 trafficking contributes to hepatic glucose production. Liver-specific CAV1 knockout mice (AAV or Cre-lox), glucose tolerance tests, fasting blood glucose and insulin measurements, in vivo glucose production assessment bioRxivpreprint Medium
2023 G6PC1 and G6PC2 overexpression in 832/13 islet-derived cells blunted glucose-stimulated signaling (as measured by a transcriptional fusion gene assay), reflecting their role in reducing intraluminal G6P flux. However, G6PC1 and G6PC2 overexpression had minimal effect on glucocorticoid-stimulated HSD11B1 activity in either 832/13 or HepG2 cells, and G6pc2 knockout mice showed metabolic changes unaffected by G6PC2 absence, indicating G6PC1/G6PC2 activity does not significantly modulate HSD11B1-dependent glucocorticoid conversion. Transcriptional fusion gene assay, overexpression in 832/13 and HepG2 cells, G6pc2 knockout mice treated with 11-DHC Journal of molecular endocrinology Medium 37855366
2019 Mice were generated with a conditional null allele for G6pc (loxP sites flanking Exon 3). EIIa-Cre-mediated deletion of Exon 3 produced a null phenotype mimicking G6Pase-alpha-deficient mice and human GSD-Ia, establishing that Exon 3 is essential for G6PC function in vivo. Conditional knockout mouse generation (loxP/Cre), phenotypic characterization Genesis (New York, N.Y. : 2000) Medium 19548314
2019 Five novel G6PC1 mutations (p.V99Cfs*3, p.G125R, IVS1-2A>T, IVS3+39G>A, IVS3+42G>A) were identified in Indian GSD-1a patients. Functional characterization showed that mutant proteins p.G125R, p.R149Q, p.G118D, p.A331V, and p.V99Cfs*3 completely abrogated glucose-6-phosphatase activity without significant changes in mRNA or protein expression levels, indicating these residues are required for catalytic activity rather than protein stability. Direct DNA sequencing, glucose-6-phosphatase activity assay, RT-PCR and Western blot for expression Gene Medium 30890478
2009 In contrast to prevailing dogma, increased transcriptional expression of G6PC does not account for increased gluconeogenesis and fasting hyperglycemia in type 2 diabetes patients or in rodent models of fasting hyperglycemia (STZ/HFF rats and portal infusion models). Hepatic G6PC expression was not elevated in insulin-sensitive, insulin-resistant, or untreated T2DM patients undergoing bariatric surgery. Liver biopsy samples from human patients, rat models with portal vein infusion; mRNA quantification, endogenous glucose production measurement by isotope tracer Proceedings of the National Academy of Sciences of the United States of America Medium 19587243

Source papers

Stage 0 corpus · 45 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2009 Fasting hyperglycemia is not associated with increased expression of PEPCK or G6Pc in patients with Type 2 Diabetes. Proceedings of the National Academy of Sciences of the United States of America 133 19587243
2008 Mutations in the glucose-6-phosphatase-alpha (G6PC) gene that cause type Ia glycogen storage disease. Human mutation 124 18449899
2010 Complete normalization of hepatic G6PC deficiency in murine glycogen storage disease type Ia using gene therapy. Molecular therapy : the journal of the American Society of Gene Therapy 69 20389290
2018 G6PC mRNA Therapy Positively Regulates Fasting Blood Glucose and Decreases Liver Abnormalities in a Mouse Model of Glycogen Storage Disease 1a. Molecular therapy : the journal of the American Society of Gene Therapy 62 29428299
2021 tRNA-derived fragment tRFLys-CTT-010 promotes triple-negative breast cancer progression by regulating glucose metabolism via G6PC. Carcinogenesis 36 34216208
2023 MiR-494 induces metabolic changes through G6pc targeting and modulates sorafenib response in hepatocellular carcinoma. Journal of experimental & clinical cancer research : CR 34 37301960
2019 Glycerol induces G6pc in primary mouse hepatocytes and is the preferred substrate for gluconeogenesis both in vitro and in vivo. The Journal of biological chemistry 33 31645433
2015 Genetic and molecular analyses reveal G6PC as a key element connecting glucose metabolism and cell cycle control in ovarian cancer. Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine 32 25926381
2020 Large-scale transcriptome profiles reveal robust 20-signatures metabolic prediction models and novel role of G6PC in clear cell renal cell carcinoma. Journal of cellular and molecular medicine 31 32567187
2011 Berberine regulated Gck, G6pc, Pck1 and Srebp-1c expression and activated AMP-activated protein kinase in primary rat hepatocytes. International journal of biological sciences 27 21647250
2013 The upstream enhancer elements of the G6PC promoter are critical for optimal G6PC expression in murine glycogen storage disease type Ia. Molecular genetics and metabolism 25 23856420
1999 Enzymatic characterization of four new mutations in the glucose-6 phosphatase (G6PC) gene which cause glycogen storage disease type 1a. Annals of human genetics 24 10738525
2020 Predominance of the c.648G > T G6PC gene mutation and late complications in Korean patients with glycogen storage disease type Ia. Orphanet journal of rare diseases 19 32046761
2023 Hepatic retinaldehyde deficiency is involved in diabetes deterioration by enhancing PCK1- and G6PC-mediated gluconeogenesis. Acta pharmaceutica Sinica. B 18 37719384
2017 3'-UTR SNP rs2229611 in G6PC1 affects mRNA stability, expression and Glycogen Storage Disease type-Ia risk. Clinica chimica acta; international journal of clinical chemistry 18 28502559
2019 Hepatic Gluconeogenic Response to Single and Long-Term SGLT2 Inhibition in Lean/Obese Male Hepatic G6pc-Reporter Mice. Endocrinology 17 31517956
2019 A Proteomic Analysis of GSD-1a in Mouse Livers: Evidence for Metabolic Reprogramming, Inflammation, and Macrophage Polarization. Journal of proteome research 14 31173686
2009 Generation of mice with a conditional allele for G6pc. Genesis (New York, N.Y. : 2000) 13 19548314
2020 Gene therapy using a novel G6PC-S298C variant enhances the long-term efficacy for treating glycogen storage disease type Ia. Biochemical and biophysical research communications 12 32430177
2021 The Mediator complex kinase module is necessary for fructose regulation of liver glycogen levels through induction of glucose-6-phosphatase catalytic subunit (G6pc). Molecular metabolism 11 33812059
2025 METTL14-Induced M6A Methylation Increases G6pc Biosynthesis, Hepatic Glucose Production and Metabolic Disorders in Obesity. Advanced science (Weinheim, Baden-Wurttemberg, Germany) 10 40278833
2014 Three novel mutations of the G6PC gene identified in Chinese patients with glycogen storage disease type Ia. European journal of pediatrics 10 24980439
2021 The Transplantation Resistance of Type II Diabetes Mellitus Adipose-Derived Stem Cells Is Due to G6PC and IGF1 Genes Related to the FoxO Signaling Pathway. International journal of molecular sciences 9 34205470
2025 Structural insights into glucose-6-phosphate recognition and hydrolysis by human G6PC1. Proceedings of the National Academy of Sciences of the United States of America 8 39847333
2025 HKDC1 promotes ovarian cancer progression through boosting lipid metabolism and immune escape by stabilizing G6PC/G6PC2. Communications biology 7 40234623
2023 A splice-switching oligonucleotide treatment ameliorates glycogen storage disease type 1a in mice with G6PC c.648G>T. The Journal of clinical investigation 7 37788110
2013 Determining mutations in G6PC and SLC37A4 genes in a sample of Brazilian patients with glycogen storage disease types Ia and Ib. Genetics and molecular biology 7 24385852
2011 Treatment of newborn G6pc(-/-) mice with bone marrow-derived myelomonocytes induces liver repair. Journal of hepatology 7 21703205
2024 The FOXO1/G6PC axis promotes gastric cancer progression and mediates 5-fluorouracil resistance by targeting the PI3K/AKT/mTOR signaling pathway. Molecular carcinogenesis 6 38224261
2013 A novel homozygous no-stop mutation in G6PC gene from a Chinese patient with glycogen storage disease type Ia. Gene 6 24355556
2021 Classifying molecular phenotypes of G6PC variants for pathogenic properties and to guide therapeutic development. JIMD reports 5 34258141
2021 Chronic AT1 blockade improves hyperglycemia by decreasing adipocyte inflammation and decreasing hepatic PCK1 and G6PC1 expression in obese rats. American journal of physiology. Endocrinology and metabolism 5 34658252
2021 Glycogen Storage Disease Type Ia Screening Using Dried Blood Spots on Filter Paper: Application of COP-PCR for Detection of the c.648G>T G6PC Gene Mutation. The Kobe journal of medical sciences 4 34795158
2021 DBS Screening for Glycogen Storage Disease Type 1a: Detection of c.648G>T Mutation in G6PC by Combination of Modified Competitive Oligonucleotide Priming-PCR and Melting Curve Analysis. International journal of neonatal screening 4 34842616
2025 The induced-fit and catalytic mechanisms of human G6PC1. Cell discovery 3 40664655
2019 Mutational spectrum and identification of five novel mutations in G6PC1 gene from a cohort of Glycogen Storage Disease Type 1a. Gene 3 30890478
2023 Rare functional variants in the CRP and G6PC genes modify the relationship between obesity and serum C-reactive protein in white British population. Molecular genetics & genomic medicine 2 37493001
2020 The rs2229611 (G6PC:c.*23 T>C) is associated with glycogen storage disease type Ia in Brazilian patients. Molecular genetics and metabolism reports 2 33101979
2025 Tissue-specific profiling of human protein phosphatases identifies G6PC1 as a liver cancer-selective biomarker. Discover oncology 1 40864347
2023 G6PC1 and G6PC2 influence G6P flux but not HSD11B1 activity. Journal of molecular endocrinology 1 37855366
2021 [G6PC knockdown blocks AKT/mTOR pathway to inhibit proliferation, invasion and migration of cervical cancer HeLa cells]. Xi bao yu fen zi mian yi xue za zhi = Chinese journal of cellular and molecular immunology 1 34060447
2026 A FOXO1-G6PC transcriptional axis restrains renal cell carcinoma progression: multi-omics, epigenetic, and mechanistic evidence. Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico 0 41770520
2026 G6PC Downregulation Promotes Renal Calcium Oxalate Stone Formation via Lactate-Induced SNAIL1 K206 Lactylation and Epithelial-Mesenchymal Transition. Advanced science (Weinheim, Baden-Wurttemberg, Germany) 0 42107057
2023 The Peptide AWRK6 Alleviates Lipid Accumulation in Hepatocytes by Inhibiting miR-5100 Targeting G6PC. International journal of molecular sciences 0 38003331
2022 Phylogeny of g6pc1 Genes and Their Functional Divergence among Sarcopterygian Vertebrates: Implications for Thermoregulatory Strategies. Zoological science 0 36205363

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