Affinage

PFKL

ATP-dependent 6-phosphofructokinase, liver type · UniProt P17858

Length
780 aa
Mass
85.0 kDa
Annotated
2026-06-10
32 papers in source corpus 21 papers cited in narrative 22 extracted findings
Cross-family judge vs UniProt: tie faithfulness: 8/8 claims corpus-supported (100%)

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

PFKL is the liver-type subunit of phosphofructokinase-1, the rate-limiting glycolytic enzyme whose activity is governed by allosteric control, post-translational modification, and protein turnover (PMID:34320407, PMID:6455664). The L-subunit randomly tetramerizes with M and P subunits, and its gene resides on chromosome 21, producing gene-dosage effects in trisomy 21 (PMID:6455664). Catalytic output is set by R-state tetramer formation: small molecules (NA-11) and a covalent electrophile conjugate bind the AMP/ADP-type allosteric effector site to stabilize the active tetramer and raise glycolytic flux while damping the pentose phosphate pathway and NADPH-oxidase-driven oxidative burst (PMID:34320407, PMID:41256653), whereas PTGES3 docks on PFKL to deliver locally generated prostaglandin E2 that allosterically inhibits it (PMID:37831605). A layer of post-translational marks tunes the same tetramerization/activity axis: Ser775 phosphorylation downstream of innate immune (LPS) signaling activates PFKL to elevate glycolysis, HIF1α, and IL-1β (PMID:39085210); HDAC6-mediated deacetylation at K563 promotes tetramer assembly and activity (PMID:41421488); and PRMT9-mediated methylation at R301, triggered by lactate, inactivates PFKL and redirects flux toward the pentose phosphate pathway and NETosis (PMID:40222696). PFKL abundance is further controlled by opposing ubiquitin-proteasome and lysosomal pathways—the E3 ligases A20 and PDLIM2 promote its degradation, while the deubiquitinases USP14 and a DNAAF5/USP39 complex stabilize it, and Caveolin-1 protects it from SQSTM1-mediated lysosomal degradation (PMID:32015333, PMID:38388430, PMID:36276075, PMID:37116593). Its transcription is repressed by EGR1 and activated by SREBF1 and KLF7 (PMID:38287371, PMID:35720503, PMID:36810848). Beyond glycolysis, PFKL moonlights under glucose deprivation as a protein kinase that phosphorylates PLIN2 on lipid droplets to tether them to mitochondria and promote fatty acid oxidation (PMID:38773347). Across tissues, PFKL-driven glycolysis shapes innate immune activation, cardiac and vascular remodeling, brain glucose flux, and tumor cell metabolism (PMID:39085210, PMID:36810848, PMID:9813288, PMID:41421488).

Mechanistic history

Synthesis pass · year-by-year structured walk · 9 steps
  1. 1981 High

    Established the genetic and biochemical identity of PFKL as a distinct PFK subunit, locating its gene and showing it tetramerizes combinatorially with other PFK subunits.

    Evidence Somatic cell hybrid mapping and subunit-specific monoclonal antibody immunoprecipitation with isozyme chromatography

    PMID:6455664

    Open questions at the time
    • No catalytic or structural mechanism addressed
    • Functional consequence of trisomy-21 dosage elevation not resolved
  2. 1994 Medium

    Showed that PFKL overexpression produces tissue- and developmental-stage-specific increases in PFK activity, demonstrating dosage-sensitive control of glycolytic capacity in vivo.

    Evidence Transgenic mice with a PFKL gene-cDNA construct, enzymatic assays across tissues and developmental stages

    PMID:8172601

    Open questions at the time
    • No measurement of downstream metabolic flux
    • Mechanism of stage-specific regulation unknown
  3. 1998 Medium

    Connected elevated PFKL protein to altered organ-level glucose flux, showing it directly accelerates cerebral glucose metabolism.

    Evidence In vivo [1-13C]-glucose NMR flux measurement in transgenic mice

    PMID:9813288

    Open questions at the time
    • Does not address allosteric or PTM regulation
    • Single transgenic model
  4. 2020 Medium

    Identified ubiquitin-proteasome control as a determinant of PFKL abundance, with A20 as a degrading E3 ligase that lowers glycolysis.

    Evidence Co-IP, ubiquitination assay, and knockdown rescue in hepatocellular carcinoma cells

    PMID:32015333

    Open questions at the time
    • Ubiquitination site not mapped
    • Single lab, no in vivo validation
  5. 2021 High

    Defined a druggable allosteric activation mechanism: stabilizing the R-state tetramer at the AMP/ADP site raises glycolytic flux and suppresses pentose-phosphate-fueled oxidative burst, with structural proof of isoform selectivity.

    Evidence Chemical proteomics, high-resolution crystal structure of PFKL bound to NA-11, neutrophil ROS/NETosis assays

    PMID:34320407

    Open questions at the time
    • Endogenous physiological ligand occupancy of the site not quantified
    • Selectivity over PFKM/PFKP defined structurally but in limited cell contexts
  6. 2022 Medium

    Revealed PFKL abundance is set by competing degradation and stabilization pathways and by transcriptional inputs, embedding glycolysis in cancer feedback loops.

    Evidence MeRIP, Co-IP via EFTUD2, ubiquitination, luciferase promoter, and Seahorse assays across HCC, LSCC, and liver cancer models (YTHDF3, PDLIM2, SREBF1)

    PMID:35511493 PMID:35720503 PMID:35723199 PMID:36471428

    Open questions at the time
    • Interaction interfaces not mapped by mutagenesis
    • Several findings rest on single Co-IP without reciprocal validation
  7. 2023 Medium

    Established allosteric inhibition of PFKL by a locally delivered metabolite and added lysosomal and transcriptional layers of control with defined tissue phenotypes.

    Evidence CRISPR screen, Co-IP, enzymatic and flux assays (PTGES3-PGE2), cardiac-specific KLF7/PFKL epistasis mice, and HSC Cav1/SQSTM1 competition

    PMID:36810848 PMID:37116593 PMID:37831605

    Open questions at the time
    • Structural basis of PTGES3 docking unknown
    • Quantitative contribution of each regulatory layer in vivo not resolved
  8. 2024 High

    Uncovered a non-glycolytic moonlighting role and an activating phosphorylation, broadening PFKL from metabolic enzyme to a signaling and lipid-droplet regulator.

    Evidence In vitro kinase assay and PLIN2 phosphosite mutagenesis with LD-mitochondria imaging; Ser775 knock-in mouse with LPS inflammation phenotyping; USP14/DNAAF5-USP39 deubiquitinase Co-IP and rescue; EGR1 promoter repression

    PMID:36276075 PMID:38287371 PMID:38388430 PMID:38773347 PMID:39085210

    Open questions at the time
    • Kinase that phosphorylates PFKL to switch on the moonlighting function not identified
    • Substrate repertoire of the PFKL kinase activity beyond PLIN2 unknown
    • Identity of the Ser775 kinase not established
  9. 2025 Medium

    Demonstrated that acetylation and methylation directly control tetramer assembly and metabolic routing, and that the allosteric site can be covalently engaged for therapeutic activation.

    Evidence HDAC6 deacetylation at K563 with native-gel tetramer assay and K563R/K563Q mutants in VSMC/neointima models; lactate-driven PRMT9 methylation at R301 with NETosis phenotyping; covalent EDC modifying K677 (preprint)

    PMID:40222696 PMID:41256653 PMID:41421488

    Open questions at the time
    • Crosstalk between K563 acetylation, R301 methylation, and S775 phosphorylation untested
    • EDC mechanism reported only in preprint

Open questions

Synthesis pass · forward-looking unresolved questions
  • How the multiple competing PTMs, allosteric ligands, and the moonlighting kinase switch are integrated to set PFKL state in a given cell remains unresolved.
  • No unified model of combinatorial PTM control on the tetramer
  • Functional relevance of the oxidized-actin interaction unestablished
  • Upstream kinase for the glucose-deprivation moonlighting switch unknown

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0016740 transferase activity 3 GO:0098772 molecular function regulator activity 3 GO:0140096 catalytic activity, acting on a protein 1
Localization
GO:0005829 cytosol 2 GO:0005811 lipid droplet 1
Pathway
R-HSA-1430728 Metabolism 3 R-HSA-74160 Gene expression (Transcription) 3 R-HSA-168256 Immune System 2
Partners
A20DNAAF5HDAC6PDLIM2PLIN2PTGES3USP14YTHDF3
Complex memberships
phosphofructokinase-1 tetramer

Evidence

Reading pass · 22 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
2021 Small-molecule NA-11 (and precursor LDC7559) selectively activates PFKL by binding to the AMP/ADP allosteric activation site, stabilizing the R-state tetramer. This increases glycolytic flux, dampens pentose phosphate pathway activity, and suppresses NADPH oxidase NOX2-dependent oxidative burst, NETosis, and tissue damage in neutrophils. A high-resolution crystal structure of PFKL confirmed binding of NA-11 to this allosteric site and explained isoform selectivity over PFKP and PFKM. Chemical proteomics (two unbiased strategies), high-resolution crystal structure of PFKL bound to NA-11, neutrophil functional assays (ROS, NETosis), pharmacological activation with analog design Cell High 34320407
2024 Under glucose deprivation, PFKL is phosphorylated, reducing its glycolytic activity and promoting its interaction with PLIN2 on lipid droplets. In this context PFKL acts as a protein kinase and phosphorylates PLIN2, which triggers PLIN2 binding to CPT1A, tethering lipid droplets to mitochondria and recruiting adipose triglyceride lipase (ATGL) to promote fatty acid oxidation. This 'moonlighting' kinase function of PFKL supports tumor cell proliferation under energy stress. Co-immunoprecipitation, in vitro kinase assay, phosphorylation-site mutagenesis, lipid droplet-mitochondria co-localization imaging, genetic knockdown/overexpression, xenograft mouse model Nature metabolism High 38773347
2020 The E3 ubiquitin ligase A20 directly interacts with PFKL and promotes its ubiquitin-mediated proteasomal degradation, thereby reducing glycolytic flux in hepatocellular carcinoma cells. Co-immunoprecipitation, ubiquitination assay, RNA interference knockdown of A20 and PFKL, glycolysis measurement Cell death & disease Medium 32015333
1981 Using somatic cell hybrids and an anti-L-subunit-specific monoclonal antibody, the PFKL gene was mapped to human chromosome 21. The L-subunit randomly tetramerizes with M and P subunits to form multiple PFK isozymes. Trisomy 21 individuals show a gene-dosage-dependent elevation of PFKL-containing isozymes in erythrocytes. Somatic cell hybrid panel, enzyme immunoprecipitation with monoclonal antibody, ion exchange chromatography of isozymes, chromosome marker analysis Proceedings of the National Academy of Sciences of the United States of America High 6455664
2024 PFKL is phosphorylated at Ser775 in macrophages following innate immune stimulation (e.g., LPS). This phosphorylation increases PFKL catalytic activity, elevating glycolytic flux, HIF1α, and IL-1β levels. A knock-in mouse model (PfklS775A/S775A) preventing this phosphorylation showed reduced glycolysis, lower HIF1α and IL-1β after LPS treatment, and reduced MCP-1 and IL-1β in an in vivo inflammation model. Biochemical phosphorylation assay, glycolysis monitoring in cells expressing phosphorylation-defective PFKL variants, genetic knock-in mouse model, in vivo inflammation model Nature communications High 39085210
2023 PTGES3 binds directly to PFKL and generates a local source of prostaglandin E2 (PGE2) that allosterically inhibits PFKL enzymatic activity, reducing glycolytic and TCA-cycle flux. Loss of PTGES3 in ovarian cancer disrupts this PTGES3-PGE2-PFKL inhibitory axis, leading to hyperactivation of glucose oxidation and enhanced tumor cell motility/invasiveness. Genome-wide CRISPR-Cas9 screen, co-immunoprecipitation of PTGES3 and PFKL, enzymatic activity assay, metabolic flux measurements, loss-of-function in ovarian cancer cells Cell reports Medium 37831605
2023 The transcription factor KLF7 directly targets the PFKL promoter to regulate its expression. Cardiac-specific knockout of KLF7 elevates PFKL-driven glycolysis and causes adult concentric hypertrophy, while cardiac-specific knockdown of PFKL partially rescues this hypertrophy, placing PFKL downstream of KLF7 in a KLF7/PFKL/ACADL metabolic axis. ChIP or promoter analysis, cardiac-specific KLF7 knockout and overexpression mice, cardiac-specific PFKL knockdown (AAV), echocardiographic and metabolic flux measurements Nature communications Medium 36810848
1994 Transgenic mice overexpressing murine PFKL show tissue-specific elevated PFK activity that mirrors endogenous expression patterns. Embryonic transgenic brains, but not adult brains, exhibit nearly doubled PFK specific activity, demonstrating developmental stage-specific gene-dosage effects of PFKL overexpression. Transgenic mouse generation (PFKL 'gene-cDNA' hybrid construct), enzymatic activity assays in multiple tissues at different developmental stages The Biochemical journal Medium 8172601
1998 Transgenic-PFKL mice with elevated PFKL show increased cerebral glucose metabolic rate (58% faster initial utilization) measured by in vivo [1-13C]-glucose NMR, despite slower peripheral blood glucose clearance, demonstrating that PFKL overexpression directly alters brain glucose flux. In vivo [1-13C]-glucose infusion followed by NMR spectroscopy, blood glucose clearance assay, enzymatic activity measurements in blood and brain Brain research Medium 9813288
2022 YTHDF3 promotes PFKL mRNA stability via m6A modification, increasing PFKL protein levels. In turn, PFKL interacts with YTHDF3 through the spliceosome subunit EFTUD2 and inhibits ubiquitination of YTHDF3, stabilizing it. This bidirectional positive feedback loop enhances aerobic glycolysis in hepatocellular carcinoma. Methylated RNA immunoprecipitation (MeRIP), co-immunoprecipitation, immunofluorescence, ubiquitination assay, gain/loss-of-function in vitro and in vivo Journal of experimental & clinical cancer research : CR Medium 36471428
2024 DNAAF5 directly binds PFKL and recruits the deubiquitinase USP39 to form a ternary complex, stabilizing PFKL protein by promoting its deubiquitination and preventing its proteasomal degradation, thereby enhancing glycolysis in HCC cells. Co-immunoprecipitation, mass spectrometry, ubiquitination assay, USP39 knockdown functional rescue, xenograft mouse model Frontiers in oncology Medium 36276075
2024 USP14 directly interacts with PFKL and stabilizes it through deubiquitination, preventing its proteasomal degradation and enhancing PFKL-mediated glycolysis in oral squamous cell carcinoma. Co-immunoprecipitation, ubiquitination assay, knockdown/overexpression in OSCC cells, glycolysis measurement Journal of translational medicine Medium 38388430
2022 PDLIM2, an E3 ubiquitin ligase, promotes ubiquitination and degradation of PFKL. M2 macrophage-derived exosomes deliver miR-222-3p into LSCC cells to suppress PDLIM2, thereby stabilizing PFKL and enhancing glycolysis. Ubiquitination assay, luciferase assay (miRNA target validation), extracellular acidification rate (Seahorse), knockdown in FaDu cells, xenograft mouse model Neoplasma Medium 35723199
2023 Caveolin-1 (Cav1) in hepatic stellate cells competes with SQSTM1 for binding to the regulatory domain of PFKL, thereby blocking SQSTM1-mediated autophagy-independent lysosomal degradation of PFKL and sustaining elevated PFKL levels and glycolysis during HSC activation. HSC-specific Cav1 knockdown in mice, co-immunoprecipitation (Cav1, SQSTM1, PFKL), lysosomal pathway assays, fibrosis phenotyping Free radical biology & medicine Medium 37116593
2025 HDAC6 acts as the deacetylase of PFKL, interacting with PFKL and deacetylating it primarily at K563. Deacetylation of PFKL by HDAC6 promotes PFKL tetrameric assembly and increases enzymatic activity, enhancing aerobic glycolysis and VSMC proliferation. The acetylation-mimicking mutant K563Q attenuates, while the deacetylation-mimicking K563R mutant aggravates PDGF-BB-induced VSMC proliferation and neointimal formation. Co-immunoprecipitation (HDAC6-PFKL), site-directed mutagenesis (K563R/K563Q), recombinant adenoviral overexpression, HDAC inhibitor (TSA/siHDAC6), glycolysis measurement, native gel for tetramer formation, in vivo ligation-induced neointima model The Journal of biological chemistry High 41421488
2025 Lactate produced by cardiomyocytes triggers PRMT9-mediated methylation of PFKL at residue R301 in neutrophils, resulting in PFKL inactivation, reduced glycolysis, and redirection of metabolic flux from glycolysis toward the pentose phosphate pathway, thereby promoting NETosis. Mass spectrometry imaging, in vivo/in vitro lactate supplementation and withdrawal, cardiomyocyte-specific PDK4 knockout mouse, PRMT9 methylation assay, NETosis phenotyping Pharmacological research Medium 40222696
2025 A covalent electrophile-drug conjugate (EDC) site-specifically modifies K677 in the allosteric effector site of PFKL, stabilizing the R-state tetramer and activating PFKL, which induces metabolic imbalance and delivers a cytotoxic payload to cancer cells in vitro and in vivo. Chemical proteomics (proteome-wide selectivity profiling), site-specific covalent modification at K677 confirmed biochemically, PFKL R-state tetramer stabilization assay, in vitro and in vivo tumor growth assays bioRxivpreprint Medium 41256653
2022 PFKL preferentially interacts with oxidized methionine-containing actin peptides (Met44/Met47 oxidized) compared with reduced forms, and this differential interaction is also observed with full-length actin protein, suggesting methionine oxidation on actin regulates the actin-PFKL interaction. Photo-crosslinking peptide pulldown, mass spectrometry-based proteomics, full-length actin interaction assay RSC chemical biology Low 36320891
2022 PFKL interacts with YTHDF3 through EFTUD2 (a core spliceosome subunit), and this interaction inhibits ubiquitination of YTHDF3, stabilizing it post-translationally. Co-immunoprecipitation, ubiquitination assay Journal of experimental & clinical cancer research : CR Low 36471428
2024 EGR1 transcription factor binds directly to the PFKL promoter and represses PFKL gene expression, thereby inhibiting PFKL-mediated aerobic glycolysis in hepatocellular carcinoma. ChIP or promoter-binding assay (reporter/EMSA implied), EGR1 overexpression/knockdown, glycolysis measurement, xenograft and organoid models Journal of experimental & clinical cancer research : CR Medium 38287371
2022 SREBF1 (SREBP1) binds to and activates the PFKL promoter, increasing PFKL transcription. ApoM knockout upregulates SREBF1, which in turn elevates PFKL expression and promotes liver cancer cell proliferation and migration. Dual-luciferase reporter assay (PFKL promoter with SREBF1 binding sites), ApoM knockout cells, functional proliferation and invasion assays Oncology letters Medium 35720503
2022 Tiam1 directly interacts with PFKL and promotes glycolysis in a PFKL-dependent manner in breast cancer cells. Co-immunoprecipitation (Tiam1-PFKL), PFKL knockdown functional rescue, glycolysis measurement, in vivo xenograft Carcinogenesis Low 35511493

Source papers

Stage 0 corpus · 32 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2021 Selective activation of PFKL suppresses the phagocytic oxidative burst. Cell 124 34320407
2024 Glycolytic enzyme PFKL governs lipolysis by promoting lipid droplet-mitochondria tethering to enhance β-oxidation and tumor cell proliferation. Nature metabolism 107 38773347
2020 A20 targets PFKL and glycolysis to inhibit the progression of hepatocellular carcinoma. Cell death & disease 89 32015333
1981 Assignment of the human gene for liver-type 6-phosphofructokinase isozyme (PFKL) to chromosome 21 by using somatic cell hybrids and monoclonal anti-L antibody. Proceedings of the National Academy of Sciences of the United States of America 89 6455664
2021 Targeting PFKL with penfluridol inhibits glycolysis and suppresses esophageal cancer tumorigenesis in an AMPK/FOXO3a/BIM-dependent manner. Acta pharmaceutica Sinica. B 84 35530161
2022 A functional loop between YTH domain family protein YTHDF3 mediated m6A modification and phosphofructokinase PFKL in glycolysis of hepatocellular carcinoma. Journal of experimental & clinical cancer research : CR 58 36471428
2024 EGR1 suppresses HCC growth and aerobic glycolysis by transcriptionally downregulating PFKL. Journal of experimental & clinical cancer research : CR 50 38287371
2023 The KLF7/PFKL/ACADL axis modulates cardiac metabolic remodelling during cardiac hypertrophy in male mice. Nature communications 39 36810848
2019 125I suppressed the Warburg effect viaregulating miR-338/PFKL axis in hepatocellular carcinoma. Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie 37 31514072
2024 Phosphorylation of PFKL regulates metabolic reprogramming in macrophages following pattern recognition receptor activation. Nature communications 25 39085210
1994 Overexpression of liver-type phosphofructokinase (PFKL) in transgenic-PFKL mice: implication for gene dosage in trisomy 21. The Biochemical journal 25 8172601
2022 Exosomes from M2 macrophages promoted glycolysis in FaDu cells by inhibiting PDLIM2 expression to stabilize PFKL. Neoplasma 18 35723199
1998 Altered brain glucose metabolism in transgenic-PFKL mice with elevated L-phosphofructokinase: in vivo NMR studies. Brain research 18 9813288
2022 DNAAF5 promotes hepatocellular carcinoma malignant progression by recruiting USP39 to improve PFKL protein stability. Frontiers in oncology 17 36276075
2023 Allosterically inhibited PFKL via prostaglandin E2 withholds glucose metabolism and ovarian cancer invasiveness. Cell reports 16 37831605
2021 Inhibition of miR-185-3p Confers Erlotinib Resistance Through Upregulation of PFKL/MET in Lung Cancers. Frontiers in cell and developmental biology 15 34368128
2021 Antitumor effects of the small molecule DMAMCL in neuroblastoma via suppressing aerobic glycolysis and targeting PFKL. Cancer cell international 15 34819091
2024 Ubiquitin-specific protease 14 targets PFKL-mediated glycolysis to promote the proliferation and migration of oral squamous cell carcinoma. Journal of translational medicine 13 38388430
2023 Caveolin-1 depletion attenuates hepatic fibrosis via promoting SQSTM1-mediated PFKL degradation in HSCs. Free radical biology & medicine 13 37116593
2024 EIF4A3-Induced CircDHTKD1 regulates glycolysis in non-small cell lung cancer via stabilizing PFKL. Journal of cellular and molecular medicine 12 39022816
2022 miR-21-5p/Tiam1-mediated glycolysis reprogramming drives breast cancer progression via enhancing PFKL stabilization. Carcinogenesis 12 35511493
2022 ApoM regulates PFKL through the transcription factor SREBF1 to inhibit the proliferation, migration and metastasis of liver cancer cells. Oncology letters 11 35720503
2021 Bta-miR-6517 promotes proliferation and inhibits differentiation of pre-adipocytes by targeting PFKL. Journal of animal physiology and animal nutrition 8 34791721
1988 A DNA polymorphism with KpnI of the human liver-type phosphofructokinase (PFKL) gene. Nucleic acids research 7 2902561
2025 Cardiac PDK4 promotes neutrophilic PFKL methylation and drives the innate immune response in diabetic myocardial infarction. Pharmacological research 6 40222696
2022 PFKL, a novel regulatory node for NOX2-dependent oxidative burst and NETosis. Journal of Zhejiang University. Science. B 4 35794690
2024 PFKL promotes cell viability and glycolysis and inhibits cisplatin chemosensitivity of laryngeal squamous cell carcinoma. Biochemical and biophysical research communications 2 38991254
2025 piR-hsa-35410 promotes triple-negative breast cancer progression via enhancing PFKL mediated glycolysis. Biochemical pharmacology 0 40953645
2025 Hypoxia-Induced m6A modification via YTHDF2 stabilizes PFKL to fuel MDSC Glycolysis and hepatocellular carcinoma progression. Functional & integrative genomics 0 41225244
2025 A Covalent PFKL Activator Suppresses Tumor Growth. bioRxiv : the preprint server for biology 0 41256653
2025 HDAC6-mediated PFKL deacetylation enhances aerobic glycolysis and promotes VSMC proliferation. The Journal of biological chemistry 0 41421488
2022 A peptide-crosslinking approach identifies HSPA8 and PFKL as selective interactors of an actin-derived peptide containing reduced and oxidized methionine. RSC chemical biology 0 36320891

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