Affinage

TRIM9

E3 ubiquitin-protein ligase TRIM9 · UniProt Q9C026

Length
710 aa
Mass
79.2 kDa
Annotated
2026-06-10
37 papers in source corpus 17 papers cited in narrative 17 extracted findings
Cross-family judge vs UniProt: Affinage preferred faithfulness: 7/7 claims corpus-supported (100%)

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

TRIM9 is a brain-enriched RING-domain E3 ubiquitin ligase that controls neuronal morphogenesis and netrin-1-dependent axon guidance by ubiquitinating cytoskeletal and receptor substrates at the growth cone (PMID:20085810, PMID:26702829, PMID:27147649). At filopodial tips it binds the netrin receptor DCC and ubiquitinates the actin polymerase VASP to limit VASP tip localization and filopodial stability; netrin stimulation reverses this, deubiquitinating VASP to promote filopodial stability and axon guidance (PMID:26702829). TRIM9 also ubiquitinates DCC itself, blocking the DCC–FAK interaction and FAK activation until netrin-1 triggers DCC multimerization, reduced ubiquitination, FAK activity, and exocytic vesicle fusion driving axon branching (PMID:28701345). It engages both the attractive DCC and the repulsive UNC5C receptors and is required for netrin-1-dependent changes in their surface levels and for both attractive and repulsive turning responses (PMID:39871643). Loss of TRIM9 in mice causes excessive dendritic arborization, mislocalization of adult-born dentate granule neurons, and spatial learning deficits (PMID:27147649), and its role in the netrin/UNC-40 attraction pathway upstream of MIG-10 is conserved in C. elegans (PMID:21338947). Beyond neurons, TRIM9 dampens NF-κB-dependent neuroinflammation by sequestering β-TrCP from the SCF complex to block IκBα degradation, with Trim9-deficient mice showing uncontrolled neuroinflammation after ischemic stroke (PMID:30970257), and its short isoform scaffolds GSK3β to TBK1 via K63-linked auto-ubiquitination to activate IRF3 and type I interferon signaling during viral infection (PMID:26915459). In cancer settings TRIM9 ubiquitinates additional substrates including HNRNPU via K11-linkage to suppress pancreatic tumor growth (PMID:41050689) and MKK6 via K63-linkage to potentiate p38 signaling (PMID:29669288).

Mechanistic history

Synthesis pass · year-by-year structured walk · 14 steps
  1. 2010 Medium

    Established TRIM9 as a bona fide E3 ubiquitin ligase and placed it in neurons, defining its biochemical activity and primary tissue context.

    Evidence In vitro ubiquitin ligase assay with E2 UbcH5b plus IHC localization in brain

    PMID:20085810

    Open questions at the time
    • No substrate identified at this stage
    • Linkage type and physiological target unknown
  2. 2011 High

    Showed RING-dependent E3 activity is required for TRIM9 function in netrin/UNC-40 axon guidance, genetically placing it upstream of the effector MIG-10.

    Evidence C. elegans genetic epistasis and in vitro ligase assay with RING-domain requirement

    PMID:21338947

    Open questions at the time
    • Direct ubiquitination substrate in the worm not defined
    • Mammalian conservation of the MIG-10 axis not tested here
  3. 2014 Medium

    Linked activity-regulated TRIM9 protein levels to fine-scale topographic separation of presynaptic terminals, extending its role to synaptic-level wiring.

    Evidence Drosophila genetics with single-neuron clonal analysis and activity manipulation

    PMID:24746793

    Open questions at the time
    • Substrate mediating terminal topography unknown
    • Mechanism coupling neural activity to TRIM9 levels not defined
  4. 2015 High

    Identified VASP as a TRIM9 substrate at filopodial tips, providing a molecular mechanism (ubiquitin-controlled actin polymerase localization) for netrin-driven filopodial dynamics and guidance.

    Evidence Co-IP, in vitro ubiquitination, non-ubiquitinatable VASP mutant, TIRF, Trim9-/- neurons and in vivo guidance assays

    PMID:26702829

    Open questions at the time
    • Identity of the netrin-induced deubiquitinase not defined
    • Ubiquitin linkage type on VASP not specified
  5. 2016 High

    Demonstrated that loss of TRIM9 causes excessive dendritic arborization and adult-born neuron mislocalization with behavioral consequences, tying the molecular activity to hippocampal circuit function.

    Evidence Trim9-/- mouse with in vitro/in vivo morphology and spatial learning behavioral testing

    PMID:27147649

    Open questions at the time
    • Substrates driving dendritic phenotype not pinned down
    • Cell-autonomous vs non-autonomous contribution unresolved
  6. 2016 High

    Revealed a non-degradative scaffolding role for the short isoform in innate antiviral immunity, bridging GSK3β to TBK1 through K63-linked auto-ubiquitination to boost type I IFN.

    Evidence Reciprocal Co-IP, K63-specific ubiquitination assays, gain/loss-of-function with IFN/cytokine readouts under viral infection

    PMID:26915459

    Open questions at the time
    • Structural basis of the GSK3β–TRIM9s–TBK1 bridge not resolved
    • Relationship between neuronal and immune isoform functions unclear
  7. 2017 High

    Defined how TRIM9 gates DCC signaling: ubiquitination blocks DCC–FAK coupling, and netrin reverses this to enable FAK activation and exocytosis-dependent axon branching.

    Evidence Co-IP, DCC ubiquitination assays, FAK activity and SNARE assays, Trim9-/- neurons with in vitro/in vivo branching and FAK inhibitor experiments

    PMID:28701345

    Open questions at the time
    • Spatiotemporal control of DCC deubiquitination not fully resolved
    • Direct ubiquitination site(s) on DCC not mapped
  8. 2017 Medium

    Extended TRIM9's cell-shape control to immune cells, showing it is required for macrophage chemotaxis and architecture in vivo.

    Evidence Zebrafish loss-of-function with in vivo macrophage motility and morphology assays

    PMID:29021367

    Open questions at the time
    • Substrate driving macrophage motility not identified
    • Conservation to mammalian macrophages not tested here
  9. 2018 High

    Uncovered a TRIM9s–MKK6 positive feedback loop in which K63 ubiquitination outcompetes K48 ubiquitination at Lys82 to stabilize MKK6 and potentiate p38 signaling.

    Evidence Site-directed K82 and Ser76/80 mutants, K63/K48-specific ubiquitination and phosphorylation assays, reciprocal Co-IP in glioblastoma cells

    PMID:29669288

    Open questions at the time
    • In vivo relevance of the feedback loop not established
    • Tissue specificity beyond glioblastoma unclear
  10. 2019 High

    Identified a ligase-independent mechanism whereby TRIM9 sequesters β-TrCP from the SCF complex to stabilize IκBα and restrain NF-κB neuroinflammation after stroke.

    Evidence Co-IP, IκBα degradation assay, Trim9-/- ischemic stroke mouse model with AAV rescue

    PMID:30970257

    Open questions at the time
    • Whether sequestration involves ubiquitination of β-TrCP not resolved
    • Cell type mediating the neuroinflammatory phenotype not defined
  11. 2020 Medium

    Mapped a TRIM9/TRIM67 proximity interactome in cortical neurons, implicating Myo16 in TRIM9- and netrin-dependent control of filopodia and branching.

    Evidence BioID proximity labeling, TIRF colocalization, Myo16 RNAi with morphological readouts

    PMID:33378226

    Open questions at the time
    • Most interactome members not functionally validated
    • Whether interactors are ubiquitination substrates unknown
  12. 2024 Medium

    Extended the substrate repertoire to cancer-relevant targets, with K11-linked ubiquitination of HNRNPU suppressing pancreatic tumor growth and ubiquitination of PKM2 reprogramming glycolysis in breast cancer.

    Evidence K11-linkage ubiquitination assays with RING mutant and in vivo xenograft rescue (HNRNPU); Co-IP and oligomerization/metabolic assays (PKM2)

    PMID:38263865 PMID:41050689

    Open questions at the time
    • PKM2 ubiquitination lacks site-level and linkage mechanistic detail
    • How tumor-suppressive substrate selection is achieved unclear
  13. 2025 High

    Showed TRIM9 engages both attractive (DCC) and repulsive (UNC5C) netrin receptors, regulating their surface levels and bidirectional turning responses while negatively regulating FAK in the absence of netrin.

    Evidence Co-IP for both receptors, microfluidic netrin gradients, Trim9-/- neurons, surface receptor quantification, FAK assays, pH-mScarlet reporter

    PMID:39871643

    Open questions at the time
    • Whether UNC5C is a direct ubiquitination substrate not established
    • Mechanism integrating attractive and repulsive outputs unclear
  14. 2026 Medium

    Implicated TRIM9 in proteostasis of disease-linked aggregating proteins, mediating degradation of the ALS-associated UBQLN2P497H mutant, and reinforced VASP-dependent control of focal adhesions and motility in melanoma.

    Evidence APEX2 proximity proteomics, Co-IP, fractionation, proteasome inhibition and siRNA (UBQLN2P497H); Co-IP, TIRF and Trim9 KO melanoma model (VASP)

    PMID:41582437 PMID:41889914

    Open questions at the time
    • Melanoma study is a preprint (single lab)
    • How TRIM9 selectively recognizes the mutant UBQLN2 conformer not defined

Open questions

Synthesis pass · forward-looking unresolved questions
  • How TRIM9 selects among its diverse substrates and switches between degradative ubiquitination, regulatory linkage signaling, and ligase-independent sequestration across neuronal, immune, and tumor contexts remains unresolved.
  • No unifying model for substrate/linkage selection
  • Isoform-specific regulation across tissues not integrated
  • No structural model of substrate or partner engagement

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0016874 ligase activity 6 GO:0140096 catalytic activity, acting on a protein 4 GO:0060090 molecular adaptor activity 2 GO:0098772 molecular function regulator activity 1
Localization
GO:0005829 cytosol 2 GO:0005856 cytoskeleton 2
Pathway
R-HSA-1266738 Developmental Biology 5 R-HSA-162582 Signal Transduction 3 R-HSA-168256 Immune System 3 R-HSA-392499 Metabolism of proteins 3
Partners
BTRCDCCGSK3BHNRNPUMKK6TBK1UNC5CVASP

Evidence

Reading pass · 17 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
2010 TRIM9 functions as an E3 ubiquitin ligase collaborating with the E2 ubiquitin conjugating enzyme UbcH5b, and is localized to neurons in the brain. In vitro ubiquitin ligase assay with UbcH5b; immunohistochemistry and immunoblotting for localization Neurobiology of disease Medium 20085810
2016 The short isoform of TRIM9 (TRIM9s) undergoes Lys-63-linked auto-polyubiquitination upon viral infection and acts as a scaffold bridging GSK3β to TBK1, thereby activating IRF3 signaling and enhancing type I IFN production while selectively suppressing pro-inflammatory cytokine production. Co-immunoprecipitation, ubiquitination assays (K63-linkage specific), overexpression/knockdown in cells with viral infection readouts Cell research High 26915459
2015 TRIM9 localizes to filopodial tips, binds the netrin receptor DCC, and ubiquitinates the barbed-end actin polymerase VASP to reduce VASP filopodial tip localization and stability; netrin stimulation causes VASP deubiquitination, promoting VASP tip localization and filopodial stability to drive axon guidance. Co-IP (TRIM9–DCC, TRIM9–VASP), in vitro ubiquitination assay, non-ubiquitinatable VASP mutant, TIRF microscopy, Trim9−/− cortical neurons, in vivo axon guidance assays Developmental cell High 26702829
2019 TRIM9 sequesters β-TrCP from the Skp-Cullin-F-box ubiquitin ligase complex, blocking IκBα degradation and thereby dampening NF-κB-dependent proinflammatory mediator production; Trim9-deficient mice show uncontrolled neuroinflammation after ischemic stroke. Co-IP (TRIM9–β-TrCP interaction), IκBα degradation assay, Trim9−/− mouse ischemic stroke model with NF-κB pathway readouts, AAV-mediated TRIM9 rescue Cell reports High 30970257
2017 TRIM9-dependent ubiquitination of DCC blocks the interaction between DCC and FAK and prevents FAK phosphorylation; upon netrin-1 stimulation TRIM9 promotes DCC multimerization but reduces DCC ubiquitination, enabling FAK activation and downstream exocytic vesicle fusion and axon branching. Co-IP (DCC–FAK), ubiquitination assays on DCC, FAK activity assays, SNARE complex assays, Trim9−/− neurons, in vitro and in vivo axon branching assays, FAK inhibitor experiments Molecular biology of the cell High 28701345
2016 TRIM9 regulates embryonic and adult hippocampal neuron morphogenesis; Trim9 deletion causes excessive dendritic arborization and mislocalization of adult-born dentate granule neurons in vivo, associated with severe deficits in spatial learning and memory. Trim9−/− mouse KO, in vitro and in vivo morphological analysis of hippocampal neurons, behavioral testing (spatial learning/memory) The Journal of neuroscience High 27147649
2011 C. elegans TRIM-9 exhibits E3 ubiquitin ligase activity in vitro (RING domain-dependent) and functions in the UNC-6/netrin–UNC-40 attraction pathway upstream of MIG-10, the downstream effector of UNC-40, to regulate ventral axon guidance. In vitro ubiquitin ligase assay, C. elegans genetic epistasis analysis (trim-9 mutants, unc-6/unc-40 pathway double mutants), MIG-10 localization assay Journal of genetics and genomics High 21338947
2018 TRIM9s promotes K63-linked ubiquitination of MKK6 at Lys82, which inhibits competing K48-linked ubiquitination at the same site to stabilize MKK6 and potentiate p38 signaling; MKK6 in turn stabilizes TRIM9s by promoting p38-dependent phosphorylation of TRIM9s at Ser76/80, blocking its proteasomal degradation—forming a positive feedback loop. Ubiquitination assays (K63- and K48-linkage specific, site-directed mutagenesis at K82), phosphorylation assays (Ser76/80 mutants), co-IP, proteasome inhibitor experiments, glioblastoma cell functional assays Cell reports High 29669288
2020 TRIM9 and TRIM67 form a proximity interaction network in developing cortical neurons that includes cytoskeletal regulators (Myo16, Coro1A, MAP1B), exocytic/endocytic regulators (ExoC1), and synaptic proteins (GRIP1, PRG-1, KIF1A); knockdown of the unconventional myosin Myo16 altered growth cone filopodia density and axonal branching in a TRIM9- and netrin-1-dependent manner. BioID proximity labeling in cortical neurons, TIRF microscopy for colocalization, RNAi knockdown with morphological readouts Molecular biology of the cell Medium 33378226
2014 In Drosophila, Trim9 protein levels (regulated by neural activity) direct fine-scale topographic separation of presynaptic terminals of adjacent nociceptive neurons; neural activity regulates Trim9 protein levels to control axon terminal topography. Drosophila genetics (trim9 mutants, single-neuron clonal analysis), in vivo imaging of presynaptic terminals, activity manipulation experiments Current biology Medium 24746793
2017 Trim9 disruption impairs macrophage chemotaxis and cellular architecture in zebrafish larvae in vivo, demonstrating a role for TRIM9 in macrophage motility beyond neurons. Zebrafish Trim9 loss-of-function model, in vivo macrophage motility and morphology assays after immune stimulation Journal of leukocyte biology Medium 29021367
2025 TRIM9 localizes and interacts with both the attractive netrin receptor DCC and the repulsive netrin receptor UNC5C in the growth cone; deletion of Trim9 alters both attractive and repulsive axon turning and growth cone size responses to netrin-1 and is required for netrin-1-dependent changes in surface levels of DCC and UNC5C; TRIM9 negatively regulates FAK activity in the absence of netrin-1. Co-IP (TRIM9–UNC5C, TRIM9–DCC), microfluidic netrin gradient assays, Trim9−/− cortical neurons, surface receptor quantification, FAK activity assays, pH-mScarlet UNC5C reporter Journal of neurochemistry High 39871643
2023 TRIM9 interacts with ZEB1 and promotes ZEB1 protein degradation via the ubiquitin-proteasome pathway, suppressing esophageal cancer cell viability and invasion. Co-IP (TRIM9–ZEB1), ubiquitination blocking experiments, cell viability and invasion assays with TRIM9 overexpression/knockdown BioMed research international Low 37124931
2024 TRIM9 promotes K11-linked ubiquitination and proteasomal degradation of HNRNPU in a RING domain-dependent manner in pancreatic cancer cells; TRIM9 overexpression suppressed tumor growth in vivo and was rescued by HNRNPU co-expression. In vitro and cell-based ubiquitination assays (K11-linkage), RING domain mutant, Co-IP (TRIM9–HNRNPU), overexpression/knockdown with proliferation/migration assays, in vivo xenograft rescue experiment Frontiers in immunology Medium 41050689
2024 TRIM9 promotes ubiquitination of PKM2, driving its transition from tetramer to dimer and reprogramming glucose metabolism from oxidative phosphorylation to aerobic glycolysis in triple-negative breast cancer cells. Ubiquitination assay (TRIM9-mediated PKM2 ubiquitination), Co-IP, PKM2 oligomerization assay, metabolic assays (glycolysis vs. OXPHOS), TRIM9 knockdown/overexpression Journal of cellular and molecular medicine Low 38263865
2026 TRIM9 and TRIM26 are selectively enriched in proximity to the ALS-linked UBQLN2P497H mutant (not wild-type UBQLN2 or P497S mutant), co-accumulate with UBQLN2P497H in the insoluble fraction, and mediate ubiquitination and proteasomal degradation of UBQLN2P497H; individual knockdown of TRIM9 increased the abundance of a C-terminal UBQLN2 fragment. APEX2 proximity labeling with LC-MS/MS, co-IP followed by Western blot, fractionation analysis, proteasome inhibitor treatment, TRIM9/TRIM26 siRNA knockdown ACS chemical biology Medium 41582437
2026 In melanoma cells, TRIM9 interacts with VASP, alters VASP modification, localization, and dynamics, negatively regulates focal adhesion formation and mesenchymal motility; TRIM9 deletion increases actin stress fibers, focal adhesions, VASP accumulation at adhesions, and mesenchymal migration in vitro, while in vivo loss of TRIM9 slows tumor growth and alters metastasis. Co-IP (TRIM9–VASP in melanoma), TIRF microscopy, VASP modification assays, focal adhesion quantification, Trim9 KO mouse melanoma model with in vivo tumor growth and metastasis readouts bioRxivpreprint Medium 41889914

Source papers

Stage 0 corpus · 37 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2010 TRIM9, a novel brain-specific E3 ubiquitin ligase, is repressed in the brain of Parkinson's disease and dementia with Lewy bodies. Neurobiology of disease 89 20085810
2016 TRIM9 short isoform preferentially promotes DNA and RNA virus-induced production of type I interferon by recruiting GSK3β to TBK1. Cell research 74 26915459
2015 The E3 Ubiquitin Ligase TRIM9 Is a Filopodia Off Switch Required for Netrin-Dependent Axon Guidance. Developmental cell 71 26702829
2019 TRIM9-Mediated Resolution of Neuroinflammation Confers Neuroprotection upon Ischemic Stroke in Mice. Cell reports 52 30970257
2016 Trim9 Deletion Alters the Morphogenesis of Developing and Adult-Born Hippocampal Neurons and Impairs Spatial Learning and Memory. The Journal of neuroscience : the official journal of the Society for Neuroscience 49 27147649
2019 TRIM9 and TRIM67 Are New Targets in Paraneoplastic Cerebellar Degeneration. Cerebellum (London, England) 42 30350014
2017 TRIM9-dependent ubiquitination of DCC constrains kinase signaling, exocytosis, and axon branching. Molecular biology of the cell 41 28701345
2020 The TRIM9/TRIM67 neuronal interactome reveals novel activators of morphogenesis. Molecular biology of the cell 39 33378226
2002 TRIM9 is specifically expressed in the embryonic and adult nervous system. Mechanisms of development 39 11960705
2018 Mutual Stabilization between TRIM9 Short Isoform and MKK6 Potentiates p38 Signaling to Synergistically Suppress Glioblastoma Progression. Cell reports 30 29669288
2019 An E3 ubiquitin ligase TRIM9 is involved in WSSV infection via interaction with β-TrCP. Developmental and comparative immunology 24 30910419
2015 Promoter methylation of TRIM9 as a marker for detection of circulating tumor DNA in breast cancer patients. SpringerPlus 23 26543769
2020 TRIM9 overexpression promotes uterine leiomyoma cell proliferation and inhibits cell apoptosis via NF-κB signaling pathway. Life sciences 22 32679146
2014 Trim9 regulates activity-dependent fine-scale topography in Drosophila. Current biology : CB 22 24746793
2024 METTL14/miR-29c-3p axis drives aerobic glycolysis to promote triple-negative breast cancer progression though TRIM9-mediated PKM2 ubiquitination. Journal of cellular and molecular medicine 18 38263865
2011 TRIM-9 functions in the UNC-6/UNC-40 pathway to regulate ventral guidance. Journal of genetics and genomics = Yi chuan xue bao 18 21338947
2016 The first molluscan TRIM9 is involved in the negative regulation of NF-κB activity in the Hong Kong oyster, Crassostrea hongkongensis. Fish & shellfish immunology 16 27393236
2023 TRIM9 Interacts with ZEB1 to Suppress Esophageal Cancer by Promoting ZEB1 Protein Degradation via the UPP Pathway. BioMed research international 10 37124931
2023 Detection of High-Risk Paraneoplastic Antibodies against TRIM9 and TRIM67 Proteins. Annals of neurology 10 37632288
2017 Disruption of Trim9 function abrogates macrophage motility in vivo. Journal of leukocyte biology 10 29021367
2022 A Novel TRIM9 Protein Promotes NF-κB Activation Through Interacting With LvIMD in Shrimp During WSSV Infection. Frontiers in immunology 9 35281067
2019 MicroRNA-653 Inhibits Thymocyte Proliferation and Induces Thymocyte Apoptosis in Mice with Autoimmune Myasthenia Gravis by Downregulating TRIM9. Neuroimmunomodulation 9 30703767
2024 Exercise-induced upregulation of TRIM9 attenuates neuroinflammation in Alzheimer's disease-like rat. International immunopharmacology 7 39580859
2021 TRIM9 is involved in facilitating Vibrio parahaemolyticus infection by inhibition of relish pathway in Penaeus monodon. Molecular immunology 6 33636432
2023 Targeting TRIM9 by miR-218-5p Restricts Cell Proliferation and Epithelial-Mesenchymal Transition in Non-Small Cell Lung Cancer. Annals of clinical and laboratory science 5 36889762
2021 Knockdown of TRIM9 attenuates irinotecan‑induced intestinal mucositis in IEC‑6 cells by regulating DUSP6 expression via the P38 pathway. Molecular medicine reports 5 34676875
2021 miR-181a Ameliorates the Progression of Myasthenia Gravis by Regulating TRIM9. Evidence-based complementary and alternative medicine : eCAM 5 34925522
2025 TRIM9 Controls Growth Cone Responses to Netrin Through DCC and UNC5C. Journal of neurochemistry 3 39871643
2024 TRIM9 controls growth cone responses to netrin through DCC and UNC5C. bioRxiv : the preprint server for biology 2 38765979
2024 Explorations of novel MDR-related hub genes and the potential roles TRIM9 played in drug-resistant hepatocellular carcinoma. International journal of biological macromolecules 2 39706432
2023 TRIM9 promotes Müller cell-derived retinal stem cells to differentiate into retinal ganglion cells by regulating Atoh7. In vitro cellular & developmental biology. Animal 2 37792226
2025 [Retracted] Knockdown of TRIM9 attenuates irinotecan‑induced intestinal mucositis in IEC‑6 cells by regulating DUSP6 expression via the P38 pathway. Molecular medicine reports 1 40145576
2025 Single-cell and multi-omics analysis identifies TRIM9 as a key ubiquitination regulator in pancreatic cancer. Frontiers in immunology 1 41050689
2026 TRIM9 and TRIM26 Interact with UBQLN2P497H to Modulate Its Proteasomal Degradation. ACS chemical biology 0 41582437
2026 TRIM9 switches the morphological phenotype of melanoma cells. bioRxiv : the preprint server for biology 0 41889914
2025 Correction to "TRIM9 Interacts with ZEB1 to Suppress Esophageal Cancer by Promoting ZEB1 Protein Degradation via the UPP Pathway". BioMed research international 0 41146861
2023 Trim9 regulates the directional differentiation of retinal Müller cells to retinal ganglion cells. Zhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences 0 38432885

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