{"gene":"VCL","run_date":"2026-06-11T09:02:06","timeline":{"discoveries":[{"year":2019,"finding":"Mechanical forces from cardiac contractility regulate the localization and activation of vinculin (VCL) in cardiomyocytes; VCL recruits the phosphatase SSH1 and its effector cofilin (CFL) to regulate F-actin rearrangement and promote myofilament maturation via the VCL-SSH1-CFL axis.","method":"Zebrafish genetic model (contracting vs. non-contracting cardiomyocytes), VCL interactome analysis (proteomics/co-IP), loss-of-function with myofilament maturation readout","journal":"Developmental Cell","confidence":"High","confidence_rationale":"Tier 2 / Moderate — reciprocal interactome in two conditions, loss-of-function with defined phenotype, multiple orthogonal methods in a single rigorous study","pmids":["31495694"],"is_preprint":false},{"year":2024,"finding":"Vinculin phosphorylation at tyrosine residue 822 (pY822) regulates the balance between cadherin-based cell-cell adhesion and integrin-based cell-matrix adhesion in cardiomyocytes; Y822F knock-in mice show reduced vinculin and adherens junction proteins at junctions and increased α5/β1 integrin and fibronectin at lateral borders, with cardiac dysfunction emerging at 28 weeks.","method":"Mouse knock-in (Y822F point mutation), immunofluorescence, cardiac function assessment","journal":"bioRxiv (preprint)","confidence":"Medium","confidence_rationale":"Tier 2 / Moderate — in vivo knock-in with defined molecular and functional phenotype, but preprint and single lab","pmids":["bio_10.1101_2024.10.28.620745"],"is_preprint":true},{"year":2021,"finding":"A pool of vinculin (VCL) is covalently PARylated (poly-ADP-ribosylated) by tankyrase (TNKS) at the plasma membrane in epithelial cells; VCL contains conserved tankyrase-binding motifs (TBMs), and overexpression of a TBM-II point mutant (GgVCL/*TBM) induced mesenchymal-like cell shape changes, implicating this modification in adherens junction regulation and cell shape maintenance.","method":"Affinity precipitation with PAR-binding reagent followed by western blot, TNKS inhibitor experiments, transfection of TBM point-mutant VCL with morphological readout","journal":"PeerJ","confidence":"Medium","confidence_rationale":"Tier 2 / Weak — biochemical PARylation confirmed by affinity precipitation, functional mutant experiment in single lab with overexpression system","pmids":["34123588"],"is_preprint":false},{"year":2021,"finding":"Loss-of-function (p.D256fs) and gain-of-function (p.L555V, conferring enhanced protein stability) VCL variants identified in human neural tube defect patients affect planar cell polarity (PCP) pathway regulation and cell migration, consistent with VCL's role in cell skeleton remodeling during neural tube closure.","method":"Targeted next-generation sequencing of human NTD cohort, functional assays for PCP pathway activity and cell migration","journal":"Molecular Genetics & Genomic Medicine","confidence":"Medium","confidence_rationale":"Tier 2 / Weak — variant-level functional evaluation with PCP and migration assays, single study","pmids":["33491343"],"is_preprint":false},{"year":2024,"finding":"miR-6721-5p directly targets the 3'-UTR of meta-VCL (the muscle-specific splice isoform of VCL) and suppresses its expression, as validated by dual-luciferase reporter assay; meta-VCL downregulation was associated with reduced anti-inflammatory cytokine levels (IL-10, TNF-α).","method":"Dual-luciferase reporter assay, cell-based ectopic expression, qPCR","journal":"Non-coding RNA Research","confidence":"Medium","confidence_rationale":"Tier 3 / Moderate — direct interaction validated by luciferase assay in cells, functional consequence assessed, replicated in patient serum and bioinformatics","pmids":["39296643"],"is_preprint":false},{"year":2023,"finding":"miR-29a-3p directly targets VCL (and CTNNB1) 3'-UTR in nasal epithelial cells, suppressing VCL expression and disrupting adherens and tight junction integrity; miR-29a-3p antagomir treatment in OVA-induced allergic rhinitis mice restored VCL/Ctnnb1 expression and improved epithelial barrier function.","method":"Dual-luciferase reporter assay, miRNA mimic/inhibitor transfection, in vivo antagomir mouse model with barrier function readout","journal":"International Immunopharmacology","confidence":"Medium","confidence_rationale":"Tier 2 / Moderate — direct targeting validated by luciferase assay, in vivo rescue experiment, multiple methods in single lab","pmids":["37262956"],"is_preprint":false},{"year":2024,"finding":"RBM10 loss causes aberrant exon inclusion in VCL transcripts; knockdown of the VCL exon-inclusion isoform in RBM10-null cells reduced cell velocity, placing this VCL isoform in the pathway linking RBM10 loss to increased cell motility and metastatic fitness.","method":"RNA-seq, isoform-specific knockdown with cell velocity readout, mouse Hras/Rbm10 KO model with combined VCL/CD44/TNC knockdown rescue","journal":"bioRxiv (preprint)","confidence":"Medium","confidence_rationale":"Tier 2 / Moderate — genetic epistasis via isoform-specific knockdown with defined motility phenotype, in vivo mouse model with rescue; preprint, single lab","pmids":["bio_10.1101_2024.07.09.602730"],"is_preprint":true},{"year":2025,"finding":"In a rat model of lung injury, anti-VCL intervention reduced plasma VCL levels, mitigated alveolar edema, and restored alveolar-capillary barrier integrity, demonstrating that VCL modulation affects vascular leakage and extravasation; multi-omics analysis identified VCL's involvement in the VCL/ICAM-1 signaling pathway associated with Omicron-induced endothelial dysfunction.","method":"Rat lung injury model with anti-VCL treatment, histological staining, electron microscopy, plasma proteomics and metabolomics","journal":"Nature Communications","confidence":"Medium","confidence_rationale":"Tier 2 / Moderate — functional intervention (anti-VCL) in animal model with defined vascular/barrier phenotype and multi-omics pathway context, single study","pmids":["40268929"],"is_preprint":false},{"year":1992,"finding":"The vinculin gene (VCL) was mapped to human chromosome 10q22.1-q23 by physical (somatic hybrid panel hybridization, flow-sorted translocation chromosome hybridization) and genetic recombination mapping.","method":"Human-rodent somatic hybrid panel hybridization, fluorescence in situ hybridization to flow-sorted chromosomes, genetic recombination mapping in MEN2 families","journal":"Genomics","confidence":"High","confidence_rationale":"Tier 1 / Strong — multiple independent physical and genetic mapping methods, replicated across approaches in a single study","pmids":["1505973"],"is_preprint":false}],"current_model":"Vinculin (VCL) is a mechanosensitive cytoskeletal adaptor protein that links filamentous actin to cell-matrix and cell-cell adhesions; in cardiomyocytes it responds to mechanical forces by recruiting the SSH1 phosphatase and cofilin to regulate F-actin remodeling and myofilament maturation (VCL-SSH1-CFL axis), and its phosphorylation at Y822 balances cadherin vs. integrin adhesion organization; VCL is covalently PARylated by tankyrase at adherens junctions, and its expression is post-transcriptionally regulated by miRNAs (miR-6721-5p targeting meta-VCL; miR-29a-3p targeting VCL in epithelial junctions); loss-of-function or gain-of-function VCL variants impair PCP signaling and cell migration, and aberrant VCL splicing driven by RBM10 loss promotes cell motility and metastatic competency."},"narrative":{"mechanistic_narrative":"Vinculin (VCL) is a mechanosensitive cytoskeletal adaptor that couples filamentous actin to both cell-matrix (integrin) and cell-cell (cadherin) adhesions and translates mechanical force into adhesion and cytoskeletal remodeling [PMID:31495694, PMID:bio_10.1101_2024.10.28.620745]. In cardiomyocytes, mechanical force from contractility controls VCL localization and activation, and VCL recruits the SSH1 phosphatase together with cofilin to drive F-actin rearrangement and myofilament maturation through the VCL-SSH1-CFL axis [PMID:31495694]. The balance between cadherin- and integrin-based adhesion is set by VCL phosphorylation at tyrosine 822: loss of this phosphorylation reduces junctional VCL and adherens-junction proteins while increasing α5/β1 integrin and fibronectin at lateral borders, with cardiac dysfunction as the in vivo consequence [PMID:bio_10.1101_2024.10.28.620745]. VCL function at adherens junctions is further regulated by covalent poly-ADP-ribosylation by tankyrase via conserved tankyrase-binding motifs, a modification linked to cell shape maintenance [PMID:34123588]. Beyond adhesion, VCL participates in planar cell polarity signaling and cell migration—where human loss- and gain-of-function variants are associated with neural tube defects [PMID:33491343]—and its abundance and isoform usage are tightly controlled post-transcriptionally, by miRNAs targeting the muscle-specific meta-VCL isoform [PMID:39296643] and epithelial VCL [PMID:37262956] and by RBM10-dependent splicing that links an exon-inclusion isoform to cell motility [PMID:bio_10.1101_2024.07.09.602730].","teleology":[{"year":1992,"claim":"Establishing the chromosomal location of VCL provided the genomic anchor needed to connect the gene to human phenotypes and to distinguish it from neighboring loci.","evidence":"Somatic hybrid panel hybridization, FISH to flow-sorted chromosomes, and genetic recombination mapping in MEN2 families","pmids":["1505973"],"confidence":"High","gaps":["Mapping alone does not address protein function","No isoform or splice structure resolved"]},{"year":2019,"claim":"It was unknown how mechanical force is converted into cytoskeletal maturation in heart muscle; this work showed VCL is a force-responsive node that recruits SSH1 and cofilin to remodel F-actin and mature myofilaments.","evidence":"Zebrafish contracting vs. non-contracting cardiomyocyte model with VCL interactome and loss-of-function myofilament readout","pmids":["31495694"],"confidence":"High","gaps":["Direct vs. bridged nature of the VCL-SSH1 interaction not resolved","Generality beyond cardiomyocytes untested in this study"]},{"year":2021,"claim":"How VCL is covalently regulated at junctions was unclear; this established that a membrane pool of VCL is PARylated by tankyrase through conserved binding motifs, linking the modification to adherens-junction and cell-shape control.","evidence":"PAR-binding affinity precipitation, tankyrase inhibition, and TBM point-mutant overexpression with morphological readout in epithelial cells","pmids":["34123588"],"confidence":"Medium","gaps":["Functional readout relies on overexpression of a mutant","Endogenous consequences of blocking PARylation not measured"]},{"year":2021,"claim":"Whether VCL contributes to human developmental disease was open; identification of loss- and gain-of-function variants in neural tube defect patients tied VCL to PCP signaling and migration during neural tube closure.","evidence":"Targeted sequencing of an NTD cohort with PCP-activity and cell-migration assays","pmids":["33491343"],"confidence":"Medium","gaps":["Causality at the organismal level not demonstrated","Mechanistic link from VCL to PCP components undefined"]},{"year":2023,"claim":"The post-transcriptional control of VCL in epithelial barriers was unknown; miR-29a-3p was shown to directly repress VCL and disrupt junctional integrity, with antagomir rescue restoring barrier function.","evidence":"Dual-luciferase 3'-UTR assay, miRNA mimic/inhibitor transfection, and in vivo antagomir allergic-rhinitis mouse model","pmids":["37262956"],"confidence":"Medium","gaps":["Effects shared with co-target CTNNB1 not fully separated","Single epithelial context"]},{"year":2024,"claim":"How phosphorylation tunes VCL between adhesion systems was unresolved; a Y822F knock-in showed pY822 sets the cadherin-versus-integrin adhesion balance with late-onset cardiac dysfunction.","evidence":"Mouse Y822F knock-in with immunofluorescence and cardiac function assessment (preprint)","pmids":["bio_10.1101_2024.10.28.620745"],"confidence":"Medium","gaps":["Preprint, single lab","Upstream kinase and signal triggering Y822 phosphorylation not identified"]},{"year":2024,"claim":"Isoform-specific regulation of VCL was clarified by showing miR-6721-5p directly represses the muscle-specific meta-VCL isoform, coupling it to inflammatory cytokine changes.","evidence":"Dual-luciferase reporter assay, ectopic expression, and qPCR","pmids":["39296643"],"confidence":"Medium","gaps":["Mechanism linking meta-VCL loss to cytokine changes unresolved","In vivo relevance limited"]},{"year":2024,"claim":"It was unclear how RBM10 loss promotes motility; aberrant VCL exon inclusion was placed in the pathway, with isoform-specific knockdown reducing cell velocity and contributing to metastatic fitness.","evidence":"RNA-seq, isoform-specific knockdown with velocity readout, and Hras/Rbm10 KO mouse with combined-knockdown rescue (preprint)","pmids":["bio_10.1101_2024.07.09.602730"],"confidence":"Medium","gaps":["Preprint, single lab","Molecular difference of the exon-inclusion isoform not characterized"]},{"year":2025,"claim":"Whether VCL participates in vascular barrier failure was open; anti-VCL intervention reduced alveolar edema and restored barrier integrity, implicating a VCL/ICAM-1 axis in endothelial dysfunction.","evidence":"Rat lung injury model with anti-VCL treatment, histology, electron microscopy, and plasma multi-omics","pmids":["40268929"],"confidence":"Medium","gaps":["Mechanism of plasma VCL action on endothelium undefined","VCL/ICAM-1 relationship correlative"]},{"year":null,"claim":"How the distinct VCL regulatory layers—force sensing, Y822 phosphorylation, tankyrase PARylation, and splicing/miRNA control—are integrated to set adhesion identity in a given cell type remains unresolved.","evidence":"","pmids":[],"confidence":"Medium","gaps":["No unified model connecting modifications and isoforms","Upstream regulators of each modification largely unknown","Cross-tissue generality untested"]}],"mechanism_profile":{"molecular_activity":[{"term_id":"GO:0008092","term_label":"cytoskeletal protein binding","supporting_discovery_ids":[0]},{"term_id":"GO:0060090","term_label":"molecular adaptor activity","supporting_discovery_ids":[0,1]}],"localization":[{"term_id":"GO:0005886","term_label":"plasma membrane","supporting_discovery_ids":[1,2]},{"term_id":"GO:0005856","term_label":"cytoskeleton","supporting_discovery_ids":[0]}],"pathway":[{"term_id":"R-HSA-1474244","term_label":"Extracellular matrix organization","supporting_discovery_ids":[1]},{"term_id":"R-HSA-1500931","term_label":"Cell-Cell communication","supporting_discovery_ids":[1,5]}],"complexes":["adherens junction"],"partners":["SSH1","CFL","TNKS"],"other_free_text":[]}},"prefetch_data":{"uniprot":{"accession":"P18206","full_name":"Vinculin","aliases":["Metavinculin","MV"],"length_aa":1134,"mass_kda":123.8,"function":"Actin filament (F-actin)-binding protein involved in cell-matrix adhesion and cell-cell adhesion. Regulates cell-surface E-cadherin expression and potentiates mechanosensing by the E-cadherin complex. May also play important roles in cell morphology and locomotion","subcellular_location":"Cell membrane; Cell junction, adherens junction; Cell junction, focal adhesion; Cytoplasm, cytoskeleton; Cell membrane, sarcolemma; Cell projection, podosome; Cytoplasm, perinuclear region","url":"https://www.uniprot.org/uniprotkb/P18206/entry"},"depmap":{"release":"DepMap","has_data":true,"is_common_essential":false,"resolved_as":"","url":"https://depmap.org/portal/gene/VCL","classification":"Not Classified","n_dependent_lines":306,"n_total_lines":1208,"dependency_fraction":0.2533112582781457},"opencell":{"profiled":true,"resolved_as":"","ensg_id":"ENSG00000035403","cell_line_id":"CID000622","localizations":[{"compartment":"cell_contact","grade":3},{"compartment":"cytoplasmic","grade":3},{"compartment":"focal_adhesions","grade":3}],"interactors":[{"gene":"ARHGAP17","stoichiometry":0.2},{"gene":"CLTA","stoichiometry":0.2},{"gene":"INPPL1","stoichiometry":0.2},{"gene":"BRCA1","stoichiometry":0.2},{"gene":"CTNNA1","stoichiometry":0.2},{"gene":"TLN1","stoichiometry":0.2},{"gene":"HSPBP1","stoichiometry":0.2},{"gene":"RCC2","stoichiometry":0.2},{"gene":"LLGL1","stoichiometry":0.2},{"gene":"RPAP2","stoichiometry":0.2}],"url":"https://opencell.sf.czbiohub.org/target/CID000622","total_profiled":1310},"omim":[{"mim_id":"620884","title":"FER1-LIKE FAMILY, MEMBER 6; FER1L6","url":"https://www.omim.org/entry/620884"},{"mim_id":"618441","title":"ADHESION G PROTEIN-COUPLED RECEPTOR G3; ADGRG3","url":"https://www.omim.org/entry/618441"},{"mim_id":"616970","title":"MARVEL DOMAIN-CONTAINING PROTEIN 1; MARVELD1","url":"https://www.omim.org/entry/616970"},{"mim_id":"616821","title":"THROMBOSPONDIN TYPE 1 DOMAIN-CONTAINING PROTEIN 1; THSD1","url":"https://www.omim.org/entry/616821"},{"mim_id":"614606","title":"FOCADHESIN; FOCAD","url":"https://www.omim.org/entry/614606"}],"hpa":{"profiled":true,"resolved_as":"","reliability":"Enhanced","locations":[{"location":"Focal adhesion sites","reliability":"Enhanced"}],"tissue_specificity":"Low tissue specificity","tissue_distribution":"Detected in all","driving_tissues":[],"url":"https://www.proteinatlas.org/search/VCL"},"hgnc":{"alias_symbol":["VINC"],"prev_symbol":[]},"alphafold":{"accession":"P18206","domains":[{"cath_id":"1.20.120.230","chopping":"6-126","consensus_level":"medium","plddt":91.551,"start":6,"end":126},{"cath_id":"1.20.120.230","chopping":"150-254","consensus_level":"medium","plddt":91.3568,"start":150,"end":254},{"cath_id":"1.20.120.810","chopping":"259-483","consensus_level":"medium","plddt":91.0086,"start":259,"end":483},{"cath_id":"1.20.120.810","chopping":"492-588","consensus_level":"high","plddt":91.2331,"start":492,"end":588},{"cath_id":"1.20.120.810","chopping":"601-710","consensus_level":"medium","plddt":93.1189,"start":601,"end":710},{"cath_id":"1.20.120.230","chopping":"718-837","consensus_level":"medium","plddt":94.448,"start":718,"end":837},{"cath_id":"1.20.120.230","chopping":"963-1113","consensus_level":"high","plddt":90.6166,"start":963,"end":1113}],"viewer_url":"https://alphafold.ebi.ac.uk/entry/P18206","model_url":"https://alphafold.ebi.ac.uk/files/AF-P18206-F1-model_v6.cif","pae_url":"https://alphafold.ebi.ac.uk/files/AF-P18206-F1-predicted_aligned_error_v6.png","plddt_mean":86.56},"mouse_models":{"mgi_url":"https://www.informatics.jax.org/marker/summary?nomen=VCL","jax_strain_url":"https://www.jax.org/strain/search?query=VCL"},"sequence":{"accession":"P18206","fasta_url":"https://rest.uniprot.org/uniprotkb/P18206.fasta","uniprot_url":"https://www.uniprot.org/uniprotkb/P18206/entry","alphafold_viewer_url":"https://alphafold.ebi.ac.uk/entry/P18206"}},"corpus_meta":[{"pmid":"21076462","id":"PMC_21076462","title":"Renal 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immunopharmacology","url":"https://pubmed.ncbi.nlm.nih.gov/37262956","citation_count":4,"is_preprint":false},{"pmid":"35975534","id":"PMC_35975534","title":"MicroRNA-21-5p Regulates CD3+T Lymphocytes Through VCL and LTF in Patients with Immune Thrombocytopenia.","date":"2022","source":"Clinical laboratory","url":"https://pubmed.ncbi.nlm.nih.gov/35975534","citation_count":3,"is_preprint":false},{"pmid":"38287421","id":"PMC_38287421","title":"Identification of a hub gene VCL for atherosclerotic plaques and discovery of potential therapeutic targets by molecular docking.","date":"2024","source":"BMC medical genomics","url":"https://pubmed.ncbi.nlm.nih.gov/38287421","citation_count":2,"is_preprint":false},{"pmid":"33491343","id":"PMC_33491343","title":"Loss-of-function or gain-of-function variations in VINCULIN (VCL) are risk factors of human neural tube defects.","date":"2021","source":"Molecular genetics & genomic 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\"method\": \"Zebrafish genetic model (contracting vs. non-contracting cardiomyocytes), VCL interactome analysis (proteomics/co-IP), loss-of-function with myofilament maturation readout\",\n      \"journal\": \"Developmental Cell\",\n      \"confidence\": \"High\",\n      \"confidence_rationale\": \"Tier 2 / Moderate — reciprocal interactome in two conditions, loss-of-function with defined phenotype, multiple orthogonal methods in a single rigorous study\",\n      \"pmids\": [\"31495694\"],\n      \"is_preprint\": false\n    },\n    {\n      \"year\": 2024,\n      \"finding\": \"Vinculin phosphorylation at tyrosine residue 822 (pY822) regulates the balance between cadherin-based cell-cell adhesion and integrin-based cell-matrix adhesion in cardiomyocytes; Y822F knock-in mice show reduced vinculin and adherens junction proteins at junctions and increased α5/β1 integrin and fibronectin at lateral borders, with cardiac dysfunction emerging at 28 weeks.\",\n      \"method\": \"Mouse knock-in (Y822F point mutation), immunofluorescence, cardiac function assessment\",\n      \"journal\": \"bioRxiv (preprint)\",\n      \"confidence\": \"Medium\",\n      \"confidence_rationale\": \"Tier 2 / Moderate — in vivo knock-in with defined molecular and functional phenotype, but preprint and single lab\",\n      \"pmids\": [\"bio_10.1101_2024.10.28.620745\"],\n      \"is_preprint\": true\n    },\n    {\n      \"year\": 2021,\n      \"finding\": \"A pool of vinculin (VCL) is covalently PARylated (poly-ADP-ribosylated) by tankyrase (TNKS) at the plasma membrane in epithelial cells; VCL contains conserved tankyrase-binding motifs (TBMs), and overexpression of a TBM-II point mutant (GgVCL/*TBM) induced mesenchymal-like cell shape changes, implicating this modification in adherens junction regulation and cell shape maintenance.\",\n      \"method\": \"Affinity precipitation with PAR-binding reagent followed by western blot, TNKS inhibitor experiments, transfection of TBM point-mutant VCL with morphological readout\",\n      \"journal\": \"PeerJ\",\n      \"confidence\": \"Medium\",\n      \"confidence_rationale\": \"Tier 2 / Weak — biochemical PARylation confirmed by affinity precipitation, functional mutant experiment in single lab with overexpression system\",\n      \"pmids\": [\"34123588\"],\n      \"is_preprint\": false\n    },\n    {\n      \"year\": 2021,\n      \"finding\": \"Loss-of-function (p.D256fs) and gain-of-function (p.L555V, conferring enhanced protein stability) VCL variants identified in human neural tube defect patients affect planar cell polarity (PCP) pathway regulation and cell migration, consistent with VCL's role in cell skeleton remodeling during neural tube closure.\",\n      \"method\": \"Targeted next-generation sequencing of human NTD cohort, functional assays for PCP pathway activity and cell migration\",\n      \"journal\": \"Molecular Genetics & Genomic Medicine\",\n      \"confidence\": \"Medium\",\n      \"confidence_rationale\": \"Tier 2 / Weak — variant-level functional evaluation with PCP and migration assays, single study\",\n      \"pmids\": [\"33491343\"],\n      \"is_preprint\": false\n    },\n    {\n      \"year\": 2024,\n      \"finding\": \"miR-6721-5p directly targets the 3'-UTR of meta-VCL (the muscle-specific splice isoform of VCL) and suppresses its expression, as validated by dual-luciferase reporter assay; meta-VCL downregulation was associated with reduced anti-inflammatory cytokine levels (IL-10, TNF-α).\",\n      \"method\": \"Dual-luciferase reporter assay, cell-based ectopic expression, qPCR\",\n      \"journal\": \"Non-coding RNA Research\",\n      \"confidence\": \"Medium\",\n      \"confidence_rationale\": \"Tier 3 / Moderate — direct interaction validated by luciferase assay in cells, functional consequence assessed, replicated in patient serum and bioinformatics\",\n      \"pmids\": [\"39296643\"],\n      \"is_preprint\": false\n    },\n    {\n      \"year\": 2023,\n      \"finding\": \"miR-29a-3p directly targets VCL (and CTNNB1) 3'-UTR in nasal epithelial cells, suppressing VCL expression and disrupting adherens and tight junction integrity; miR-29a-3p antagomir treatment in OVA-induced allergic rhinitis mice restored VCL/Ctnnb1 expression and improved epithelial barrier function.\",\n      \"method\": \"Dual-luciferase reporter assay, miRNA mimic/inhibitor transfection, in vivo antagomir mouse model with barrier function readout\",\n      \"journal\": \"International Immunopharmacology\",\n      \"confidence\": \"Medium\",\n      \"confidence_rationale\": \"Tier 2 / Moderate — direct targeting validated by luciferase assay, in vivo rescue experiment, multiple methods in single lab\",\n      \"pmids\": [\"37262956\"],\n      \"is_preprint\": false\n    },\n    {\n      \"year\": 2024,\n      \"finding\": \"RBM10 loss causes aberrant exon inclusion in VCL transcripts; knockdown of the VCL exon-inclusion isoform in RBM10-null cells reduced cell velocity, placing this VCL isoform in the pathway linking RBM10 loss to increased cell motility and metastatic fitness.\",\n      \"method\": \"RNA-seq, isoform-specific knockdown with cell velocity readout, mouse Hras/Rbm10 KO model with combined VCL/CD44/TNC knockdown rescue\",\n      \"journal\": \"bioRxiv (preprint)\",\n      \"confidence\": \"Medium\",\n      \"confidence_rationale\": \"Tier 2 / Moderate — genetic epistasis via isoform-specific knockdown with defined motility phenotype, in vivo mouse model with rescue; preprint, single lab\",\n      \"pmids\": [\"bio_10.1101_2024.07.09.602730\"],\n      \"is_preprint\": true\n    },\n    {\n      \"year\": 2025,\n      \"finding\": \"In a rat model of lung injury, anti-VCL intervention reduced plasma VCL levels, mitigated alveolar edema, and restored alveolar-capillary barrier integrity, demonstrating that VCL modulation affects vascular leakage and extravasation; multi-omics analysis identified VCL's involvement in the VCL/ICAM-1 signaling pathway associated with Omicron-induced endothelial dysfunction.\",\n      \"method\": \"Rat lung injury model with anti-VCL treatment, histological staining, electron microscopy, plasma proteomics and metabolomics\",\n      \"journal\": \"Nature Communications\",\n      \"confidence\": \"Medium\",\n      \"confidence_rationale\": \"Tier 2 / Moderate — functional intervention (anti-VCL) in animal model with defined vascular/barrier phenotype and multi-omics pathway context, single study\",\n      \"pmids\": [\"40268929\"],\n      \"is_preprint\": false\n    },\n    {\n      \"year\": 1992,\n      \"finding\": \"The vinculin gene (VCL) was mapped to human chromosome 10q22.1-q23 by physical (somatic hybrid panel hybridization, flow-sorted translocation chromosome hybridization) and genetic recombination mapping.\",\n      \"method\": \"Human-rodent somatic hybrid panel hybridization, fluorescence in situ hybridization to flow-sorted chromosomes, genetic recombination mapping in MEN2 families\",\n      \"journal\": \"Genomics\",\n      \"confidence\": \"High\",\n      \"confidence_rationale\": \"Tier 1 / Strong — multiple independent physical and genetic mapping methods, replicated across approaches in a single study\",\n      \"pmids\": [\"1505973\"],\n      \"is_preprint\": false\n    }\n  ],\n  \"current_model\": \"Vinculin (VCL) is a mechanosensitive cytoskeletal adaptor protein that links filamentous actin to cell-matrix and cell-cell adhesions; in cardiomyocytes it responds to mechanical forces by recruiting the SSH1 phosphatase and cofilin to regulate F-actin remodeling and myofilament maturation (VCL-SSH1-CFL axis), and its phosphorylation at Y822 balances cadherin vs. integrin adhesion organization; VCL is covalently PARylated by tankyrase at adherens junctions, and its expression is post-transcriptionally regulated by miRNAs (miR-6721-5p targeting meta-VCL; miR-29a-3p targeting VCL in epithelial junctions); loss-of-function or gain-of-function VCL variants impair PCP signaling and cell migration, and aberrant VCL splicing driven by RBM10 loss promotes cell motility and metastatic competency.\"\n}\n```","stage2_raw":"{\n  \"mechanistic_narrative\": \"Vinculin (VCL) is a mechanosensitive cytoskeletal adaptor that couples filamentous actin to both cell-matrix (integrin) and cell-cell (cadherin) adhesions and translates mechanical force into adhesion and cytoskeletal remodeling [#0, #1]. In cardiomyocytes, mechanical force from contractility controls VCL localization and activation, and VCL recruits the SSH1 phosphatase together with cofilin to drive F-actin rearrangement and myofilament maturation through the VCL-SSH1-CFL axis [#0]. The balance between cadherin- and integrin-based adhesion is set by VCL phosphorylation at tyrosine 822: loss of this phosphorylation reduces junctional VCL and adherens-junction proteins while increasing α5/β1 integrin and fibronectin at lateral borders, with cardiac dysfunction as the in vivo consequence [#1]. VCL function at adherens junctions is further regulated by covalent poly-ADP-ribosylation by tankyrase via conserved tankyrase-binding motifs, a modification linked to cell shape maintenance [#2]. Beyond adhesion, VCL participates in planar cell polarity signaling and cell migration—where human loss- and gain-of-function variants are associated with neural tube defects [#3]—and its abundance and isoform usage are tightly controlled post-transcriptionally, by miRNAs targeting the muscle-specific meta-VCL isoform [#4] and epithelial VCL [#5] and by RBM10-dependent splicing that links an exon-inclusion isoform to cell motility [#6].\",\n  \"teleology\": [\n    {\n      \"year\": 1992,\n      \"claim\": \"Establishing the chromosomal location of VCL provided the genomic anchor needed to connect the gene to human phenotypes and to distinguish it from neighboring loci.\",\n      \"evidence\": \"Somatic hybrid panel hybridization, FISH to flow-sorted chromosomes, and genetic recombination mapping in MEN2 families\",\n      \"pmids\": [\"1505973\"],\n      \"confidence\": \"High\",\n      \"gaps\": [\"Mapping alone does not address protein function\", \"No isoform or splice structure resolved\"]\n    },\n    {\n      \"year\": 2019,\n      \"claim\": \"It was unknown how mechanical force is converted into cytoskeletal maturation in heart muscle; this work showed VCL is a force-responsive node that recruits SSH1 and cofilin to remodel F-actin and mature myofilaments.\",\n      \"evidence\": \"Zebrafish contracting vs. non-contracting cardiomyocyte model with VCL interactome and loss-of-function myofilament readout\",\n      \"pmids\": [\"31495694\"],\n      \"confidence\": \"High\",\n      \"gaps\": [\"Direct vs. bridged nature of the VCL-SSH1 interaction not resolved\", \"Generality beyond cardiomyocytes untested in this study\"]\n    },\n    {\n      \"year\": 2021,\n      \"claim\": \"How VCL is covalently regulated at junctions was unclear; this established that a membrane pool of VCL is PARylated by tankyrase through conserved binding motifs, linking the modification to adherens-junction and cell-shape control.\",\n      \"evidence\": \"PAR-binding affinity precipitation, tankyrase inhibition, and TBM point-mutant overexpression with morphological readout in epithelial cells\",\n      \"pmids\": [\"34123588\"],\n      \"confidence\": \"Medium\",\n      \"gaps\": [\"Functional readout relies on overexpression of a mutant\", \"Endogenous consequences of blocking PARylation not measured\"]\n    },\n    {\n      \"year\": 2021,\n      \"claim\": \"Whether VCL contributes to human developmental disease was open; identification of loss- and gain-of-function variants in neural tube defect patients tied VCL to PCP signaling and migration during neural tube closure.\",\n      \"evidence\": \"Targeted sequencing of an NTD cohort with PCP-activity and cell-migration assays\",\n      \"pmids\": [\"33491343\"],\n      \"confidence\": \"Medium\",\n      \"gaps\": [\"Causality at the organismal level not demonstrated\", \"Mechanistic link from VCL to PCP components undefined\"]\n    },\n    {\n      \"year\": 2023,\n      \"claim\": \"The post-transcriptional control of VCL in epithelial barriers was unknown; miR-29a-3p was shown to directly repress VCL and disrupt junctional integrity, with antagomir rescue restoring barrier function.\",\n      \"evidence\": \"Dual-luciferase 3'-UTR assay, miRNA mimic/inhibitor transfection, and in vivo antagomir allergic-rhinitis mouse model\",\n      \"pmids\": [\"37262956\"],\n      \"confidence\": \"Medium\",\n      \"gaps\": [\"Effects shared with co-target CTNNB1 not fully separated\", \"Single epithelial context\"]\n    },\n    {\n      \"year\": 2024,\n      \"claim\": \"How phosphorylation tunes VCL between adhesion systems was unresolved; a Y822F knock-in showed pY822 sets the cadherin-versus-integrin adhesion balance with late-onset cardiac dysfunction.\",\n      \"evidence\": \"Mouse Y822F knock-in with immunofluorescence and cardiac function assessment (preprint)\",\n      \"pmids\": [\"bio_10.1101_2024.10.28.620745\"],\n      \"confidence\": \"Medium\",\n      \"gaps\": [\"Preprint, single lab\", \"Upstream kinase and signal triggering Y822 phosphorylation not identified\"]\n    },\n    {\n      \"year\": 2024,\n      \"claim\": \"Isoform-specific regulation of VCL was clarified by showing miR-6721-5p directly represses the muscle-specific meta-VCL isoform, coupling it to inflammatory cytokine changes.\",\n      \"evidence\": \"Dual-luciferase reporter assay, ectopic expression, and qPCR\",\n      \"pmids\": [\"39296643\"],\n      \"confidence\": \"Medium\",\n      \"gaps\": [\"Mechanism linking meta-VCL loss to cytokine changes unresolved\", \"In vivo relevance limited\"]\n    },\n    {\n      \"year\": 2024,\n      \"claim\": \"It was unclear how RBM10 loss promotes motility; aberrant VCL exon inclusion was placed in the pathway, with isoform-specific knockdown reducing cell velocity and contributing to metastatic fitness.\",\n      \"evidence\": \"RNA-seq, isoform-specific knockdown with velocity readout, and Hras/Rbm10 KO mouse with combined-knockdown rescue (preprint)\",\n      \"pmids\": [\"bio_10.1101_2024.07.09.602730\"],\n      \"confidence\": \"Medium\",\n      \"gaps\": [\"Preprint, single lab\", \"Molecular difference of the exon-inclusion isoform not characterized\"]\n    },\n    {\n      \"year\": 2025,\n      \"claim\": \"Whether VCL participates in vascular barrier failure was open; anti-VCL intervention reduced alveolar edema and restored barrier integrity, implicating a VCL/ICAM-1 axis in endothelial dysfunction.\",\n      \"evidence\": \"Rat lung injury model with anti-VCL treatment, histology, electron microscopy, and plasma multi-omics\",\n      \"pmids\": [\"40268929\"],\n      \"confidence\": \"Medium\",\n      \"gaps\": [\"Mechanism of plasma VCL action on endothelium undefined\", \"VCL/ICAM-1 relationship correlative\"]\n    },\n    {\n      \"year\": null,\n      \"claim\": \"How the distinct VCL regulatory layers—force sensing, Y822 phosphorylation, tankyrase PARylation, and splicing/miRNA control—are integrated to set adhesion identity in a given cell type remains unresolved.\",\n      \"evidence\": \"\",\n      \"pmids\": [],\n      \"confidence\": \"Medium\",\n      \"gaps\": [\"No unified model connecting modifications and isoforms\", \"Upstream regulators of each modification largely unknown\", \"Cross-tissue generality untested\"]\n    }\n  ],\n  \"mechanism_profile\": {\n    \"molecular_activity\": [\n      {\"term_id\": \"GO:0008092\", \"supporting_discovery_ids\": [0]},\n      {\"term_id\": \"GO:0060090\", \"supporting_discovery_ids\": [0, 1]}\n    ],\n    \"localization\": [\n      {\"term_id\": \"GO:0005886\", \"supporting_discovery_ids\": [1, 2]},\n      {\"term_id\": \"GO:0005856\", \"supporting_discovery_ids\": [0]}\n    ],\n    \"pathway\": [\n      {\"term_id\": \"R-HSA-1474244\", \"supporting_discovery_ids\": [1]},\n      {\"term_id\": \"R-HSA-1500931\", \"supporting_discovery_ids\": [1, 5]}\n    ],\n    \"complexes\": [\"adherens junction\"],\n    \"partners\": [\"SSH1\", \"CFL\", \"TNKS\"],\n    \"other_free_text\": []\n  }\n}","audit_flag":null,"evaluation":{"pairwise":"win","faith_supported":4,"faith_total":4,"faith_pct":100.0}}