{"gene":"ACTBL2","run_date":"2026-06-09T22:02:40","timeline":{"discoveries":[{"year":2021,"finding":"ACTBL2 (actbl2) protein can polymerize and forms complexes with gelsolin in human melanoma cells. Knockout of ACTBL2 or its overexpression alters invasion, focal adhesion formation, actin polymerization ratio, lamellipodia formation, and stress fiber formation, establishing actbl2 as the seventh actin isoform with an essential role in cell motility.","method":"CRISPR knockout and overexpression in melanoma cell lines; phylogenetic/bioinformatic analysis; functional assays for invasion, focal adhesion formation, actin polymerization","journal":"Scientific reports","confidence":"Medium","confidence_rationale":"Tier 2 / Moderate — clean KO and OE with multiple defined cellular phenotypes (invasion, focal adhesion, polymerization, lamellipodia, stress fibers), single lab, multiple orthogonal readouts","pmids":["33558623"],"is_preprint":false},{"year":2015,"finding":"Actbl2 physically interacts with gelsolin in human melanoma cells, detected separately in cytoplasmic and nuclear compartments.","method":"Immunoprecipitation followed by mass spectrometry, confirmed by Western blot, proximity ligation assay, and confocal microscopy","journal":"European journal of cell biology","confidence":"Medium","confidence_rationale":"Tier 2 / Moderate — reciprocal Co-IP with MS, confirmed by PLA and confocal; single lab, multiple orthogonal methods","pmids":["26598132"],"is_preprint":false},{"year":2014,"finding":"The transcription factor TonEBP/NFAT5 directly controls ACTBL2 expression in vascular smooth muscle cells (VSMCs) under biomechanical stretch: stretch promotes NFAT5 nuclear translocation, NFAT5 binds the ACTBL2 promoter region, and siRNA-mediated NFAT5 knockdown reduces ACTBL2 expression. Kappa-actin (ACTBL2) aligns with stress fibers under static conditions, disperses into lamellipodia under stretch, and its knockdown reduces VSMC lateral migration.","method":"Automated immunofluorescence, Western blot, in silico promoter analysis, siRNA knockdown, migration assay","journal":"Frontiers in physiology","confidence":"Medium","confidence_rationale":"Tier 2 / Moderate — siRNA knockdown with defined migration phenotype plus promoter binding evidence; single lab, multiple orthogonal methods","pmids":["25520667"],"is_preprint":false},{"year":2020,"finding":"ACTBL2 competes with the E3 ligase RBCK1 for binding to MTSS1, thereby counteracting MTSS1-mediated RBCK1-facilitated ubiquitination and degradation of p65 (NF-κB subunit), leading to p65 stabilization and enhanced NF-κB signaling.","method":"Co-immunoprecipitation (Co-IP) competition assay, ubiquitination assay, Western blot for p65 levels; genetic perturbation of MTSS1 and ACTBL2 in breast cancer cell lines and mouse models","journal":"Nature cancer","confidence":"High","confidence_rationale":"Tier 2 / Strong — reciprocal Co-IP, competitive binding assay, ubiquitination assay, multiple cell line and in vivo models; published in high-tier journal with mechanistic rigor","pmids":["35122005"],"is_preprint":false},{"year":2021,"finding":"siRNA knockdown of ACTBL2 in epithelial ovarian cancer (EOC) cell lines significantly reduces cellular viability, proliferation, and migration. siRNA knockdown of NFAT5 downregulates ACTBL2 and produces concordant decreases in migration, confirming a NFAT5→ACTBL2 regulatory axis in EOC cells.","method":"siRNA knockdown; cellular viability, proliferation (functional assay), and migration assays in EOC cell lines","journal":"Frontiers in oncology","confidence":"Medium","confidence_rationale":"Tier 2 / Moderate — siRNA KD with multiple defined functional phenotypes in EOC cells; single lab, multiple orthogonal readouts confirming NFAT5-ACTBL2 axis","pmids":["34631538"],"is_preprint":false}],"current_model":"ACTBL2 (kappa-actin/actbl2) is a seventh actin isoform capable of polymerization that interacts with gelsolin, aligns with stress fibers, and localizes to lamellipodia; its expression is transcriptionally driven by TonEBP/NFAT5 in response to biomechanical stretch; it promotes cell motility, invasion, and focal adhesion formation in melanoma and ovarian cancer cells; and it competes with the E3 ligase RBCK1 for MTSS1 binding, thereby stabilizing NF-κB p65 and enhancing NF-κB signaling."},"narrative":{"mechanistic_narrative":"ACTBL2 (kappa-actin) is a polymerization-competent actin isoform that controls cytoskeletal dynamics underlying cell motility and invasion [PMID:33558623]. It forms complexes with the actin-severing protein gelsolin in both cytoplasmic and nuclear compartments, aligns with stress fibers, and redistributes into lamellipodia, with loss-of-function altering invasion, focal adhesion formation, actin polymerization, and migration [PMID:33558623, PMID:26598132]. Its expression is transcriptionally driven by the osmosensitive/mechanosensitive transcription factor TonEBP/NFAT5, which translocates to the nucleus under biomechanical stretch and binds the ACTBL2 promoter; this NFAT5→ACTBL2 axis governs migration in vascular smooth muscle and ovarian cancer cells [PMID:25520667, PMID:34631538]. Beyond its cytoskeletal role, ACTBL2 functions in NF-κB signaling by competing with the E3 ligase RBCK1 for binding to MTSS1, thereby blocking RBCK1-mediated ubiquitination and degradation of the NF-κB subunit p65 and stabilizing NF-κB activity [PMID:35122005].","teleology":[{"year":2014,"claim":"Established how ACTBL2 expression is controlled, identifying NFAT5 as a direct mechanosensitive transcriptional driver and linking ACTBL2 to stretch-responsive cytoskeletal remodeling.","evidence":"Immunofluorescence, Western blot, in silico promoter analysis, NFAT5 siRNA knockdown, and migration assays in vascular smooth muscle cells","pmids":["25520667"],"confidence":"Medium","gaps":["Direct NFAT5 occupancy of the ACTBL2 promoter shown by in silico analysis rather than ChIP","Mechanism linking ACTBL2 to lamellipodia redistribution under stretch not resolved"]},{"year":2015,"claim":"Identified a direct physical partner for ACTBL2, showing it complexes with the actin-regulatory protein gelsolin in distinct subcellular compartments.","evidence":"Reciprocal Co-IP with mass spectrometry, confirmed by PLA and confocal microscopy in melanoma cells","pmids":["26598132"],"confidence":"Medium","gaps":["Functional consequence of the gelsolin interaction not defined","Significance of separate nuclear vs cytoplasmic pools unclear"]},{"year":2020,"claim":"Revealed a non-cytoskeletal signaling role, showing ACTBL2 stabilizes NF-κB p65 by competing with RBCK1 for MTSS1, thereby blocking p65 ubiquitination.","evidence":"Reciprocal Co-IP competition and ubiquitination assays plus genetic perturbation in breast cancer cell lines and mouse models","pmids":["35122005"],"confidence":"High","gaps":["Whether actin polymerization activity is required for the MTSS1/RBCK1 competition is unknown","Structural basis of competitive binding not determined"]},{"year":2021,"claim":"Defined ACTBL2 as the seventh actin isoform with an essential role in motility, demonstrating that its loss or overexpression remodels actin-dependent structures and invasion.","evidence":"CRISPR knockout and overexpression with invasion, focal adhesion, polymerization, lamellipodia, and stress fiber assays in melanoma cell lines","pmids":["33558623"],"confidence":"Medium","gaps":["Single-lab phenotyping","Atomic structure and copolymerization behavior with canonical actins not established"]},{"year":2021,"claim":"Generalized the NFAT5→ACTBL2 axis beyond vascular cells, showing it supports viability, proliferation, and migration in epithelial ovarian cancer.","evidence":"siRNA knockdown of ACTBL2 and NFAT5 with viability, proliferation, and migration assays in EOC cell lines","pmids":["34631538"],"confidence":"Medium","gaps":["Mechanism linking ACTBL2 to proliferation versus migration not separated","No in vivo confirmation in ovarian cancer"]},{"year":null,"claim":"How ACTBL2's cytoskeletal/actin-polymerization function mechanistically connects to its role in NF-κB signaling, and whether it copolymerizes with canonical actins in cells, remains unresolved.","evidence":"","pmids":[],"confidence":"Medium","gaps":["No structural model of ACTBL2 filaments or interaction interfaces","Tissue-level physiological function not established"]}],"mechanism_profile":{"molecular_activity":[{"term_id":"GO:0005198","term_label":"structural molecule activity","supporting_discovery_ids":[0]},{"term_id":"GO:0008092","term_label":"cytoskeletal protein binding","supporting_discovery_ids":[0,1]}],"localization":[{"term_id":"GO:0005856","term_label":"cytoskeleton","supporting_discovery_ids":[0,2]},{"term_id":"GO:0005829","term_label":"cytosol","supporting_discovery_ids":[1]},{"term_id":"GO:0005634","term_label":"nucleus","supporting_discovery_ids":[1]}],"pathway":[{"term_id":"R-HSA-162582","term_label":"Signal Transduction","supporting_discovery_ids":[3]}],"complexes":[],"partners":["GSN","MTSS1","RBCK1"],"other_free_text":[]}},"prefetch_data":{"uniprot":{"accession":"Q562R1","full_name":"Beta-actin-like protein 2","aliases":["Kappa-actin"],"length_aa":376,"mass_kda":42.0,"function":"Actins are highly conserved proteins that are involved in various types of cell motility and are ubiquitously expressed in all eukaryotic cells","subcellular_location":"Cytoplasm, cytoskeleton","url":"https://www.uniprot.org/uniprotkb/Q562R1/entry"},"depmap":{"release":"DepMap","has_data":true,"is_common_essential":false,"resolved_as":"","url":"https://depmap.org/portal/gene/ACTBL2","classification":"Not Classified","n_dependent_lines":0,"n_total_lines":1208,"dependency_fraction":0.0},"opencell":{"profiled":false,"resolved_as":"","ensg_id":"","cell_line_id":"","localizations":[],"interactors":[{"gene":"BCAR1","stoichiometry":4.0},{"gene":"CALD1","stoichiometry":0.2},{"gene":"CAPZB","stoichiometry":0.2}],"url":"https://opencell.sf.czbiohub.org/search/ACTBL2","total_profiled":1310},"omim":[{"mim_id":"620170","title":"SPERMATOGENIC FAILURE 78; SPGF78","url":"https://www.omim.org/entry/620170"},{"mim_id":"620160","title":"IQ MOTIF-CONTAINING PROTEIN N; IQCN","url":"https://www.omim.org/entry/620160"},{"mim_id":"614835","title":"ACTIN, BETA-LIKE, 2; ACTBL2","url":"https://www.omim.org/entry/614835"}],"hpa":{"profiled":true,"resolved_as":"","reliability":"","locations":[],"tissue_specificity":"Not detected","tissue_distribution":"Not detected","driving_tissues":[],"url":"https://www.proteinatlas.org/search/ACTBL2"},"hgnc":{"alias_symbol":["DKFZp686D0972"],"prev_symbol":[]},"alphafold":{"accession":"Q562R1","domains":[{"cath_id":"3.30.420.40","chopping":"10-139_340-375","consensus_level":"medium","plddt":94.5811,"start":10,"end":375},{"cath_id":"3.30.420.40","chopping":"145-181_274-338","consensus_level":"medium","plddt":97.2865,"start":145,"end":338},{"cath_id":"3.90.640.10","chopping":"184-268","consensus_level":"high","plddt":96.0686,"start":184,"end":268}],"viewer_url":"https://alphafold.ebi.ac.uk/entry/Q562R1","model_url":"https://alphafold.ebi.ac.uk/files/AF-Q562R1-F1-model_v6.cif","pae_url":"https://alphafold.ebi.ac.uk/files/AF-Q562R1-F1-predicted_aligned_error_v6.png","plddt_mean":94.81},"mouse_models":{"mgi_url":"https://www.informatics.jax.org/marker/summary?nomen=ACTBL2","jax_strain_url":"https://www.jax.org/strain/search?query=ACTBL2"},"sequence":{"accession":"Q562R1","fasta_url":"https://rest.uniprot.org/uniprotkb/Q562R1.fasta","uniprot_url":"https://www.uniprot.org/uniprotkb/Q562R1/entry","alphafold_viewer_url":"https://alphafold.ebi.ac.uk/entry/Q562R1"}},"corpus_meta":[{"pmid":"36871648","id":"PMC_36871648","title":"Towards 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Ribosomal Proteins RPeL27, RPeL43, and RPeL41 Are Upregulated in Nasopharyngeal Carcinoma Cell Lines.","date":"2016","source":"Disease markers","url":"https://pubmed.ncbi.nlm.nih.gov/28018022","citation_count":6,"is_preprint":false},{"pmid":"37775079","id":"PMC_37775079","title":"Enhanced ileum function in weaned piglets via Laminaria digitata and alginate lyase dietary inclusion: A combined proteomics and metabolomics analysis.","date":"2023","source":"Journal of proteomics","url":"https://pubmed.ncbi.nlm.nih.gov/37775079","citation_count":5,"is_preprint":false},{"pmid":"35770079","id":"PMC_35770079","title":"Proteomic Analysis of Potential Targets for Non-Response to Infliximab in Patients With Ulcerative Colitis.","date":"2022","source":"Frontiers in pharmacology","url":"https://pubmed.ncbi.nlm.nih.gov/35770079","citation_count":5,"is_preprint":false},{"pmid":"31737203","id":"PMC_31737203","title":"Proteomic analysis for identifying the differences in molecular profiling between fanconi anaemia and aplastic anaemia.","date":"2019","source":"American journal of translational research","url":"https://pubmed.ncbi.nlm.nih.gov/31737203","citation_count":5,"is_preprint":false},{"pmid":"34966852","id":"PMC_34966852","title":"ACTB and GAPDH appear at multiple SDS-PAGE positions, thus not suitable as reference genes for determining protein loading in techniques like Western blotting.","date":"2021","source":"Open life sciences","url":"https://pubmed.ncbi.nlm.nih.gov/34966852","citation_count":4,"is_preprint":false},{"pmid":"40199047","id":"PMC_40199047","title":"The effect of high-level dietary Laminaria digitata on the muscle proteome and metabolome of weaned piglets.","date":"2025","source":"Research in veterinary science","url":"https://pubmed.ncbi.nlm.nih.gov/40199047","citation_count":1,"is_preprint":false},{"pmid":"33277874","id":"PMC_33277874","title":"The expression pattern of ACTBL2 in thymoma reveals its potential therapeutic target 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Switzerland)","url":"https://pubmed.ncbi.nlm.nih.gov/41635560","citation_count":0,"is_preprint":false}],"cost":{"stage1":{"model":"claude-sonnet-4-6","input_tokens":13908,"output_tokens":1382,"usd":0.031227,"stage1_stop_reason":"end_turn"},"stage2":{"model":"claude-opus-4-8","input_tokens":8102,"output_tokens":2072,"usd":0.046155,"stage2_stop_reason":"end_turn"},"total_usd":0.077382,"stage1_batch_id":"msgbatch_0179Z2pxRYBsXi2xADneafRw","stage2_batch_id":"msgbatch_01LaY9ZaVdgjWArcZo9eqQE5","note":"batch pricing = 50% of standard"},"stage1_raw":"```json\n{\n  \"discoveries\": [\n    {\n      \"year\": 2021,\n      \"finding\": \"ACTBL2 (actbl2) protein can polymerize and forms complexes with gelsolin in human melanoma cells. Knockout of ACTBL2 or its overexpression alters invasion, focal adhesion formation, actin polymerization ratio, lamellipodia formation, and stress fiber formation, establishing actbl2 as the seventh actin isoform with an essential role in cell motility.\",\n      \"method\": \"CRISPR knockout and overexpression in melanoma cell lines; phylogenetic/bioinformatic analysis; functional assays for invasion, focal adhesion formation, actin polymerization\",\n      \"journal\": \"Scientific reports\",\n      \"confidence\": \"Medium\",\n      \"confidence_rationale\": \"Tier 2 / Moderate — clean KO and OE with multiple defined cellular phenotypes (invasion, focal adhesion, polymerization, lamellipodia, stress fibers), single lab, multiple orthogonal readouts\",\n      \"pmids\": [\"33558623\"],\n      \"is_preprint\": false\n    },\n    {\n      \"year\": 2015,\n      \"finding\": \"Actbl2 physically interacts with gelsolin in human melanoma cells, detected separately in cytoplasmic and nuclear compartments.\",\n      \"method\": \"Immunoprecipitation followed by mass spectrometry, confirmed by Western blot, proximity ligation assay, and confocal microscopy\",\n      \"journal\": \"European journal of cell biology\",\n      \"confidence\": \"Medium\",\n      \"confidence_rationale\": \"Tier 2 / Moderate — reciprocal Co-IP with MS, confirmed by PLA and confocal; single lab, multiple orthogonal methods\",\n      \"pmids\": [\"26598132\"],\n      \"is_preprint\": false\n    },\n    {\n      \"year\": 2014,\n      \"finding\": \"The transcription factor TonEBP/NFAT5 directly controls ACTBL2 expression in vascular smooth muscle cells (VSMCs) under biomechanical stretch: stretch promotes NFAT5 nuclear translocation, NFAT5 binds the ACTBL2 promoter region, and siRNA-mediated NFAT5 knockdown reduces ACTBL2 expression. Kappa-actin (ACTBL2) aligns with stress fibers under static conditions, disperses into lamellipodia under stretch, and its knockdown reduces VSMC lateral migration.\",\n      \"method\": \"Automated immunofluorescence, Western blot, in silico promoter analysis, siRNA knockdown, migration assay\",\n      \"journal\": \"Frontiers in physiology\",\n      \"confidence\": \"Medium\",\n      \"confidence_rationale\": \"Tier 2 / Moderate — siRNA knockdown with defined migration phenotype plus promoter binding evidence; single lab, multiple orthogonal methods\",\n      \"pmids\": [\"25520667\"],\n      \"is_preprint\": false\n    },\n    {\n      \"year\": 2020,\n      \"finding\": \"ACTBL2 competes with the E3 ligase RBCK1 for binding to MTSS1, thereby counteracting MTSS1-mediated RBCK1-facilitated ubiquitination and degradation of p65 (NF-κB subunit), leading to p65 stabilization and enhanced NF-κB signaling.\",\n      \"method\": \"Co-immunoprecipitation (Co-IP) competition assay, ubiquitination assay, Western blot for p65 levels; genetic perturbation of MTSS1 and ACTBL2 in breast cancer cell lines and mouse models\",\n      \"journal\": \"Nature cancer\",\n      \"confidence\": \"High\",\n      \"confidence_rationale\": \"Tier 2 / Strong — reciprocal Co-IP, competitive binding assay, ubiquitination assay, multiple cell line and in vivo models; published in high-tier journal with mechanistic rigor\",\n      \"pmids\": [\"35122005\"],\n      \"is_preprint\": false\n    },\n    {\n      \"year\": 2021,\n      \"finding\": \"siRNA knockdown of ACTBL2 in epithelial ovarian cancer (EOC) cell lines significantly reduces cellular viability, proliferation, and migration. siRNA knockdown of NFAT5 downregulates ACTBL2 and produces concordant decreases in migration, confirming a NFAT5→ACTBL2 regulatory axis in EOC cells.\",\n      \"method\": \"siRNA knockdown; cellular viability, proliferation (functional assay), and migration assays in EOC cell lines\",\n      \"journal\": \"Frontiers in oncology\",\n      \"confidence\": \"Medium\",\n      \"confidence_rationale\": \"Tier 2 / Moderate — siRNA KD with multiple defined functional phenotypes in EOC cells; single lab, multiple orthogonal readouts confirming NFAT5-ACTBL2 axis\",\n      \"pmids\": [\"34631538\"],\n      \"is_preprint\": false\n    }\n  ],\n  \"current_model\": \"ACTBL2 (kappa-actin/actbl2) is a seventh actin isoform capable of polymerization that interacts with gelsolin, aligns with stress fibers, and localizes to lamellipodia; its expression is transcriptionally driven by TonEBP/NFAT5 in response to biomechanical stretch; it promotes cell motility, invasion, and focal adhesion formation in melanoma and ovarian cancer cells; and it competes with the E3 ligase RBCK1 for MTSS1 binding, thereby stabilizing NF-κB p65 and enhancing NF-κB signaling.\"\n}\n```","stage2_raw":"{\n  \"mechanistic_narrative\": \"ACTBL2 (kappa-actin) is a polymerization-competent actin isoform that controls cytoskeletal dynamics underlying cell motility and invasion [#0]. It forms complexes with the actin-severing protein gelsolin in both cytoplasmic and nuclear compartments, aligns with stress fibers, and redistributes into lamellipodia, with loss-of-function altering invasion, focal adhesion formation, actin polymerization, and migration [#0, #1]. Its expression is transcriptionally driven by the osmosensitive/mechanosensitive transcription factor TonEBP/NFAT5, which translocates to the nucleus under biomechanical stretch and binds the ACTBL2 promoter; this NFAT5→ACTBL2 axis governs migration in vascular smooth muscle and ovarian cancer cells [#2, #4]. Beyond its cytoskeletal role, ACTBL2 functions in NF-\\u03baB signaling by competing with the E3 ligase RBCK1 for binding to MTSS1, thereby blocking RBCK1-mediated ubiquitination and degradation of the NF-\\u03baB subunit p65 and stabilizing NF-\\u03baB activity [#3].\",\n  \"teleology\": [\n    {\n      \"year\": 2014,\n      \"claim\": \"Established how ACTBL2 expression is controlled, identifying NFAT5 as a direct mechanosensitive transcriptional driver and linking ACTBL2 to stretch-responsive cytoskeletal remodeling.\",\n      \"evidence\": \"Immunofluorescence, Western blot, in silico promoter analysis, NFAT5 siRNA knockdown, and migration assays in vascular smooth muscle cells\",\n      \"pmids\": [\"25520667\"],\n      \"confidence\": \"Medium\",\n      \"gaps\": [\"Direct NFAT5 occupancy of the ACTBL2 promoter shown by in silico analysis rather than ChIP\", \"Mechanism linking ACTBL2 to lamellipodia redistribution under stretch not resolved\"]\n    },\n    {\n      \"year\": 2015,\n      \"claim\": \"Identified a direct physical partner for ACTBL2, showing it complexes with the actin-regulatory protein gelsolin in distinct subcellular compartments.\",\n      \"evidence\": \"Reciprocal Co-IP with mass spectrometry, confirmed by PLA and confocal microscopy in melanoma cells\",\n      \"pmids\": [\"26598132\"],\n      \"confidence\": \"Medium\",\n      \"gaps\": [\"Functional consequence of the gelsolin interaction not defined\", \"Significance of separate nuclear vs cytoplasmic pools unclear\"]\n    },\n    {\n      \"year\": 2020,\n      \"claim\": \"Revealed a non-cytoskeletal signaling role, showing ACTBL2 stabilizes NF-\\u03baB p65 by competing with RBCK1 for MTSS1, thereby blocking p65 ubiquitination.\",\n      \"evidence\": \"Reciprocal Co-IP competition and ubiquitination assays plus genetic perturbation in breast cancer cell lines and mouse models\",\n      \"pmids\": [\"35122005\"],\n      \"confidence\": \"High\",\n      \"gaps\": [\"Whether actin polymerization activity is required for the MTSS1/RBCK1 competition is unknown\", \"Structural basis of competitive binding not determined\"]\n    },\n    {\n      \"year\": 2021,\n      \"claim\": \"Defined ACTBL2 as the seventh actin isoform with an essential role in motility, demonstrating that its loss or overexpression remodels actin-dependent structures and invasion.\",\n      \"evidence\": \"CRISPR knockout and overexpression with invasion, focal adhesion, polymerization, lamellipodia, and stress fiber assays in melanoma cell lines\",\n      \"pmids\": [\"33558623\"],\n      \"confidence\": \"Medium\",\n      \"gaps\": [\"Single-lab phenotyping\", \"Atomic structure and copolymerization behavior with canonical actins not established\"]\n    },\n    {\n      \"year\": 2021,\n      \"claim\": \"Generalized the NFAT5→ACTBL2 axis beyond vascular cells, showing it supports viability, proliferation, and migration in epithelial ovarian cancer.\",\n      \"evidence\": \"siRNA knockdown of ACTBL2 and NFAT5 with viability, proliferation, and migration assays in EOC cell lines\",\n      \"pmids\": [\"34631538\"],\n      \"confidence\": \"Medium\",\n      \"gaps\": [\"Mechanism linking ACTBL2 to proliferation versus migration not separated\", \"No in vivo confirmation in ovarian cancer\"]\n    },\n    {\n      \"year\": null,\n      \"claim\": \"How ACTBL2's cytoskeletal/actin-polymerization function mechanistically connects to its role in NF-\\u03baB signaling, and whether it copolymerizes with canonical actins in cells, remains unresolved.\",\n      \"evidence\": \"\",\n      \"pmids\": [],\n      \"confidence\": \"Medium\",\n      \"gaps\": [\"No structural model of ACTBL2 filaments or interaction interfaces\", \"Tissue-level physiological function not established\"]\n    }\n  ],\n  \"mechanism_profile\": {\n    \"molecular_activity\": [\n      {\"term_id\": \"GO:0005198\", \"supporting_discovery_ids\": [0]},\n      {\"term_id\": \"GO:0008092\", \"supporting_discovery_ids\": [0, 1]}\n    ],\n    \"localization\": [\n      {\"term_id\": \"GO:0005856\", \"supporting_discovery_ids\": [0, 2]},\n      {\"term_id\": \"GO:0005829\", \"supporting_discovery_ids\": [1]},\n      {\"term_id\": \"GO:0005634\", \"supporting_discovery_ids\": [1]}\n    ],\n    \"pathway\": [\n      {\"term_id\": \"R-HSA-162582\", \"supporting_discovery_ids\": [3]}\n    ],\n    \"complexes\": [],\n    \"partners\": [\"GSN\", \"MTSS1\", \"RBCK1\"],\n    \"other_free_text\": []\n  }\n}","audit_flag":null,"evaluation":{"pairwise":"win","faith_supported":4,"faith_total":4,"faith_pct":100.0}}