{"gene":"TNRC6B","run_date":"2026-06-10T10:51:55","timeline":{"discoveries":[{"year":2009,"finding":"The N-terminal GW-repeat-containing region of TNRC6B interacts with all four human Argonaute proteins (AGO1-AGO4), as demonstrated by interaction assays.","method":"Protein interaction assays (pulldown/co-immunoprecipitation of N-terminal GW-repeat domain with AGO1-AGO4)","journal":"RNA (New York, N.Y.)","confidence":"High","confidence_rationale":"Tier 2 / Strong — reciprocal interaction mapping across all four AGO paralogs, replicated across three TNRC6 family members in the same study with domain-level resolution","pmids":["19383768"],"is_preprint":false},{"year":2009,"finding":"The C-terminal silencing domain of TNRC6B is sufficient to silence bound mRNAs independently of its interaction with Argonaute proteins, acting through translational repression and/or mRNA destabilization including deadenylation.","method":"Tethering assays with isolated C-terminal domain constructs; mRNA stability and protein expression measurements; deadenylation assays","journal":"RNA (New York, N.Y.)","confidence":"High","confidence_rationale":"Tier 1-2 / Strong — domain dissection with functional tethering assays, multiple orthogonal readouts (protein expression, mRNA stability, deadenylation) in a single rigorous study","pmids":["19383768"],"is_preprint":false},{"year":2009,"finding":"TNRC6B is recruited to miRNA targets via interaction between its N-terminal domain and an Argonaute protein, after which its C-terminal silencing domain promotes translational repression and/or degradation of miRNA targets.","method":"Domain mapping experiments combined with functional silencing assays; genetic dissection of N-terminal vs C-terminal domain activities","journal":"RNA (New York, N.Y.)","confidence":"High","confidence_rationale":"Tier 2 / Strong — epistasis between N-terminal AGO-binding and C-terminal silencing established by domain separation experiments with functional readouts, multiple orthogonal methods in one study","pmids":["19383768"],"is_preprint":false},{"year":2024,"finding":"A synonymous variant c.3141G>A in TNRC6B causes exon 7 skipping, demonstrating that this variant disrupts normal RNA splicing of the TNRC6B transcript.","method":"Minigene assay and Sanger sequencing to verify aberrant splicing","journal":"Molecular biology reports","confidence":"Medium","confidence_rationale":"Tier 2 / Weak — functional minigene splicing assay with Sanger sequencing validation, but single lab and single method","pmids":["39115759"],"is_preprint":false},{"year":2026,"finding":"miR-329-3p directly interacts with TNRC6B 3'UTR and negatively regulates TNRC6B expression, as confirmed by dual-luciferase reporter assay.","method":"Dual-luciferase reporter assay; RT-qPCR for expression correlation","journal":"Annals of hematology","confidence":"Low","confidence_rationale":"Tier 3 / Weak — single luciferase assay establishing miR-329-3p binding to TNRC6B, single lab, no further mechanistic follow-up on TNRC6B protein function","pmids":["41882181"],"is_preprint":false}],"current_model":"TNRC6B (a vertebrate GW182-family protein) is recruited to miRNA targets via its N-terminal GW-repeat domain binding to Argonaute proteins (AGO1–AGO4), after which its C-terminal silencing domain independently promotes translational repression and mRNA destabilization (including deadenylation) of bound transcripts; haploinsufficiency of TNRC6B causes a neurodevelopmental disorder featuring developmental delay, intellectual disability, autism, and ADHD."},"narrative":{"mechanistic_narrative":"TNRC6B is a GW-repeat-containing effector of the miRNA silencing pathway that bridges Argonaute-loaded miRNA complexes to the machinery that represses bound transcripts [PMID:19383768]. Its N-terminal GW-repeat region binds all four human Argonaute proteins (AGO1–AGO4), recruiting TNRC6B to miRNA targets [PMID:19383768]. Once recruited, its C-terminal silencing domain acts autonomously — independently of the AGO interaction — to silence the bound mRNA through translational repression and mRNA destabilization, including deadenylation [PMID:19383768]. TNRC6B expression is itself subject to miRNA control, with miR-329-3p binding the TNRC6B 3'UTR to downregulate it [PMID:41882181]. A synonymous variant (c.3141G>A) disrupts normal splicing by causing exon 7 skipping, linking TNRC6B sequence integrity to transcript processing [PMID:39115759]. Beyond the AGO-binding and silencing-domain architecture established in [PMID:19383768], no further mechanistic detail of substrate selection or recruitment of downstream deadenylation factors has been characterized in the available corpus.","teleology":[{"year":2009,"claim":"Established how TNRC6B is recruited to miRNA targets by mapping the physical interface to Argonaute proteins, answering whether this GW182-family protein couples to the core silencing effectors.","evidence":"Pulldown/co-immunoprecipitation of the N-terminal GW-repeat domain against AGO1–AGO4 in human cells","pmids":["19383768"],"confidence":"High","gaps":["Does not resolve the stoichiometry or relative affinity across the four AGO paralogs","Structural basis of GW-repeat recognition not determined"]},{"year":2009,"claim":"Defined the downstream effector activity by showing the C-terminal silencing domain is sufficient to repress a tethered mRNA without AGO, distinguishing recruitment from execution of silencing.","evidence":"Tethering assays with isolated C-terminal constructs plus protein-expression, mRNA-stability, and deadenylation readouts","pmids":["19383768"],"confidence":"High","gaps":["Identity of the deadenylase and decay factors recruited by the C-terminal domain not established in the corpus","Relative contribution of translational repression versus mRNA decay not quantified"]},{"year":2009,"claim":"Integrated the two domains into a recruitment-then-silencing model, establishing that N-terminal AGO binding and C-terminal silencing are separable and epistatically ordered.","evidence":"Domain-separation genetic dissection coupled to functional silencing assays","pmids":["19383768"],"confidence":"High","gaps":["In vivo physiological targets of TNRC6B-mediated silencing not identified","All three mechanistic findings derive from a single study"]},{"year":2024,"claim":"Addressed how a clinically observed synonymous variant could be pathogenic by showing it disrupts splicing rather than coding, expanding the interpretation of TNRC6B sequence variants.","evidence":"Minigene assay with Sanger sequencing confirming c.3141G>A-induced exon 7 skipping","pmids":["39115759"],"confidence":"Medium","gaps":["Single lab and single method","Effect of the truncated/altered transcript on protein function not assessed"]},{"year":2026,"claim":"Identified upstream regulation of TNRC6B itself, showing the silencing effector is a miRNA target, establishing a feedback layer on the pathway.","evidence":"Dual-luciferase reporter assay of miR-329-3p against the TNRC6B 3'UTR with RT-qPCR correlation","pmids":["41882181"],"confidence":"Low","gaps":["Single luciferase assay without orthogonal validation or mutagenesis of the seed site","No follow-up linking miR-329-3p regulation to TNRC6B protein function or downstream silencing"]},{"year":null,"claim":"The endogenous mRNA targets of TNRC6B and the identity of the decay/deadenylation factors it recruits in cells remain unresolved.","evidence":"","pmids":[],"confidence":"Low","gaps":["No transcriptome-wide target set characterized in the corpus","Downstream deadenylase/decay partners not identified","No structural model of the AGO–GW interface"]}],"mechanism_profile":{"molecular_activity":[{"term_id":"GO:0060090","term_label":"molecular adaptor activity","supporting_discovery_ids":[0,2]},{"term_id":"GO:0098772","term_label":"molecular function regulator activity","supporting_discovery_ids":[1,2]}],"localization":[],"pathway":[{"term_id":"R-HSA-8953854","term_label":"Metabolism of RNA","supporting_discovery_ids":[0,1,2]}],"complexes":[],"partners":["AGO1","AGO2","AGO3","AGO4"],"other_free_text":[]}},"prefetch_data":{"uniprot":{"accession":"Q9UPQ9","full_name":"Trinucleotide repeat-containing gene 6B protein","aliases":[],"length_aa":1833,"mass_kda":194.0,"function":"Plays a role in RNA-mediated gene silencing by both micro-RNAs (miRNAs) and short interfering RNAs (siRNAs) (PubMed:16289642, PubMed:19167051, PubMed:19304925, PubMed:32354837). Required for miRNA-dependent translational repression and siRNA-dependent endonucleolytic cleavage of complementary mRNAs by argonaute family proteins (PubMed:16289642, PubMed:19167051, PubMed:19304925, PubMed:32354837). As scaffolding protein associates with argonaute proteins bound to partially complementary mRNAs and simultaneously can recruit CCR4-NOT and PAN deadenylase complexes (PubMed:21981923)","subcellular_location":"Cytoplasm, P-body","url":"https://www.uniprot.org/uniprotkb/Q9UPQ9/entry"},"depmap":{"release":"DepMap","has_data":true,"is_common_essential":false,"resolved_as":"","url":"https://depmap.org/portal/gene/TNRC6B","classification":"Not Classified","n_dependent_lines":12,"n_total_lines":1208,"dependency_fraction":0.009933774834437087},"opencell":{"profiled":false,"resolved_as":"","ensg_id":"","cell_line_id":"","localizations":[],"interactors":[{"gene":"AGO1","stoichiometry":10.0},{"gene":"AGO2","stoichiometry":10.0},{"gene":"CAPZB","stoichiometry":0.2},{"gene":"DCP1B","stoichiometry":0.2},{"gene":"MIF","stoichiometry":0.2}],"url":"https://opencell.sf.czbiohub.org/search/TNRC6B","total_profiled":1310},"omim":[{"mim_id":"619408","title":"TRIPARTITE MOTIF-CONTAINING PROTEIN 65; TRIM65","url":"https://www.omim.org/entry/619408"},{"mim_id":"619243","title":"GLOBAL DEVELOPMENTAL DELAY WITH SPEECH AND BEHAVIORAL ABNORMALITIES; GDSBA","url":"https://www.omim.org/entry/619243"},{"mim_id":"610742","title":"MOV10 RISC COMPLEX RNA HELICASE; MOV10","url":"https://www.omim.org/entry/610742"},{"mim_id":"610740","title":"TRINUCLEOTIDE REPEAT-CONTAINING GENE 6B; TNRC6B","url":"https://www.omim.org/entry/610740"}],"hpa":{"profiled":true,"resolved_as":"","reliability":"","locations":[],"tissue_specificity":"Low tissue specificity","tissue_distribution":"Detected in all","driving_tissues":[],"url":"https://www.proteinatlas.org/search/TNRC6B"},"hgnc":{"alias_symbol":["KIAA1093"],"prev_symbol":[]},"alphafold":{"accession":"Q9UPQ9","domains":[{"cath_id":"-","chopping":"1654-1659_1674-1693_1702-1728","consensus_level":"medium","plddt":93.3955,"start":1654,"end":1728}],"viewer_url":"https://alphafold.ebi.ac.uk/entry/Q9UPQ9","model_url":"https://alphafold.ebi.ac.uk/files/AF-Q9UPQ9-F1-model_v6.cif","pae_url":"https://alphafold.ebi.ac.uk/files/AF-Q9UPQ9-F1-predicted_aligned_error_v6.png","plddt_mean":39.12},"mouse_models":{"mgi_url":"https://www.informatics.jax.org/marker/summary?nomen=TNRC6B","jax_strain_url":"https://www.jax.org/strain/search?query=TNRC6B"},"sequence":{"accession":"Q9UPQ9","fasta_url":"https://rest.uniprot.org/uniprotkb/Q9UPQ9.fasta","uniprot_url":"https://www.uniprot.org/uniprotkb/Q9UPQ9/entry","alphafold_viewer_url":"https://alphafold.ebi.ac.uk/entry/Q9UPQ9"}},"corpus_meta":[{"pmid":"19383768","id":"PMC_19383768","title":"The C-terminal domains of human TNRC6A, TNRC6B, and TNRC6C silence bound transcripts independently of Argonaute proteins.","date":"2009","source":"RNA (New York, N.Y.)","url":"https://pubmed.ncbi.nlm.nih.gov/19383768","citation_count":119,"is_preprint":false},{"pmid":"23604678","id":"PMC_23604678","title":"BET1L and TNRC6B associate with uterine fibroid risk among European Americans.","date":"2013","source":"Human genetics","url":"https://pubmed.ncbi.nlm.nih.gov/23604678","citation_count":32,"is_preprint":false},{"pmid":"32152250","id":"PMC_32152250","title":"Pathogenic variants in TNRC6B cause a genetic disorder characterised by developmental delay/intellectual disability and a spectrum of neurobehavioural phenotypes including autism and ADHD.","date":"2020","source":"Journal of medical genetics","url":"https://pubmed.ncbi.nlm.nih.gov/32152250","citation_count":25,"is_preprint":false},{"pmid":"23892540","id":"PMC_23892540","title":"Variants in BET1L and TNRC6B associate with increasing fibroid volume and fibroid type among European Americans.","date":"2013","source":"Human genetics","url":"https://pubmed.ncbi.nlm.nih.gov/23892540","citation_count":25,"is_preprint":false},{"pmid":"31960988","id":"PMC_31960988","title":"Circular RNA circABCC4 regulates lung adenocarcinoma progression via miR-3186-3p/TNRC6B axis.","date":"2020","source":"Journal of cellular biochemistry","url":"https://pubmed.ncbi.nlm.nih.gov/31960988","citation_count":19,"is_preprint":false},{"pmid":"37014625","id":"PMC_37014625","title":"Circular RNA circ-TNRC6B inhibits the proliferation and invasion of esophageal squamous cell carcinoma cells by regulating the miR-452-5p/DAG1 axis.","date":"2023","source":"Molecular oncology","url":"https://pubmed.ncbi.nlm.nih.gov/37014625","citation_count":18,"is_preprint":false},{"pmid":"32450521","id":"PMC_32450521","title":"FOXA1-induced LINC01207 facilitates head and neck squamous cell carcinoma via up-regulation of TNRC6B.","date":"2020","source":"Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie","url":"https://pubmed.ncbi.nlm.nih.gov/32450521","citation_count":16,"is_preprint":false},{"pmid":"38404251","id":"PMC_38404251","title":"Novel variants in TNRC6B cause global developmental delay with speech and behavioral abnormalities, short stature, low body weight, café-au-lait spots, and metabolic abnormality.","date":"2024","source":"Molecular genetics & genomic medicine","url":"https://pubmed.ncbi.nlm.nih.gov/38404251","citation_count":4,"is_preprint":false},{"pmid":"39115759","id":"PMC_39115759","title":"Identification of the synonymous variant c.3141G > A in TNRC6B gene that altered RNA splicing by minigene assay.","date":"2024","source":"Molecular biology reports","url":"https://pubmed.ncbi.nlm.nih.gov/39115759","citation_count":3,"is_preprint":false},{"pmid":"41147347","id":"PMC_41147347","title":"A Case Report: Co-Occurrence of TNRC6B Gene Variant and Xq28 Microdeletion Syndrome With Comprehensive Literature Review.","date":"2025","source":"Birth defects research","url":"https://pubmed.ncbi.nlm.nih.gov/41147347","citation_count":1,"is_preprint":false},{"pmid":"41882181","id":"PMC_41882181","title":"Clinical value of miR-329-3p in thalassemia and its regulation of TNRC6B expression.","date":"2026","source":"Annals of hematology","url":"https://pubmed.ncbi.nlm.nih.gov/41882181","citation_count":0,"is_preprint":false},{"pmid":"42074582","id":"PMC_42074582","title":"Expansion of the Phenotypic Spectrum of TNRC6B-Related Neurodevelopmental Disorder in a Three-Generation Family with 22q13.1 Deletion.","date":"2026","source":"Genes","url":"https://pubmed.ncbi.nlm.nih.gov/42074582","citation_count":0,"is_preprint":false},{"pmid":null,"id":"bio_10.1101_2025.05.15.25327674","title":"Genome-wide association studies of social participation and occupational engagement in the UK Biobank","date":"2025-05-15","source":"bioRxiv","url":"https://doi.org/10.1101/2025.05.15.25327674","citation_count":0,"is_preprint":true}],"cost":{"stage1":{"model":"claude-sonnet-4-6","input_tokens":9100,"output_tokens":1130,"usd":0.022125,"stage1_stop_reason":"end_turn"},"stage2":{"model":"claude-opus-4-8","input_tokens":7680,"output_tokens":1879,"usd":0.042688,"stage2_stop_reason":"end_turn"},"total_usd":0.064813,"stage1_batch_id":"msgbatch_017qqVz33Ga63SCDwzb35XPb","stage2_batch_id":"msgbatch_01Scr2Ei9x4HJMiRGxwrmvLK","note":"batch pricing = 50% of standard"},"stage1_raw":"```json\n{\n  \"discoveries\": [\n    {\n      \"year\": 2009,\n      \"finding\": \"The N-terminal GW-repeat-containing region of TNRC6B interacts with all four human Argonaute proteins (AGO1-AGO4), as demonstrated by interaction assays.\",\n      \"method\": \"Protein interaction assays (pulldown/co-immunoprecipitation of N-terminal GW-repeat domain with AGO1-AGO4)\",\n      \"journal\": \"RNA (New York, N.Y.)\",\n      \"confidence\": \"High\",\n      \"confidence_rationale\": \"Tier 2 / Strong — reciprocal interaction mapping across all four AGO paralogs, replicated across three TNRC6 family members in the same study with domain-level resolution\",\n      \"pmids\": [\"19383768\"],\n      \"is_preprint\": false\n    },\n    {\n      \"year\": 2009,\n      \"finding\": \"The C-terminal silencing domain of TNRC6B is sufficient to silence bound mRNAs independently of its interaction with Argonaute proteins, acting through translational repression and/or mRNA destabilization including deadenylation.\",\n      \"method\": \"Tethering assays with isolated C-terminal domain constructs; mRNA stability and protein expression measurements; deadenylation assays\",\n      \"journal\": \"RNA (New York, N.Y.)\",\n      \"confidence\": \"High\",\n      \"confidence_rationale\": \"Tier 1-2 / Strong — domain dissection with functional tethering assays, multiple orthogonal readouts (protein expression, mRNA stability, deadenylation) in a single rigorous study\",\n      \"pmids\": [\"19383768\"],\n      \"is_preprint\": false\n    },\n    {\n      \"year\": 2009,\n      \"finding\": \"TNRC6B is recruited to miRNA targets via interaction between its N-terminal domain and an Argonaute protein, after which its C-terminal silencing domain promotes translational repression and/or degradation of miRNA targets.\",\n      \"method\": \"Domain mapping experiments combined with functional silencing assays; genetic dissection of N-terminal vs C-terminal domain activities\",\n      \"journal\": \"RNA (New York, N.Y.)\",\n      \"confidence\": \"High\",\n      \"confidence_rationale\": \"Tier 2 / Strong — epistasis between N-terminal AGO-binding and C-terminal silencing established by domain separation experiments with functional readouts, multiple orthogonal methods in one study\",\n      \"pmids\": [\"19383768\"],\n      \"is_preprint\": false\n    },\n    {\n      \"year\": 2024,\n      \"finding\": \"A synonymous variant c.3141G>A in TNRC6B causes exon 7 skipping, demonstrating that this variant disrupts normal RNA splicing of the TNRC6B transcript.\",\n      \"method\": \"Minigene assay and Sanger sequencing to verify aberrant splicing\",\n      \"journal\": \"Molecular biology reports\",\n      \"confidence\": \"Medium\",\n      \"confidence_rationale\": \"Tier 2 / Weak — functional minigene splicing assay with Sanger sequencing validation, but single lab and single method\",\n      \"pmids\": [\"39115759\"],\n      \"is_preprint\": false\n    },\n    {\n      \"year\": 2026,\n      \"finding\": \"miR-329-3p directly interacts with TNRC6B 3'UTR and negatively regulates TNRC6B expression, as confirmed by dual-luciferase reporter assay.\",\n      \"method\": \"Dual-luciferase reporter assay; RT-qPCR for expression correlation\",\n      \"journal\": \"Annals of hematology\",\n      \"confidence\": \"Low\",\n      \"confidence_rationale\": \"Tier 3 / Weak — single luciferase assay establishing miR-329-3p binding to TNRC6B, single lab, no further mechanistic follow-up on TNRC6B protein function\",\n      \"pmids\": [\"41882181\"],\n      \"is_preprint\": false\n    }\n  ],\n  \"current_model\": \"TNRC6B (a vertebrate GW182-family protein) is recruited to miRNA targets via its N-terminal GW-repeat domain binding to Argonaute proteins (AGO1–AGO4), after which its C-terminal silencing domain independently promotes translational repression and mRNA destabilization (including deadenylation) of bound transcripts; haploinsufficiency of TNRC6B causes a neurodevelopmental disorder featuring developmental delay, intellectual disability, autism, and ADHD.\"\n}\n```","stage2_raw":"{\n  \"mechanistic_narrative\": \"TNRC6B is a GW-repeat-containing effector of the miRNA silencing pathway that bridges Argonaute-loaded miRNA complexes to the machinery that represses bound transcripts [#0, #2]. Its N-terminal GW-repeat region binds all four human Argonaute proteins (AGO1–AGO4), recruiting TNRC6B to miRNA targets [#0]. Once recruited, its C-terminal silencing domain acts autonomously — independently of the AGO interaction — to silence the bound mRNA through translational repression and mRNA destabilization, including deadenylation [#1, #2]. TNRC6B expression is itself subject to miRNA control, with miR-329-3p binding the TNRC6B 3'UTR to downregulate it [#4]. A synonymous variant (c.3141G>A) disrupts normal splicing by causing exon 7 skipping, linking TNRC6B sequence integrity to transcript processing [#3]. Beyond the AGO-binding and silencing-domain architecture established in [#0, #1, #2], no further mechanistic detail of substrate selection or recruitment of downstream deadenylation factors has been characterized in the available corpus.\",\n  \"teleology\": [\n    {\n      \"year\": 2009,\n      \"claim\": \"Established how TNRC6B is recruited to miRNA targets by mapping the physical interface to Argonaute proteins, answering whether this GW182-family protein couples to the core silencing effectors.\",\n      \"evidence\": \"Pulldown/co-immunoprecipitation of the N-terminal GW-repeat domain against AGO1–AGO4 in human cells\",\n      \"pmids\": [\"19383768\"],\n      \"confidence\": \"High\",\n      \"gaps\": [\"Does not resolve the stoichiometry or relative affinity across the four AGO paralogs\", \"Structural basis of GW-repeat recognition not determined\"]\n    },\n    {\n      \"year\": 2009,\n      \"claim\": \"Defined the downstream effector activity by showing the C-terminal silencing domain is sufficient to repress a tethered mRNA without AGO, distinguishing recruitment from execution of silencing.\",\n      \"evidence\": \"Tethering assays with isolated C-terminal constructs plus protein-expression, mRNA-stability, and deadenylation readouts\",\n      \"pmids\": [\"19383768\"],\n      \"confidence\": \"High\",\n      \"gaps\": [\"Identity of the deadenylase and decay factors recruited by the C-terminal domain not established in the corpus\", \"Relative contribution of translational repression versus mRNA decay not quantified\"]\n    },\n    {\n      \"year\": 2009,\n      \"claim\": \"Integrated the two domains into a recruitment-then-silencing model, establishing that N-terminal AGO binding and C-terminal silencing are separable and epistatically ordered.\",\n      \"evidence\": \"Domain-separation genetic dissection coupled to functional silencing assays\",\n      \"pmids\": [\"19383768\"],\n      \"confidence\": \"High\",\n      \"gaps\": [\"In vivo physiological targets of TNRC6B-mediated silencing not identified\", \"All three mechanistic findings derive from a single study\"]\n    },\n    {\n      \"year\": 2024,\n      \"claim\": \"Addressed how a clinically observed synonymous variant could be pathogenic by showing it disrupts splicing rather than coding, expanding the interpretation of TNRC6B sequence variants.\",\n      \"evidence\": \"Minigene assay with Sanger sequencing confirming c.3141G>A-induced exon 7 skipping\",\n      \"pmids\": [\"39115759\"],\n      \"confidence\": \"Medium\",\n      \"gaps\": [\"Single lab and single method\", \"Effect of the truncated/altered transcript on protein function not assessed\"]\n    },\n    {\n      \"year\": 2026,\n      \"claim\": \"Identified upstream regulation of TNRC6B itself, showing the silencing effector is a miRNA target, establishing a feedback layer on the pathway.\",\n      \"evidence\": \"Dual-luciferase reporter assay of miR-329-3p against the TNRC6B 3'UTR with RT-qPCR correlation\",\n      \"pmids\": [\"41882181\"],\n      \"confidence\": \"Low\",\n      \"gaps\": [\"Single luciferase assay without orthogonal validation or mutagenesis of the seed site\", \"No follow-up linking miR-329-3p regulation to TNRC6B protein function or downstream silencing\"]\n    },\n    {\n      \"year\": null,\n      \"claim\": \"The endogenous mRNA targets of TNRC6B and the identity of the decay/deadenylation factors it recruits in cells remain unresolved.\",\n      \"evidence\": \"\",\n      \"pmids\": [],\n      \"confidence\": \"Low\",\n      \"gaps\": [\"No transcriptome-wide target set characterized in the corpus\", \"Downstream deadenylase/decay partners not identified\", \"No structural model of the AGO–GW interface\"]\n    }\n  ],\n  \"mechanism_profile\": {\n    \"molecular_activity\": [\n      {\"term_id\": \"GO:0060090\", \"supporting_discovery_ids\": [0, 2]},\n      {\"term_id\": \"GO:0098772\", \"supporting_discovery_ids\": [1, 2]}\n    ],\n    \"localization\": [],\n    \"pathway\": [\n      {\"term_id\": \"R-HSA-8953854\", \"supporting_discovery_ids\": [0, 1, 2]}\n    ],\n    \"complexes\": [],\n    \"partners\": [\"AGO1\", \"AGO2\", \"AGO3\", \"AGO4\"],\n    \"other_free_text\": []\n  }\n}","audit_flag":null,"evaluation":{"pairwise":"win","faith_supported":6,"faith_total":6,"faith_pct":100.0}}