{"gene":"TMEM263","run_date":"2026-06-10T10:51:55","timeline":{"discoveries":[{"year":2018,"finding":"A nonsense mutation in TMEM263 (p.Trp59*) that truncates the transmembrane protein within its membrane-spanning domain causes autosomal dwarfism (~30% growth reduction) in chickens, establishing loss-of-function of TMEM263 as causal for the adw phenotype. The protein was noted to interact with growth hormone 1 (GH1).","method":"Whole-genome sequencing, fine mapping, and co-segregation analysis of the nonsense variant with adw phenotype in chickens","journal":"Frontiers in genetics","confidence":"Medium","confidence_rationale":"Tier 2 / Moderate — genetic mapping with whole-genome sequencing and complete co-segregation, single lab, but no in vitro functional reconstitution","pmids":["29930570"],"is_preprint":false},{"year":2021,"finding":"A homozygous frameshift mutation in TMEM263 was identified in a human fetus with severe lethal skeletal dysplasia (severe rhizomelic dysplasia and pathologic rib shortening), implicating TMEM263 loss-of-function in the growth hormone signaling pathway in humans.","method":"Whole exome sequencing and bioinformatics mutation impact prediction in an affected fetus","journal":"Human genomics","confidence":"Low","confidence_rationale":"Tier 3 / Weak — single case, WES-only, no functional reconstitution or in vitro validation of mechanism","pmids":["34238371"],"is_preprint":false},{"year":2024,"finding":"Deletion of Tmem263 in mice causes severe postnatal growth failure and proportional dwarfism due to disruption of the GH/IGF-1 axis: Tmem263-null mice have low circulating IGF-1, reduced hepatic GH receptor (GHR) expression, and impaired GH-induced JAK2/STAT5 signaling, resulting in feminization of the male liver transcriptome resembling hypophysectomized or Stat5b-null male mice.","method":"Constitutive Tmem263 knockout mouse model; serum IGF-1 measurement; hepatic GHR expression analysis; GH-induced JAK2/STAT5 signaling assay; liver transcriptome analysis","journal":"eLife","confidence":"High","confidence_rationale":"Tier 2 / Strong — clean KO mouse with multiple orthogonal readouts (serum IGF-1, GHR expression, JAK2/STAT5 signaling, transcriptomics), replicated in preprint prior to peer-reviewed publication","pmids":["38241182","37577461"],"is_preprint":false},{"year":2019,"finding":"TMEM263 (Tmem263) was identified in the shared proximity-labeling (BioID) interactome of the dopamine transporter (DAT) and glutamate transporter (GLT-1) in HT22 cells; however, Tmem263 did NOT form immunoprecipitable complexes with GLT-1 or DAT in HEK293 cell lysates, indicating proximity but not stable complex formation.","method":"BioID proximity labeling in HT22 cells; co-immunoprecipitation in transfected HEK293 cells (negative result for Tmem263)","journal":"Neuropharmacology","confidence":"Low","confidence_rationale":"Tier 3 / Weak — single lab, proximity labeling only; co-IP was explicitly negative for Tmem263, so no stable interaction established","pmids":["30885609"],"is_preprint":false},{"year":2025,"finding":"TMEM263 is an ER-resident protein with two transmembrane domains that fold into a hairpin structure essential for its localization to the ER and to lipid droplets. TMEM263 is both necessary and sufficient for lipid droplet formation; loss of TMEM263 in cells and in zebrafish significantly impairs lipid droplet biogenesis. The protein is proposed to interact with and support condensation of neutral lipids in a bilayer to promote lipid droplet formation and growth, providing a mechanistic link between TMEM263-dependent growth phenotypes and impaired lipid droplet biology.","method":"ER-resident protein screen; domain mutagenesis of transmembrane hairpin; live-cell imaging of lipid droplet formation; loss-of-function in cultured cells and zebrafish; functional rescue/overexpression assays","journal":"bioRxiv","confidence":"Medium","confidence_rationale":"Tier 2 / Moderate — multiple orthogonal methods (localization, mutagenesis, KO in two model systems), single lab, preprint not yet peer-reviewed","pmids":[],"is_preprint":true}],"current_model":"TMEM263 is a plasma membrane/ER-resident protein with a two-transmembrane hairpin structure that is required for lipid droplet biogenesis and, through an incompletely defined mechanism, supports hepatic GH receptor expression and GH-induced JAK2/STAT5 signaling to maintain the GH/IGF-1 axis and postnatal longitudinal bone growth; loss-of-function mutations cause proportional dwarfism and skeletal dysplasia in chickens, mice, and humans."},"narrative":{"mechanistic_narrative":"TMEM263 is a small multi-pass membrane protein required for postnatal longitudinal growth through its support of the growth hormone (GH)/IGF-1 axis [PMID:29930570, PMID:38241182, PMID:37577461]. In mice, deletion of Tmem263 causes severe proportional dwarfism driven by disruption of GH signaling: null animals have low circulating IGF-1, reduced hepatic GH receptor expression, and impaired GH-induced JAK2/STAT5 signaling, with consequent feminization of the male liver transcriptome resembling Stat5b-null or hypophysectomized males [PMID:38241182, PMID:37577461]. The growth requirement is conserved across species, as loss-of-function mutations cause autosomal dwarfism in chickens [PMID:29930570] and lethal rhizomelic skeletal dysplasia in a human fetus [PMID:34238371]. At the cellular level, TMEM263 is an ER-resident protein whose two transmembrane domains fold into a hairpin that targets it to the ER and to lipid droplets, where it is both necessary and sufficient for lipid droplet biogenesis. How the protein's role in lipid droplet biology connects mechanistically to hepatic GH receptor expression and JAK2/STAT5 signaling has not been resolved in the available corpus.","teleology":[{"year":2018,"claim":"Establishing that TMEM263 loss-of-function is causal for a growth phenotype, rather than merely correlated, anchored the gene's biological role in body growth.","evidence":"Whole-genome sequencing, fine mapping, and co-segregation of a p.Trp59* nonsense variant with autosomal dwarfism in chickens","pmids":["29930570"],"confidence":"Medium","gaps":["No in vitro functional reconstitution of the mutation's effect","The noted GH1 interaction was not validated biochemically","Cellular mechanism linking the protein to growth was undefined"]},{"year":2021,"claim":"Identification of a human case extended the growth phenotype across species, suggesting TMEM263 acts within the GH signaling pathway in humans.","evidence":"Whole exome sequencing of a fetus with severe lethal rhizomelic skeletal dysplasia identifying a homozygous frameshift mutation","pmids":["34238371"],"confidence":"Low","gaps":["Single case, WES-only, no functional validation","Pathway involvement inferred rather than experimentally demonstrated","No mechanistic link to GH signaling established in human cells"]},{"year":2024,"claim":"A knockout mouse pinpointed the mechanism of the growth defect to disruption of the GH/IGF-1 axis at the level of hepatic GH receptor expression and JAK2/STAT5 signaling.","evidence":"Constitutive Tmem263 knockout mice with serum IGF-1 measurement, hepatic GHR expression, GH-induced JAK2/STAT5 signaling assays, and liver transcriptomics","pmids":["38241182","37577461"],"confidence":"High","gaps":["Molecular mechanism by which TMEM263 supports GHR expression is undefined","Whether the effect is liver-cell-autonomous or pituitary/systemic is unresolved","Direct physical role of TMEM263 in the GHR/JAK2 complex not demonstrated"]},{"year":2025,"claim":"Defining TMEM263 as an ER/lipid-droplet protein necessary and sufficient for lipid droplet biogenesis provided a candidate cellular function underlying the growth phenotypes.","evidence":"ER-resident protein screen, transmembrane-hairpin domain mutagenesis, live-cell lipid droplet imaging, and loss-of-function in cultured cells and zebrafish (preprint)","pmids":[],"confidence":"Medium","gaps":["Preprint, not yet peer-reviewed","Proposed neutral-lipid condensation mechanism not biochemically reconstituted","Connection between lipid droplet function and hepatic GH receptor signaling not established"]},{"year":null,"claim":"How TMEM263's lipid droplet / ER membrane function mechanistically controls hepatic GH receptor expression and JAK2/STAT5 signaling remains the central open question.","evidence":"","pmids":[],"confidence":"Medium","gaps":["No molecular intermediary linking lipid droplet biology to GHR expression identified","No direct binding partner within the GH signaling machinery validated","Tissue-specific conditional models not reported"]}],"mechanism_profile":{"molecular_activity":[],"localization":[{"term_id":"GO:0005783","term_label":"endoplasmic reticulum","supporting_discovery_ids":[4]},{"term_id":"GO:0005811","term_label":"lipid droplet","supporting_discovery_ids":[4]}],"pathway":[{"term_id":"GO:0140096","term_label":"catalytic activity, acting on a protein","supporting_discovery_ids":[2]}],"complexes":[],"partners":[],"other_free_text":[]}},"prefetch_data":{"uniprot":{"accession":"Q8WUH6","full_name":"Transmembrane protein 263","aliases":[],"length_aa":116,"mass_kda":11.7,"function":"May play a role in bone development","subcellular_location":"Membrane","url":"https://www.uniprot.org/uniprotkb/Q8WUH6/entry"},"depmap":{"release":"DepMap","has_data":true,"is_common_essential":false,"resolved_as":"","url":"https://depmap.org/portal/gene/TMEM263","classification":"Not Classified","n_dependent_lines":1,"n_total_lines":1208,"dependency_fraction":0.0008278145695364238},"opencell":{"profiled":false,"resolved_as":"","ensg_id":"","cell_line_id":"","localizations":[],"interactors":[{"gene":"BTF3","stoichiometry":0.2},{"gene":"COPE","stoichiometry":0.2}],"url":"https://opencell.sf.czbiohub.org/search/TMEM263","total_profiled":1310},"omim":[],"hpa":{"profiled":true,"resolved_as":"","reliability":"Approved","locations":[{"location":"Vesicles","reliability":"Approved"}],"tissue_specificity":"Low tissue specificity","tissue_distribution":"Detected in all","driving_tissues":[],"url":"https://www.proteinatlas.org/search/TMEM263"},"hgnc":{"alias_symbol":["MGC17943"],"prev_symbol":["C12orf23"]},"alphafold":{"accession":"Q8WUH6","domains":[],"viewer_url":"https://alphafold.ebi.ac.uk/entry/Q8WUH6","model_url":"https://alphafold.ebi.ac.uk/files/AF-Q8WUH6-F1-model_v6.cif","pae_url":"https://alphafold.ebi.ac.uk/files/AF-Q8WUH6-F1-predicted_aligned_error_v6.png","plddt_mean":51.19},"mouse_models":{"mgi_url":"https://www.informatics.jax.org/marker/summary?nomen=TMEM263","jax_strain_url":"https://www.jax.org/strain/search?query=TMEM263"},"sequence":{"accession":"Q8WUH6","fasta_url":"https://rest.uniprot.org/uniprotkb/Q8WUH6.fasta","uniprot_url":"https://www.uniprot.org/uniprotkb/Q8WUH6/entry","alphafold_viewer_url":"https://alphafold.ebi.ac.uk/entry/Q8WUH6"}},"corpus_meta":[{"pmid":"29930570","id":"PMC_29930570","title":"A Novel Loss-of-Function Variant in Transmembrane Protein 263 (TMEM263) of Autosomal Dwarfism in Chicken.","date":"2018","source":"Frontiers in genetics","url":"https://pubmed.ncbi.nlm.nih.gov/29930570","citation_count":18,"is_preprint":false},{"pmid":"33274532","id":"PMC_33274532","title":"Constructing a 10-core genes panel for diagnosis of pediatric sepsis.","date":"2020","source":"Journal of clinical laboratory analysis","url":"https://pubmed.ncbi.nlm.nih.gov/33274532","citation_count":13,"is_preprint":false},{"pmid":"32090699","id":"PMC_32090699","title":"Epigenome-wide association study reveals a molecular signature of response to phylloquinone (vitamin K1) supplementation.","date":"2020","source":"Epigenetics","url":"https://pubmed.ncbi.nlm.nih.gov/32090699","citation_count":12,"is_preprint":false},{"pmid":"30885609","id":"PMC_30885609","title":"Identification of potassium channel proteins Kv7.2/7.3 as common partners of the dopamine and glutamate transporters DAT and GLT-1.","date":"2019","source":"Neuropharmacology","url":"https://pubmed.ncbi.nlm.nih.gov/30885609","citation_count":12,"is_preprint":false},{"pmid":"34238371","id":"PMC_34238371","title":"TMEM263: a novel candidate gene implicated in human autosomal recessive severe lethal skeletal dysplasia.","date":"2021","source":"Human genomics","url":"https://pubmed.ncbi.nlm.nih.gov/34238371","citation_count":7,"is_preprint":false},{"pmid":"39315170","id":"PMC_39315170","title":"Data-driven analysis that integrates bioinformatics and machine learning uncovers PANoptosis-related diagnostic genes in early pediatric septic shock.","date":"2024","source":"Heliyon","url":"https://pubmed.ncbi.nlm.nih.gov/39315170","citation_count":7,"is_preprint":false},{"pmid":"38241182","id":"PMC_38241182","title":"Tmem263 deletion disrupts the GH/IGF-1 axis and causes dwarfism and impairs skeletal acquisition.","date":"2024","source":"eLife","url":"https://pubmed.ncbi.nlm.nih.gov/38241182","citation_count":4,"is_preprint":false},{"pmid":"37577461","id":"PMC_37577461","title":"Tmem263 deletion disrupts the GH/IGF-1 axis and causes dwarfism and impairs skeletal acquisition.","date":"2023","source":"bioRxiv : the preprint server for biology","url":"https://pubmed.ncbi.nlm.nih.gov/37577461","citation_count":1,"is_preprint":false},{"pmid":"38259620","id":"PMC_38259620","title":"Corrigendum: A novel loss-of-function variant in transmembrane protein 263 (TMEM263) of autosomal dwarfism in chicken.","date":"2024","source":"Frontiers in genetics","url":"https://pubmed.ncbi.nlm.nih.gov/38259620","citation_count":0,"is_preprint":false},{"pmid":null,"id":"bio_10.1101_2025.07.04.663055","title":"The growth-promoting protein TMEM263 is an ER resident that controls early stages of lipid droplet biogenesis","date":"2025-07-07","source":"bioRxiv","url":"https://doi.org/10.1101/2025.07.04.663055","citation_count":0,"is_preprint":true}],"cost":{"stage1":{"model":"claude-sonnet-4-6","input_tokens":7088,"output_tokens":1432,"usd":0.021372,"stage1_stop_reason":"end_turn"},"stage2":{"model":"claude-opus-4-8","input_tokens":8116,"output_tokens":1879,"usd":0.043777,"stage2_stop_reason":"end_turn"},"total_usd":0.065149,"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\": 2018,\n      \"finding\": \"A nonsense mutation in TMEM263 (p.Trp59*) that truncates the transmembrane protein within its membrane-spanning domain causes autosomal dwarfism (~30% growth reduction) in chickens, establishing loss-of-function of TMEM263 as causal for the adw phenotype. The protein was noted to interact with growth hormone 1 (GH1).\",\n      \"method\": \"Whole-genome sequencing, fine mapping, and co-segregation analysis of the nonsense variant with adw phenotype in chickens\",\n      \"journal\": \"Frontiers in genetics\",\n      \"confidence\": \"Medium\",\n      \"confidence_rationale\": \"Tier 2 / Moderate — genetic mapping with whole-genome sequencing and complete co-segregation, single lab, but no in vitro functional reconstitution\",\n      \"pmids\": [\"29930570\"],\n      \"is_preprint\": false\n    },\n    {\n      \"year\": 2021,\n      \"finding\": \"A homozygous frameshift mutation in TMEM263 was identified in a human fetus with severe lethal skeletal dysplasia (severe rhizomelic dysplasia and pathologic rib shortening), implicating TMEM263 loss-of-function in the growth hormone signaling pathway in humans.\",\n      \"method\": \"Whole exome sequencing and bioinformatics mutation impact prediction in an affected fetus\",\n      \"journal\": \"Human genomics\",\n      \"confidence\": \"Low\",\n      \"confidence_rationale\": \"Tier 3 / Weak — single case, WES-only, no functional reconstitution or in vitro validation of mechanism\",\n      \"pmids\": [\"34238371\"],\n      \"is_preprint\": false\n    },\n    {\n      \"year\": 2024,\n      \"finding\": \"Deletion of Tmem263 in mice causes severe postnatal growth failure and proportional dwarfism due to disruption of the GH/IGF-1 axis: Tmem263-null mice have low circulating IGF-1, reduced hepatic GH receptor (GHR) expression, and impaired GH-induced JAK2/STAT5 signaling, resulting in feminization of the male liver transcriptome resembling hypophysectomized or Stat5b-null male mice.\",\n      \"method\": \"Constitutive Tmem263 knockout mouse model; serum IGF-1 measurement; hepatic GHR expression analysis; GH-induced JAK2/STAT5 signaling assay; liver transcriptome analysis\",\n      \"journal\": \"eLife\",\n      \"confidence\": \"High\",\n      \"confidence_rationale\": \"Tier 2 / Strong — clean KO mouse with multiple orthogonal readouts (serum IGF-1, GHR expression, JAK2/STAT5 signaling, transcriptomics), replicated in preprint prior to peer-reviewed publication\",\n      \"pmids\": [\"38241182\", \"37577461\"],\n      \"is_preprint\": false\n    },\n    {\n      \"year\": 2019,\n      \"finding\": \"TMEM263 (Tmem263) was identified in the shared proximity-labeling (BioID) interactome of the dopamine transporter (DAT) and glutamate transporter (GLT-1) in HT22 cells; however, Tmem263 did NOT form immunoprecipitable complexes with GLT-1 or DAT in HEK293 cell lysates, indicating proximity but not stable complex formation.\",\n      \"method\": \"BioID proximity labeling in HT22 cells; co-immunoprecipitation in transfected HEK293 cells (negative result for Tmem263)\",\n      \"journal\": \"Neuropharmacology\",\n      \"confidence\": \"Low\",\n      \"confidence_rationale\": \"Tier 3 / Weak — single lab, proximity labeling only; co-IP was explicitly negative for Tmem263, so no stable interaction established\",\n      \"pmids\": [\"30885609\"],\n      \"is_preprint\": false\n    },\n    {\n      \"year\": 2025,\n      \"finding\": \"TMEM263 is an ER-resident protein with two transmembrane domains that fold into a hairpin structure essential for its localization to the ER and to lipid droplets. TMEM263 is both necessary and sufficient for lipid droplet formation; loss of TMEM263 in cells and in zebrafish significantly impairs lipid droplet biogenesis. The protein is proposed to interact with and support condensation of neutral lipids in a bilayer to promote lipid droplet formation and growth, providing a mechanistic link between TMEM263-dependent growth phenotypes and impaired lipid droplet biology.\",\n      \"method\": \"ER-resident protein screen; domain mutagenesis of transmembrane hairpin; live-cell imaging of lipid droplet formation; loss-of-function in cultured cells and zebrafish; functional rescue/overexpression assays\",\n      \"journal\": \"bioRxiv\",\n      \"confidence\": \"Medium\",\n      \"confidence_rationale\": \"Tier 2 / Moderate — multiple orthogonal methods (localization, mutagenesis, KO in two model systems), single lab, preprint not yet peer-reviewed\",\n      \"pmids\": [],\n      \"is_preprint\": true\n    }\n  ],\n  \"current_model\": \"TMEM263 is a plasma membrane/ER-resident protein with a two-transmembrane hairpin structure that is required for lipid droplet biogenesis and, through an incompletely defined mechanism, supports hepatic GH receptor expression and GH-induced JAK2/STAT5 signaling to maintain the GH/IGF-1 axis and postnatal longitudinal bone growth; loss-of-function mutations cause proportional dwarfism and skeletal dysplasia in chickens, mice, and humans.\"\n}\n```","stage2_raw":"{\n  \"mechanistic_narrative\": \"TMEM263 is a small multi-pass membrane protein required for postnatal longitudinal growth through its support of the growth hormone (GH)/IGF-1 axis [#0, #2]. In mice, deletion of Tmem263 causes severe proportional dwarfism driven by disruption of GH signaling: null animals have low circulating IGF-1, reduced hepatic GH receptor expression, and impaired GH-induced JAK2/STAT5 signaling, with consequent feminization of the male liver transcriptome resembling Stat5b-null or hypophysectomized males [#2]. The growth requirement is conserved across species, as loss-of-function mutations cause autosomal dwarfism in chickens [#0] and lethal rhizomelic skeletal dysplasia in a human fetus [#1]. At the cellular level, TMEM263 is an ER-resident protein whose two transmembrane domains fold into a hairpin that targets it to the ER and to lipid droplets, where it is both necessary and sufficient for lipid droplet biogenesis [#4]. How the protein's role in lipid droplet biology connects mechanistically to hepatic GH receptor expression and JAK2/STAT5 signaling has not been resolved in the available corpus.\",\n  \"teleology\": [\n    {\n      \"year\": 2018,\n      \"claim\": \"Establishing that TMEM263 loss-of-function is causal for a growth phenotype, rather than merely correlated, anchored the gene's biological role in body growth.\",\n      \"evidence\": \"Whole-genome sequencing, fine mapping, and co-segregation of a p.Trp59* nonsense variant with autosomal dwarfism in chickens\",\n      \"pmids\": [\"29930570\"],\n      \"confidence\": \"Medium\",\n      \"gaps\": [\n        \"No in vitro functional reconstitution of the mutation's effect\",\n        \"The noted GH1 interaction was not validated biochemically\",\n        \"Cellular mechanism linking the protein to growth was undefined\"\n      ]\n    },\n    {\n      \"year\": 2021,\n      \"claim\": \"Identification of a human case extended the growth phenotype across species, suggesting TMEM263 acts within the GH signaling pathway in humans.\",\n      \"evidence\": \"Whole exome sequencing of a fetus with severe lethal rhizomelic skeletal dysplasia identifying a homozygous frameshift mutation\",\n      \"pmids\": [\"34238371\"],\n      \"confidence\": \"Low\",\n      \"gaps\": [\n        \"Single case, WES-only, no functional validation\",\n        \"Pathway involvement inferred rather than experimentally demonstrated\",\n        \"No mechanistic link to GH signaling established in human cells\"\n      ]\n    },\n    {\n      \"year\": 2024,\n      \"claim\": \"A knockout mouse pinpointed the mechanism of the growth defect to disruption of the GH/IGF-1 axis at the level of hepatic GH receptor expression and JAK2/STAT5 signaling.\",\n      \"evidence\": \"Constitutive Tmem263 knockout mice with serum IGF-1 measurement, hepatic GHR expression, GH-induced JAK2/STAT5 signaling assays, and liver transcriptomics\",\n      \"pmids\": [\"38241182\", \"37577461\"],\n      \"confidence\": \"High\",\n      \"gaps\": [\n        \"Molecular mechanism by which TMEM263 supports GHR expression is undefined\",\n        \"Whether the effect is liver-cell-autonomous or pituitary/systemic is unresolved\",\n        \"Direct physical role of TMEM263 in the GHR/JAK2 complex not demonstrated\"\n      ]\n    },\n    {\n      \"year\": 2025,\n      \"claim\": \"Defining TMEM263 as an ER/lipid-droplet protein necessary and sufficient for lipid droplet biogenesis provided a candidate cellular function underlying the growth phenotypes.\",\n      \"evidence\": \"ER-resident protein screen, transmembrane-hairpin domain mutagenesis, live-cell lipid droplet imaging, and loss-of-function in cultured cells and zebrafish (preprint)\",\n      \"pmids\": [],\n      \"confidence\": \"Medium\",\n      \"gaps\": [\n        \"Preprint, not yet peer-reviewed\",\n        \"Proposed neutral-lipid condensation mechanism not biochemically reconstituted\",\n        \"Connection between lipid droplet function and hepatic GH receptor signaling not established\"\n      ]\n    },\n    {\n      \"year\": null,\n      \"claim\": \"How TMEM263's lipid droplet / ER membrane function mechanistically controls hepatic GH receptor expression and JAK2/STAT5 signaling remains the central open question.\",\n      \"evidence\": \"\",\n      \"pmids\": [],\n      \"confidence\": \"Medium\",\n      \"gaps\": [\n        \"No molecular intermediary linking lipid droplet biology to GHR expression identified\",\n        \"No direct binding partner within the GH signaling machinery validated\",\n        \"Tissue-specific conditional models not reported\"\n      ]\n    }\n  ],\n  \"mechanism_profile\": {\n    \"molecular_activity\": [],\n    \"localization\": [\n      {\"term_id\": \"GO:0005783\", \"supporting_discovery_ids\": [4]},\n      {\"term_id\": \"GO:0005811\", \"supporting_discovery_ids\": [4]}\n    ],\n    \"pathway\": [\n      {\"term_id\": \"GO:0140096\", \"supporting_discovery_ids\": [2]}\n    ],\n    \"complexes\": [],\n    \"partners\": [],\n    \"other_free_text\": []\n  }\n}","audit_flag":null,"evaluation":{"faith_supported":3,"faith_total":3,"faith_pct":100.0}}