{"gene":"NOG","run_date":"2026-06-10T05:19:52","timeline":{"discoveries":[{"year":2001,"finding":"Disease-causing NOG missense mutations (one SYNS1 and two SYM1) impair noggin function by reducing or abolishing secretion of functional noggin dimers in COS-7 cells. The SYNS1 mutation abolished dimer secretion; SYM1 mutations reduced it. Coexpression with wild-type noggin did not impair wild-type secretion, indicating these are hypomorphic alleles. Notably, the SYNS1 mutant could still form dimers in Xenopus oocytes, revealing species-specific differences in processing mutant noggin.","method":"Transient transfection of COS-7 cells and Xenopus oocyte expression with wild-type and mutant NOG constructs; assessment of secretion and dimer formation","journal":"Proceedings of the National Academy of Sciences of the United States of America","confidence":"High","confidence_rationale":"Tier 1 / Moderate — in vitro functional reconstitution with multiple mutant alleles, orthogonal cell systems (COS-7 and Xenopus oocytes), single lab but multiple orthogonal methods","pmids":["11562478"],"is_preprint":false},{"year":2015,"finding":"A novel NOG missense mutation p.W150C interferes with dimerization of the NOG protein, as demonstrated by Western blot analysis of leukocyte samples from affected family members. This impaired dimerization is proposed as a pathogenic mechanism for NOG-related symphalangism spectrum disorder.","method":"Western blotting of leukocyte samples from affected patients carrying the p.W150C mutation","journal":"The Annals of otology, rhinology, and laryngology","confidence":"Medium","confidence_rationale":"Tier 3 / Weak — single Western blot from patient leukocytes, single lab, single method","pmids":["25888563"],"is_preprint":false},{"year":2022,"finding":"HIF-1α directly binds to a hypoxia response element (HRE) at position -1505 to -1502 in the NOG promoter to enhance NOG transcription, leading to increased Noggin secretion and inhibition of osteogenic differentiation of periodontal ligament stem cells (PDLSCs) under hypoxic conditions.","method":"Chromatin immunoprecipitation (ChIP), dual-luciferase reporter assay, qRT-PCR, Western blot, HIF-1α overexpression and inhibition experiments, in vivo animal model with IHC","journal":"Experimental cell research","confidence":"High","confidence_rationale":"Tier 1-2 / Moderate — ChIP and dual-luciferase reporter assay with functional validation, multiple orthogonal methods (overexpression, inhibition, in vivo), single lab","pmids":["36002046"],"is_preprint":false},{"year":2012,"finding":"NOG expression in breast cancer cells facilitates bone colonization by fostering osteoclast differentiation and bone degradation (nonautonomous function) and contributes to metastatic lesion reinitiation (autonomous function). NOG expression is acquired during late metastatic events and is selected for in bone metastatic lesions compared to lung, liver, and brain metastases.","method":"Genetic approaches (gain/loss of function) in human breast cancer cells; in vivo bone metastasis models assessing osteoclast differentiation and bone degradation","journal":"The Journal of biological chemistry","confidence":"Medium","confidence_rationale":"Tier 2 / Moderate — genetic loss/gain of function with defined cellular phenotypes (osteoclast differentiation, bone degradation, metastatic reinitiation), single lab, multiple functional readouts","pmids":["22547073"],"is_preprint":false},{"year":2002,"finding":"Heterozygous nonsense (Q110X) and frameshift (c.252-253insC) mutations in NOG that disrupt the cysteine-rich C-terminal domain cause a congenital stapes ankylosis syndrome. In contrast to most NOG mutations in SYM1/SYNS1 that preserve this domain, C-terminal disruptions produce a phenotype with conductive hearing loss but without symphalangism, demonstrating domain-specific functional consequences.","method":"Mutation identification by sequencing; genotype-phenotype correlation in human families","journal":"American journal of human genetics","confidence":"Low","confidence_rationale":"Tier 3 / Weak — genotype-phenotype correlation only, no direct biochemical functional assay, single study","pmids":["12089654"],"is_preprint":false},{"year":2021,"finding":"A 30 base pair deletion at a splice site in the NOG gene in Boxer dogs is associated with spontaneous superficial chronic corneal epithelial defects (SCCEDs). RNA-seq showed significant fold reductions in NOG, BMP4, MMP13, and NCAM1 expression, and increased BMP2 in corneal IHC of affected dogs, suggesting that NOG normally inhibits BMP signaling to regulate limbal epithelial progenitor cells in the cornea.","method":"Whole genome sequencing, RNA sequencing of corneal tissue, immunohistochemistry","journal":"BMC veterinary research","confidence":"Medium","confidence_rationale":"Tier 2 / Moderate — loss-of-function (deletion) with defined molecular and cellular phenotypes via RNA-seq and IHC, single lab, multiple methods","pmids":["34311726"],"is_preprint":false}],"current_model":"NOG encodes noggin, a secreted BMP antagonist that functions as a disulfide-linked homodimer; disease-causing missense mutations reduce or abolish dimer secretion and/or BMP binding, leading to haploinsufficiency that causes joint fusion syndromes (symphalangism, multiple synostoses) in a dosage-dependent manner, while its transcription is directly upregulated by HIF-1α binding to a promoter HRE under hypoxia, and in cancer contexts NOG promotes bone metastasis by fostering osteoclast differentiation and bone degradation."},"narrative":{"mechanistic_narrative":"NOG encodes noggin, a secreted antagonist of BMP signaling that functions as a disulfide-linked homodimer and regulates skeletal and epithelial development through dosage-sensitive inhibition of BMP activity [PMID:11562478, PMID:34311726]. Disease-causing missense mutations act as hypomorphic alleles that reduce or abolish secretion of functional noggin dimers, producing haploinsufficiency that causes joint fusion syndromes such as symphalangism (SYM1) and multiple synostoses (SYNS1) [PMID:11562478]; a distinct class of C-terminal truncating mutations that disrupt the cysteine-rich domain instead produces a stapes ankylosis phenotype without symphalangism, indicating domain-specific functional consequences [PMID:12089654]. A separate missense allele (p.W150C) interferes with noggin dimerization, reinforcing dimer formation as central to its activity [PMID:25888563]. NOG transcription is directly induced by HIF-1α binding to a hypoxia response element in its promoter, and the resulting increase in noggin secretion inhibits osteogenic differentiation of periodontal ligament stem cells under hypoxia [PMID:36002046]. In cancer, NOG expression acquired by breast cancer cells promotes bone colonization by fostering osteoclast differentiation and bone degradation while also supporting metastatic lesion reinitiation [PMID:22547073].","teleology":[{"year":2001,"claim":"Established that disease-associated NOG missense mutations are hypomorphic alleles acting by impairing secretion of functional noggin dimers, defining the molecular basis of dosage-dependent joint fusion syndromes.","evidence":"Transient transfection of wild-type and mutant NOG in COS-7 cells and Xenopus oocytes, assessing dimer formation and secretion","pmids":["11562478"],"confidence":"High","gaps":["Does not resolve the structural basis of dimer assembly","Species-specific processing differences left unexplained","Direct effect on BMP binding not measured"]},{"year":2002,"claim":"Showed that mutations disrupting the C-terminal cysteine-rich domain produce a distinct phenotype (stapes ankylosis without symphalangism), demonstrating domain-specific functional consequences of NOG alterations.","evidence":"Mutation sequencing and genotype-phenotype correlation in human families","pmids":["12089654"],"confidence":"Low","gaps":["Genotype-phenotype correlation only, no biochemical functional assay","Mechanism by which C-terminal disruption spares symphalangism not defined"]},{"year":2012,"claim":"Identified a pathological gain of NOG function in cancer, where its expression promotes bone metastasis via osteoclast-driven bone degradation and metastatic reinitiation.","evidence":"Gain/loss-of-function in human breast cancer cells with in vivo bone metastasis models scoring osteoclast differentiation and bone degradation","pmids":["22547073"],"confidence":"Medium","gaps":["Molecular pathway linking secreted NOG to osteoclast differentiation not detailed","Single lab","Relationship between autonomous and nonautonomous functions unresolved"]},{"year":2015,"claim":"Linked a specific dimerization-impairing missense allele (p.W150C) to symphalangism spectrum disorder, supporting dimerization defects as a recurrent pathogenic mechanism.","evidence":"Western blotting of leukocyte samples from affected patients","pmids":["25888563"],"confidence":"Medium","gaps":["Single Western blot from patient leukocytes, single method","BMP-binding consequence not tested"]},{"year":2021,"claim":"Implicated NOG in corneal epithelial homeostasis, where reduced expression alters BMP signaling and limbal progenitor regulation, broadening its role beyond skeletal tissue.","evidence":"Whole genome and RNA sequencing plus IHC of corneal tissue in Boxer dogs carrying a splice-site deletion","pmids":["34311726"],"confidence":"Medium","gaps":["Causal link between NOG loss and SCCEDs not established mechanistically","Effects inferred from expression changes of BMP pathway genes","Non-human model"]},{"year":2022,"claim":"Defined direct transcriptional control of NOG by HIF-1α, connecting hypoxia to BMP antagonism and inhibition of osteogenic differentiation.","evidence":"ChIP, dual-luciferase reporter assays, HIF-1α overexpression/inhibition, and in vivo IHC in periodontal ligament stem cells","pmids":["36002046"],"confidence":"High","gaps":["Whether hypoxic NOG induction operates in other tissues not tested","Downstream BMP targets in PDLSCs not enumerated"]},{"year":null,"claim":"The structural basis of noggin dimerization and direct BMP binding, and how distinct mutation classes map to tissue-specific phenotypes, remain unresolved.","evidence":"","pmids":[],"confidence":"Low","gaps":["No structural model of the noggin dimer in the corpus","Direct BMP-binding assays absent","Mechanism linking secreted NOG to osteoclast differentiation uncharacterized"]}],"mechanism_profile":{"molecular_activity":[{"term_id":"GO:0098772","term_label":"molecular function regulator activity","supporting_discovery_ids":[0,5]}],"localization":[{"term_id":"GO:0005576","term_label":"extracellular region","supporting_discovery_ids":[0,2]}],"pathway":[],"complexes":[],"partners":[],"other_free_text":[]}},"prefetch_data":{"uniprot":{"accession":"Q13253","full_name":"Noggin","aliases":[],"length_aa":232,"mass_kda":25.8,"function":"Inhibitor of bone morphogenetic proteins (BMP) signaling which is required for growth and patterning of the neural tube and somite. Essential for cartilage morphogenesis and joint formation. Inhibits chondrocyte differentiation through its interaction with GDF5 and, probably, GDF6 (PubMed:21976273, PubMed:26643732)","subcellular_location":"Secreted","url":"https://www.uniprot.org/uniprotkb/Q13253/entry"},"depmap":{"release":"DepMap","has_data":true,"is_common_essential":false,"resolved_as":"","url":"https://depmap.org/portal/gene/NOG","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":[],"url":"https://opencell.sf.czbiohub.org/search/NOG","total_profiled":1310},"omim":[{"mim_id":"619034","title":"RNA-BINDING PROTEIN, mRNA-PROCESSING FACTOR, 2; RBPMS2","url":"https://www.omim.org/entry/619034"},{"mim_id":"615589","title":"OTOSCLEROSIS 10; OTSC10","url":"https://www.omim.org/entry/615589"},{"mim_id":"615298","title":"SYMPHALANGISM, PROXIMAL, 1B; SYM1B","url":"https://www.omim.org/entry/615298"},{"mim_id":"612985","title":"IROQUOIS HOMEOBOX PROTEIN 3; IRX3","url":"https://www.omim.org/entry/612985"},{"mim_id":"612839","title":"TET METHYLCYTOSINE DIOXYGENASE 2; TET2","url":"https://www.omim.org/entry/612839"}],"hpa":{"profiled":true,"resolved_as":"","reliability":"","locations":[],"tissue_specificity":"Tissue enhanced","tissue_distribution":"Detected in some","driving_tissues":[{"tissue":"brain","ntpm":5.5},{"tissue":"placenta","ntpm":10.0}],"url":"https://www.proteinatlas.org/search/NOG"},"hgnc":{"alias_symbol":[],"prev_symbol":["SYNS1","SYM1"]},"alphafold":{"accession":"Q13253","domains":[{"cath_id":"2.10.90.10","chopping":"48-83_157-232","consensus_level":"medium","plddt":94.973,"start":48,"end":232},{"cath_id":"-","chopping":"113-125_133-153","consensus_level":"medium","plddt":89.0724,"start":113,"end":153}],"viewer_url":"https://alphafold.ebi.ac.uk/entry/Q13253","model_url":"https://alphafold.ebi.ac.uk/files/AF-Q13253-F1-model_v6.cif","pae_url":"https://alphafold.ebi.ac.uk/files/AF-Q13253-F1-predicted_aligned_error_v6.png","plddt_mean":86.06},"mouse_models":{"mgi_url":"https://www.informatics.jax.org/marker/summary?nomen=NOG","jax_strain_url":"https://www.jax.org/strain/search?query=NOG"},"sequence":{"accession":"Q13253","fasta_url":"https://rest.uniprot.org/uniprotkb/Q13253.fasta","uniprot_url":"https://www.uniprot.org/uniprotkb/Q13253/entry","alphafold_viewer_url":"https://alphafold.ebi.ac.uk/entry/Q13253"}},"corpus_meta":[{"pmid":"21238430","id":"PMC_21238430","title":"The 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The SYNS1 mutation abolished dimer secretion; SYM1 mutations reduced it. Coexpression with wild-type noggin did not impair wild-type secretion, indicating these are hypomorphic alleles. Notably, the SYNS1 mutant could still form dimers in Xenopus oocytes, revealing species-specific differences in processing mutant noggin.\",\n      \"method\": \"Transient transfection of COS-7 cells and Xenopus oocyte expression with wild-type and mutant NOG constructs; assessment of secretion and dimer formation\",\n      \"journal\": \"Proceedings of the National Academy of Sciences of the United States of America\",\n      \"confidence\": \"High\",\n      \"confidence_rationale\": \"Tier 1 / Moderate — in vitro functional reconstitution with multiple mutant alleles, orthogonal cell systems (COS-7 and Xenopus oocytes), single lab but multiple orthogonal methods\",\n      \"pmids\": [\"11562478\"],\n      \"is_preprint\": false\n    },\n    {\n      \"year\": 2015,\n      \"finding\": \"A novel NOG missense mutation p.W150C interferes with dimerization of the NOG protein, as demonstrated by Western blot analysis of leukocyte samples from affected family members. This impaired dimerization is proposed as a pathogenic mechanism for NOG-related symphalangism spectrum disorder.\",\n      \"method\": \"Western blotting of leukocyte samples from affected patients carrying the p.W150C mutation\",\n      \"journal\": \"The Annals of otology, rhinology, and laryngology\",\n      \"confidence\": \"Medium\",\n      \"confidence_rationale\": \"Tier 3 / Weak — single Western blot from patient leukocytes, single lab, single method\",\n      \"pmids\": [\"25888563\"],\n      \"is_preprint\": false\n    },\n    {\n      \"year\": 2022,\n      \"finding\": \"HIF-1α directly binds to a hypoxia response element (HRE) at position -1505 to -1502 in the NOG promoter to enhance NOG transcription, leading to increased Noggin secretion and inhibition of osteogenic differentiation of periodontal ligament stem cells (PDLSCs) under hypoxic conditions.\",\n      \"method\": \"Chromatin immunoprecipitation (ChIP), dual-luciferase reporter assay, qRT-PCR, Western blot, HIF-1α overexpression and inhibition experiments, in vivo animal model with IHC\",\n      \"journal\": \"Experimental cell research\",\n      \"confidence\": \"High\",\n      \"confidence_rationale\": \"Tier 1-2 / Moderate — ChIP and dual-luciferase reporter assay with functional validation, multiple orthogonal methods (overexpression, inhibition, in vivo), single lab\",\n      \"pmids\": [\"36002046\"],\n      \"is_preprint\": false\n    },\n    {\n      \"year\": 2012,\n      \"finding\": \"NOG expression in breast cancer cells facilitates bone colonization by fostering osteoclast differentiation and bone degradation (nonautonomous function) and contributes to metastatic lesion reinitiation (autonomous function). NOG expression is acquired during late metastatic events and is selected for in bone metastatic lesions compared to lung, liver, and brain metastases.\",\n      \"method\": \"Genetic approaches (gain/loss of function) in human breast cancer cells; in vivo bone metastasis models assessing osteoclast differentiation and bone degradation\",\n      \"journal\": \"The Journal of biological chemistry\",\n      \"confidence\": \"Medium\",\n      \"confidence_rationale\": \"Tier 2 / Moderate — genetic loss/gain of function with defined cellular phenotypes (osteoclast differentiation, bone degradation, metastatic reinitiation), single lab, multiple functional readouts\",\n      \"pmids\": [\"22547073\"],\n      \"is_preprint\": false\n    },\n    {\n      \"year\": 2002,\n      \"finding\": \"Heterozygous nonsense (Q110X) and frameshift (c.252-253insC) mutations in NOG that disrupt the cysteine-rich C-terminal domain cause a congenital stapes ankylosis syndrome. In contrast to most NOG mutations in SYM1/SYNS1 that preserve this domain, C-terminal disruptions produce a phenotype with conductive hearing loss but without symphalangism, demonstrating domain-specific functional consequences.\",\n      \"method\": \"Mutation identification by sequencing; genotype-phenotype correlation in human families\",\n      \"journal\": \"American journal of human genetics\",\n      \"confidence\": \"Low\",\n      \"confidence_rationale\": \"Tier 3 / Weak — genotype-phenotype correlation only, no direct biochemical functional assay, single study\",\n      \"pmids\": [\"12089654\"],\n      \"is_preprint\": false\n    },\n    {\n      \"year\": 2021,\n      \"finding\": \"A 30 base pair deletion at a splice site in the NOG gene in Boxer dogs is associated with spontaneous superficial chronic corneal epithelial defects (SCCEDs). RNA-seq showed significant fold reductions in NOG, BMP4, MMP13, and NCAM1 expression, and increased BMP2 in corneal IHC of affected dogs, suggesting that NOG normally inhibits BMP signaling to regulate limbal epithelial progenitor cells in the cornea.\",\n      \"method\": \"Whole genome sequencing, RNA sequencing of corneal tissue, immunohistochemistry\",\n      \"journal\": \"BMC veterinary research\",\n      \"confidence\": \"Medium\",\n      \"confidence_rationale\": \"Tier 2 / Moderate — loss-of-function (deletion) with defined molecular and cellular phenotypes via RNA-seq and IHC, single lab, multiple methods\",\n      \"pmids\": [\"34311726\"],\n      \"is_preprint\": false\n    }\n  ],\n  \"current_model\": \"NOG encodes noggin, a secreted BMP antagonist that functions as a disulfide-linked homodimer; disease-causing missense mutations reduce or abolish dimer secretion and/or BMP binding, leading to haploinsufficiency that causes joint fusion syndromes (symphalangism, multiple synostoses) in a dosage-dependent manner, while its transcription is directly upregulated by HIF-1α binding to a promoter HRE under hypoxia, and in cancer contexts NOG promotes bone metastasis by fostering osteoclast differentiation and bone degradation.\"\n}\n```","stage2_raw":"{\n  \"mechanistic_narrative\": \"NOG encodes noggin, a secreted antagonist of BMP signaling that functions as a disulfide-linked homodimer and regulates skeletal and epithelial development through dosage-sensitive inhibition of BMP activity [#0, #5]. Disease-causing missense mutations act as hypomorphic alleles that reduce or abolish secretion of functional noggin dimers, producing haploinsufficiency that causes joint fusion syndromes such as symphalangism (SYM1) and multiple synostoses (SYNS1) [#0]; a distinct class of C-terminal truncating mutations that disrupt the cysteine-rich domain instead produces a stapes ankylosis phenotype without symphalangism, indicating domain-specific functional consequences [#4]. A separate missense allele (p.W150C) interferes with noggin dimerization, reinforcing dimer formation as central to its activity [#1]. NOG transcription is directly induced by HIF-1\\u03b1 binding to a hypoxia response element in its promoter, and the resulting increase in noggin secretion inhibits osteogenic differentiation of periodontal ligament stem cells under hypoxia [#2]. In cancer, NOG expression acquired by breast cancer cells promotes bone colonization by fostering osteoclast differentiation and bone degradation while also supporting metastatic lesion reinitiation [#3].\",\n  \"teleology\": [\n    {\n      \"year\": 2001,\n      \"claim\": \"Established that disease-associated NOG missense mutations are hypomorphic alleles acting by impairing secretion of functional noggin dimers, defining the molecular basis of dosage-dependent joint fusion syndromes.\",\n      \"evidence\": \"Transient transfection of wild-type and mutant NOG in COS-7 cells and Xenopus oocytes, assessing dimer formation and secretion\",\n      \"pmids\": [\"11562478\"],\n      \"confidence\": \"High\",\n      \"gaps\": [\"Does not resolve the structural basis of dimer assembly\", \"Species-specific processing differences left unexplained\", \"Direct effect on BMP binding not measured\"]\n    },\n    {\n      \"year\": 2002,\n      \"claim\": \"Showed that mutations disrupting the C-terminal cysteine-rich domain produce a distinct phenotype (stapes ankylosis without symphalangism), demonstrating domain-specific functional consequences of NOG alterations.\",\n      \"evidence\": \"Mutation sequencing and genotype-phenotype correlation in human families\",\n      \"pmids\": [\"12089654\"],\n      \"confidence\": \"Low\",\n      \"gaps\": [\"Genotype-phenotype correlation only, no biochemical functional assay\", \"Mechanism by which C-terminal disruption spares symphalangism not defined\"]\n    },\n    {\n      \"year\": 2012,\n      \"claim\": \"Identified a pathological gain of NOG function in cancer, where its expression promotes bone metastasis via osteoclast-driven bone degradation and metastatic reinitiation.\",\n      \"evidence\": \"Gain/loss-of-function in human breast cancer cells with in vivo bone metastasis models scoring osteoclast differentiation and bone degradation\",\n      \"pmids\": [\"22547073\"],\n      \"confidence\": \"Medium\",\n      \"gaps\": [\"Molecular pathway linking secreted NOG to osteoclast differentiation not detailed\", \"Single lab\", \"Relationship between autonomous and nonautonomous functions unresolved\"]\n    },\n    {\n      \"year\": 2015,\n      \"claim\": \"Linked a specific dimerization-impairing missense allele (p.W150C) to symphalangism spectrum disorder, supporting dimerization defects as a recurrent pathogenic mechanism.\",\n      \"evidence\": \"Western blotting of leukocyte samples from affected patients\",\n      \"pmids\": [\"25888563\"],\n      \"confidence\": \"Medium\",\n      \"gaps\": [\"Single Western blot from patient leukocytes, single method\", \"BMP-binding consequence not tested\"]\n    },\n    {\n      \"year\": 2021,\n      \"claim\": \"Implicated NOG in corneal epithelial homeostasis, where reduced expression alters BMP signaling and limbal progenitor regulation, broadening its role beyond skeletal tissue.\",\n      \"evidence\": \"Whole genome and RNA sequencing plus IHC of corneal tissue in Boxer dogs carrying a splice-site deletion\",\n      \"pmids\": [\"34311726\"],\n      \"confidence\": \"Medium\",\n      \"gaps\": [\"Causal link between NOG loss and SCCEDs not established mechanistically\", \"Effects inferred from expression changes of BMP pathway genes\", \"Non-human model\"]\n    },\n    {\n      \"year\": 2022,\n      \"claim\": \"Defined direct transcriptional control of NOG by HIF-1\\u03b1, connecting hypoxia to BMP antagonism and inhibition of osteogenic differentiation.\",\n      \"evidence\": \"ChIP, dual-luciferase reporter assays, HIF-1\\u03b1 overexpression/inhibition, and in vivo IHC in periodontal ligament stem cells\",\n      \"pmids\": [\"36002046\"],\n      \"confidence\": \"High\",\n      \"gaps\": [\"Whether hypoxic NOG induction operates in other tissues not tested\", \"Downstream BMP targets in PDLSCs not enumerated\"]\n    },\n    {\n      \"year\": null,\n      \"claim\": \"The structural basis of noggin dimerization and direct BMP binding, and how distinct mutation classes map to tissue-specific phenotypes, remain unresolved.\",\n      \"evidence\": \"\",\n      \"pmids\": [],\n      \"confidence\": \"Low\",\n      \"gaps\": [\"No structural model of the noggin dimer in the corpus\", \"Direct BMP-binding assays absent\", \"Mechanism linking secreted NOG to osteoclast differentiation uncharacterized\"]\n    }\n  ],\n  \"mechanism_profile\": {\n    \"molecular_activity\": [\n      {\"term_id\": \"GO:0098772\", \"supporting_discovery_ids\": [0, 5]}\n    ],\n    \"localization\": [\n      {\"term_id\": \"GO:0005576\", \"supporting_discovery_ids\": [0, 2]}\n    ],\n    \"pathway\": [\n      {\"term_id\": \"GO:0008283\", \"supporting_discovery_ids\": [3]}\n    ],\n    \"complexes\": [],\n    \"partners\": [],\n    \"other_free_text\": []\n  }\n}","audit_flag":null,"evaluation":{"pairwise":"win","faith_supported":5,"faith_total":5,"faith_pct":100.0}}