{"gene":"OR2T6","run_date":"2026-06-10T05:19:53","timeline":{"discoveries":[{"year":2019,"finding":"OR2T6 overexpression in breast cancer cell lines (MCF-7 and MDA-MB-231) enhanced proliferation, invasion, and migration, and promoted epithelial-mesenchymal transition (EMT) by upregulating mesenchymal markers (Vimentin, N-cadherin, β-catenin) while downregulating E-cadherin.","method":"In vitro overexpression in breast cancer cell lines with functional assays (proliferation, invasion, migration) and western blot for EMT markers","journal":"Frontiers in oncology","confidence":"Medium","confidence_rationale":"Tier 3 / Moderate — single lab, multiple functional readouts but no mutagenesis or reconstitution; pathway placement by gene expression microarray confirmed by western blot","pmids":["31781505"],"is_preprint":false},{"year":2019,"finding":"OR2T6 activates the MAPK/ERK signaling pathway in breast cancer cells, as determined by human gene expression microarray and confirmed at the protein level by western blot.","method":"Gene expression microarray and western blot analysis following OR2T6 manipulation in breast cancer cell lines","journal":"Frontiers in oncology","confidence":"Medium","confidence_rationale":"Tier 3 / Moderate — single lab, two orthogonal methods (microarray + western blot) but no mutagenesis or reconstitution","pmids":["31781505"],"is_preprint":false},{"year":2025,"finding":"OR2T6 directly binds to PPP3CA (calcineurin A), as established by co-immunoprecipitation and mass spectrometry, and promotes PPP3CA protein stability and enzyme activity through the ubiquitin-proteasome system.","method":"Co-immunoprecipitation (Co-IP) and mass spectrometry (MS); ubiquitin-proteasome pathway assays","journal":"Cell death and differentiation","confidence":"High","confidence_rationale":"Tier 2 / Moderate — reciprocal Co-IP with MS identification of binding partner, plus enzymatic activity assay in single lab with multiple orthogonal methods","pmids":["41214150"],"is_preprint":false},{"year":2025,"finding":"OR2T6 promotes calcium ion influx via the Gs/cAMP/PKA channel signaling axis, which contributes to PPP3CA stabilization and activation.","method":"Signaling pathway analysis in gastric cancer cells with functional readouts","journal":"Cell death and differentiation","confidence":"Medium","confidence_rationale":"Tier 3 / Weak — single lab, mechanistic claim supported by pathway analysis but limited methodological detail in abstract","pmids":["41214150"],"is_preprint":false},{"year":2025,"finding":"OR2T6, via PPP3CA binding, suppresses the AKT/mTOR signaling pathway, thereby inhibiting tumor cell proliferation and promoting autophagy initiation in gastric cancer cells in vitro and in vivo.","method":"Loss-of-function and gain-of-function studies in gastric cancer cell lines and in vivo models; western blot for AKT/mTOR pathway components; autophagy assays","journal":"Cell death and differentiation","confidence":"High","confidence_rationale":"Tier 2 / Moderate — epistasis established through Co-IP binding plus in vitro and in vivo functional assays with defined pathway readouts in single lab","pmids":["41214150"],"is_preprint":false},{"year":2025,"finding":"OR2T6 facilitates nuclear translocation of TFEB, a key regulator of lysosomal biogenesis, leading to transcriptional inactivation of lysosomal target genes (LAMP1, MCOLN1, ATP6V1H, CTSB, CTSD), impairing lysosomal function and blocking autophagic flux in gastric cancer.","method":"TFEB nuclear translocation assays, transcriptional target gene expression analysis, lysosomal function assays in gastric cancer cells","journal":"Cell death and differentiation","confidence":"Medium","confidence_rationale":"Tier 2 / Moderate — multiple orthogonal methods (localization, transcriptional target genes, lysosomal function) in single lab without independent replication","pmids":["41214150"],"is_preprint":false}],"current_model":"OR2T6 is an olfactory receptor that, depending on cellular context, can act as an oncogene in breast cancer (activating EMT and MAPK/ERK signaling) or a tumor suppressor in gastric cancer, where it directly binds and stabilizes the phosphatase PPP3CA via the ubiquitin-proteasome system and Gs/cAMP/PKA-mediated calcium influx, consequently suppressing AKT/mTOR-driven proliferation, initiating autophagy, and blocking autophagic flux through TFEB-mediated lysosomal dysfunction."},"narrative":{"mechanistic_narrative":"OR2T6 is an olfactory-receptor-family gene that functions as a context-dependent regulator of tumor cell behavior, with opposing roles documented in breast and gastric cancer [PMID:31781505, PMID:41214150]. In breast cancer cells, OR2T6 overexpression drives proliferation, invasion, migration, and epithelial-mesenchymal transition—upregulating Vimentin, N-cadherin, and β-catenin while reducing E-cadherin—and activates MAPK/ERK signaling [PMID:31781505]. In gastric cancer, OR2T6 directly binds the calcineurin A subunit PPP3CA and stabilizes it via the ubiquitin-proteasome system, increasing PPP3CA protein levels and enzymatic activity [PMID:41214150]; this stabilization is reinforced by OR2T6-driven calcium influx through a Gs/cAMP/PKA signaling axis [PMID:41214150]. Through PPP3CA, OR2T6 suppresses AKT/mTOR signaling to inhibit proliferation and initiate autophagy [PMID:41214150], while concurrently promoting nuclear translocation of TFEB and transcriptional shutdown of lysosomal genes (LAMP1, MCOLN1, ATP6V1H, CTSB, CTSD), impairing lysosomal function and blocking autophagic flux [PMID:41214150]. The structural basis of OR2T6 ligand recognition and how a single receptor produces opposite outcomes in different tissues have not been characterized in the available corpus.","teleology":[{"year":2019,"claim":"Established the first functional role for OR2T6 in cancer, showing it acts as a pro-tumorigenic driver of EMT in breast cancer rather than a silent olfactory receptor.","evidence":"Overexpression in MCF-7 and MDA-MB-231 with proliferation/invasion/migration assays and western blot for EMT markers","pmids":["31781505"],"confidence":"Medium","gaps":["No mutagenesis or reconstitution to confirm receptor-intrinsic activity","No ligand or upstream activator identified","Mechanism linking OR2T6 to EMT markers not resolved beyond correlation"]},{"year":2019,"claim":"Placed OR2T6's breast cancer activity within a defined signaling pathway by identifying MAPK/ERK activation as a downstream effector.","evidence":"Gene expression microarray plus western blot following OR2T6 manipulation in breast cancer cell lines","pmids":["31781505"],"confidence":"Medium","gaps":["Direct coupling of the receptor to MAPK/ERK not demonstrated biochemically","Whether ERK activation is necessary for the EMT phenotype not tested"]},{"year":2025,"claim":"Identified the first direct physical partner of OR2T6, the phosphatase PPP3CA, and a mechanism of action via ubiquitin-proteasome-dependent stabilization.","evidence":"Reciprocal Co-IP with mass spectrometry and ubiquitin-proteasome pathway and enzyme-activity assays in gastric cancer cells","pmids":["41214150"],"confidence":"High","gaps":["Whether OR2T6 binds PPP3CA directly or through an adaptor not fully resolved","Identity of the ubiquitin ligase/deubiquitinase machinery involved unknown","Whether this interaction occurs in breast cancer not tested"]},{"year":2025,"claim":"Connected canonical olfactory-receptor signaling output (Gs/cAMP/PKA) to PPP3CA regulation, linking receptor activity to calcium-dependent stabilization.","evidence":"Signaling pathway analysis with functional readouts in gastric cancer cells","pmids":["41214150"],"confidence":"Medium","gaps":["Limited methodological detail for the Gs/cAMP/PKA axis","Calcium channel mediating influx not identified","Quantitative contribution of calcium versus proteasome to stabilization unclear"]},{"year":2025,"claim":"Defined OR2T6 as a gastric cancer tumor suppressor acting through PPP3CA to dampen AKT/mTOR signaling and trigger autophagy, opposite to its breast cancer role.","evidence":"Loss- and gain-of-function studies in gastric cancer cell lines and in vivo, with AKT/mTOR western blots and autophagy assays","pmids":["41214150"],"confidence":"High","gaps":["Molecular basis for the tissue-specific reversal of oncogenic/suppressive role unexplained","Whether PPP3CA phosphatase activity is required for AKT/mTOR suppression not isolated"]},{"year":2025,"claim":"Resolved the apparent paradox of autophagy initiation without productive flux by showing OR2T6 drives TFEB nuclear translocation and lysosomal gene shutdown.","evidence":"TFEB localization, lysosomal target gene expression, and lysosomal function assays in gastric cancer cells","pmids":["41214150"],"confidence":"Medium","gaps":["Mechanism by which TFEB nuclear translocation produces transcriptional inactivation rather than activation not explained","Link between PPP3CA/calcineurin activity and TFEB regulation not directly traced","Single lab without independent replication"]},{"year":null,"claim":"It remains unknown what ligand activates OR2T6 and what molecular switch determines whether it acts as an oncogene or tumor suppressor across tissues.","evidence":"","pmids":[],"confidence":"Medium","gaps":["No endogenous or synthetic OR2T6 ligand identified","No structural model of the receptor or its PPP3CA interface","Tissue-specific determinants of opposing phenotypes uncharacterized"]}],"mechanism_profile":{"molecular_activity":[{"term_id":"GO:0060089","term_label":"molecular transducer activity","supporting_discovery_ids":[3]},{"term_id":"GO:0140096","term_label":"catalytic activity, acting on a protein","supporting_discovery_ids":[2]}],"localization":[{"term_id":"GO:0005886","term_label":"plasma membrane","supporting_discovery_ids":[3]}],"pathway":[{"term_id":"R-HSA-162582","term_label":"Signal Transduction","supporting_discovery_ids":[1,3,4]},{"term_id":"R-HSA-9612973","term_label":"Autophagy","supporting_discovery_ids":[4,5]},{"term_id":"R-HSA-1643685","term_label":"Disease","supporting_discovery_ids":[0,4]}],"complexes":[],"partners":["PPP3CA"],"other_free_text":[]}},"prefetch_data":{"uniprot":{"accession":"Q8NHC8","full_name":"Olfactory receptor 2T6","aliases":["OST703","Olfactory receptor 2T9"],"length_aa":308,"mass_kda":34.8,"function":"Odorant receptor","subcellular_location":"Cell membrane","url":"https://www.uniprot.org/uniprotkb/Q8NHC8/entry"},"depmap":{"release":"DepMap","has_data":true,"is_common_essential":false,"resolved_as":"","url":"https://depmap.org/portal/gene/OR2T6","classification":"Not Classified","n_dependent_lines":4,"n_total_lines":1090,"dependency_fraction":0.003669724770642202},"opencell":{"profiled":false,"resolved_as":"","ensg_id":"","cell_line_id":"","localizations":[],"interactors":[],"url":"https://opencell.sf.czbiohub.org/search/OR2T6","total_profiled":1310},"omim":[],"hpa":{"profiled":true,"resolved_as":"","reliability":"","locations":[],"tissue_specificity":"Not detected","tissue_distribution":"Not detected","driving_tissues":[],"url":"https://www.proteinatlas.org/search/OR2T6"},"hgnc":{"alias_symbol":["OST703"],"prev_symbol":["OR2T6P","OR2T9"]},"alphafold":{"accession":"Q8NHC8","domains":[{"cath_id":"1.20.1070.10","chopping":"10-308","consensus_level":"high","plddt":89.6027,"start":10,"end":308}],"viewer_url":"https://alphafold.ebi.ac.uk/entry/Q8NHC8","model_url":"https://alphafold.ebi.ac.uk/files/AF-Q8NHC8-F1-model_v6.cif","pae_url":"https://alphafold.ebi.ac.uk/files/AF-Q8NHC8-F1-predicted_aligned_error_v6.png","plddt_mean":88.25},"mouse_models":{"mgi_url":"https://www.informatics.jax.org/marker/summary?nomen=OR2T6","jax_strain_url":"https://www.jax.org/strain/search?query=OR2T6"},"sequence":{"accession":"Q8NHC8","fasta_url":"https://rest.uniprot.org/uniprotkb/Q8NHC8.fasta","uniprot_url":"https://www.uniprot.org/uniprotkb/Q8NHC8/entry","alphafold_viewer_url":"https://alphafold.ebi.ac.uk/entry/Q8NHC8"}},"corpus_meta":[{"pmid":"31781505","id":"PMC_31781505","title":"The Olfactory Receptor Family 2, Subfamily T, Member 6 (OR2T6) Is Involved in Breast Cancer Progression via Initiating Epithelial-Mesenchymal Transition and MAPK/ERK Pathway.","date":"2019","source":"Frontiers in oncology","url":"https://pubmed.ncbi.nlm.nih.gov/31781505","citation_count":20,"is_preprint":false},{"pmid":"41214150","id":"PMC_41214150","title":"OR2T6 modulates autophagy through the PPP3CA-mediated pathways to suppress gastric cancer.","date":"2025","source":"Cell death and differentiation","url":"https://pubmed.ncbi.nlm.nih.gov/41214150","citation_count":0,"is_preprint":false}],"cost":{"stage1":{"model":"claude-sonnet-4-6","input_tokens":3265,"output_tokens":1384,"usd":0.015277,"stage1_stop_reason":"end_turn"},"stage2":{"model":"claude-opus-4-8","input_tokens":8092,"output_tokens":2521,"usd":0.051742,"stage2_stop_reason":"end_turn"},"total_usd":0.067019,"stage1_batch_id":"msgbatch_013a8chtv3AWyTqv4z4sEF4C","stage2_batch_id":"msgbatch_01AHsuW63vinsvuTgzmQ3n62","note":"batch pricing = 50% of standard"},"stage1_raw":"```json\n{\n  \"discoveries\": [\n    {\n      \"year\": 2019,\n      \"finding\": \"OR2T6 overexpression in breast cancer cell lines (MCF-7 and MDA-MB-231) enhanced proliferation, invasion, and migration, and promoted epithelial-mesenchymal transition (EMT) by upregulating mesenchymal markers (Vimentin, N-cadherin, β-catenin) while downregulating E-cadherin.\",\n      \"method\": \"In vitro overexpression in breast cancer cell lines with functional assays (proliferation, invasion, migration) and western blot for EMT markers\",\n      \"journal\": \"Frontiers in oncology\",\n      \"confidence\": \"Medium\",\n      \"confidence_rationale\": \"Tier 3 / Moderate — single lab, multiple functional readouts but no mutagenesis or reconstitution; pathway placement by gene expression microarray confirmed by western blot\",\n      \"pmids\": [\"31781505\"],\n      \"is_preprint\": false\n    },\n    {\n      \"year\": 2019,\n      \"finding\": \"OR2T6 activates the MAPK/ERK signaling pathway in breast cancer cells, as determined by human gene expression microarray and confirmed at the protein level by western blot.\",\n      \"method\": \"Gene expression microarray and western blot analysis following OR2T6 manipulation in breast cancer cell lines\",\n      \"journal\": \"Frontiers in oncology\",\n      \"confidence\": \"Medium\",\n      \"confidence_rationale\": \"Tier 3 / Moderate — single lab, two orthogonal methods (microarray + western blot) but no mutagenesis or reconstitution\",\n      \"pmids\": [\"31781505\"],\n      \"is_preprint\": false\n    },\n    {\n      \"year\": 2025,\n      \"finding\": \"OR2T6 directly binds to PPP3CA (calcineurin A), as established by co-immunoprecipitation and mass spectrometry, and promotes PPP3CA protein stability and enzyme activity through the ubiquitin-proteasome system.\",\n      \"method\": \"Co-immunoprecipitation (Co-IP) and mass spectrometry (MS); ubiquitin-proteasome pathway assays\",\n      \"journal\": \"Cell death and differentiation\",\n      \"confidence\": \"High\",\n      \"confidence_rationale\": \"Tier 2 / Moderate — reciprocal Co-IP with MS identification of binding partner, plus enzymatic activity assay in single lab with multiple orthogonal methods\",\n      \"pmids\": [\"41214150\"],\n      \"is_preprint\": false\n    },\n    {\n      \"year\": 2025,\n      \"finding\": \"OR2T6 promotes calcium ion influx via the Gs/cAMP/PKA channel signaling axis, which contributes to PPP3CA stabilization and activation.\",\n      \"method\": \"Signaling pathway analysis in gastric cancer cells with functional readouts\",\n      \"journal\": \"Cell death and differentiation\",\n      \"confidence\": \"Medium\",\n      \"confidence_rationale\": \"Tier 3 / Weak — single lab, mechanistic claim supported by pathway analysis but limited methodological detail in abstract\",\n      \"pmids\": [\"41214150\"],\n      \"is_preprint\": false\n    },\n    {\n      \"year\": 2025,\n      \"finding\": \"OR2T6, via PPP3CA binding, suppresses the AKT/mTOR signaling pathway, thereby inhibiting tumor cell proliferation and promoting autophagy initiation in gastric cancer cells in vitro and in vivo.\",\n      \"method\": \"Loss-of-function and gain-of-function studies in gastric cancer cell lines and in vivo models; western blot for AKT/mTOR pathway components; autophagy assays\",\n      \"journal\": \"Cell death and differentiation\",\n      \"confidence\": \"High\",\n      \"confidence_rationale\": \"Tier 2 / Moderate — epistasis established through Co-IP binding plus in vitro and in vivo functional assays with defined pathway readouts in single lab\",\n      \"pmids\": [\"41214150\"],\n      \"is_preprint\": false\n    },\n    {\n      \"year\": 2025,\n      \"finding\": \"OR2T6 facilitates nuclear translocation of TFEB, a key regulator of lysosomal biogenesis, leading to transcriptional inactivation of lysosomal target genes (LAMP1, MCOLN1, ATP6V1H, CTSB, CTSD), impairing lysosomal function and blocking autophagic flux in gastric cancer.\",\n      \"method\": \"TFEB nuclear translocation assays, transcriptional target gene expression analysis, lysosomal function assays in gastric cancer cells\",\n      \"journal\": \"Cell death and differentiation\",\n      \"confidence\": \"Medium\",\n      \"confidence_rationale\": \"Tier 2 / Moderate — multiple orthogonal methods (localization, transcriptional target genes, lysosomal function) in single lab without independent replication\",\n      \"pmids\": [\"41214150\"],\n      \"is_preprint\": false\n    }\n  ],\n  \"current_model\": \"OR2T6 is an olfactory receptor that, depending on cellular context, can act as an oncogene in breast cancer (activating EMT and MAPK/ERK signaling) or a tumor suppressor in gastric cancer, where it directly binds and stabilizes the phosphatase PPP3CA via the ubiquitin-proteasome system and Gs/cAMP/PKA-mediated calcium influx, consequently suppressing AKT/mTOR-driven proliferation, initiating autophagy, and blocking autophagic flux through TFEB-mediated lysosomal dysfunction.\"\n}\n```","stage2_raw":"{\n  \"mechanistic_narrative\": \"OR2T6 is an olfactory-receptor-family gene that functions as a context-dependent regulator of tumor cell behavior, with opposing roles documented in breast and gastric cancer [#0, #4]. In breast cancer cells, OR2T6 overexpression drives proliferation, invasion, migration, and epithelial-mesenchymal transition—upregulating Vimentin, N-cadherin, and \\u03b2-catenin while reducing E-cadherin—and activates MAPK/ERK signaling [#0, #1]. In gastric cancer, OR2T6 directly binds the calcineurin A subunit PPP3CA and stabilizes it via the ubiquitin-proteasome system, increasing PPP3CA protein levels and enzymatic activity [#2]; this stabilization is reinforced by OR2T6-driven calcium influx through a Gs/cAMP/PKA signaling axis [#3]. Through PPP3CA, OR2T6 suppresses AKT/mTOR signaling to inhibit proliferation and initiate autophagy [#4], while concurrently promoting nuclear translocation of TFEB and transcriptional shutdown of lysosomal genes (LAMP1, MCOLN1, ATP6V1H, CTSB, CTSD), impairing lysosomal function and blocking autophagic flux [#5]. The structural basis of OR2T6 ligand recognition and how a single receptor produces opposite outcomes in different tissues have not been characterized in the available corpus.\",\n  \"teleology\": [\n    {\n      \"year\": 2019,\n      \"claim\": \"Established the first functional role for OR2T6 in cancer, showing it acts as a pro-tumorigenic driver of EMT in breast cancer rather than a silent olfactory receptor.\",\n      \"evidence\": \"Overexpression in MCF-7 and MDA-MB-231 with proliferation/invasion/migration assays and western blot for EMT markers\",\n      \"pmids\": [\"31781505\"],\n      \"confidence\": \"Medium\",\n      \"gaps\": [\n        \"No mutagenesis or reconstitution to confirm receptor-intrinsic activity\",\n        \"No ligand or upstream activator identified\",\n        \"Mechanism linking OR2T6 to EMT markers not resolved beyond correlation\"\n      ]\n    },\n    {\n      \"year\": 2019,\n      \"claim\": \"Placed OR2T6's breast cancer activity within a defined signaling pathway by identifying MAPK/ERK activation as a downstream effector.\",\n      \"evidence\": \"Gene expression microarray plus western blot following OR2T6 manipulation in breast cancer cell lines\",\n      \"pmids\": [\"31781505\"],\n      \"confidence\": \"Medium\",\n      \"gaps\": [\n        \"Direct coupling of the receptor to MAPK/ERK not demonstrated biochemically\",\n        \"Whether ERK activation is necessary for the EMT phenotype not tested\"\n      ]\n    },\n    {\n      \"year\": 2025,\n      \"claim\": \"Identified the first direct physical partner of OR2T6, the phosphatase PPP3CA, and a mechanism of action via ubiquitin-proteasome-dependent stabilization.\",\n      \"evidence\": \"Reciprocal Co-IP with mass spectrometry and ubiquitin-proteasome pathway and enzyme-activity assays in gastric cancer cells\",\n      \"pmids\": [\"41214150\"],\n      \"confidence\": \"High\",\n      \"gaps\": [\n        \"Whether OR2T6 binds PPP3CA directly or through an adaptor not fully resolved\",\n        \"Identity of the ubiquitin ligase/deubiquitinase machinery involved unknown\",\n        \"Whether this interaction occurs in breast cancer not tested\"\n      ]\n    },\n    {\n      \"year\": 2025,\n      \"claim\": \"Connected canonical olfactory-receptor signaling output (Gs/cAMP/PKA) to PPP3CA regulation, linking receptor activity to calcium-dependent stabilization.\",\n      \"evidence\": \"Signaling pathway analysis with functional readouts in gastric cancer cells\",\n      \"pmids\": [\"41214150\"],\n      \"confidence\": \"Medium\",\n      \"gaps\": [\n        \"Limited methodological detail for the Gs/cAMP/PKA axis\",\n        \"Calcium channel mediating influx not identified\",\n        \"Quantitative contribution of calcium versus proteasome to stabilization unclear\"\n      ]\n    },\n    {\n      \"year\": 2025,\n      \"claim\": \"Defined OR2T6 as a gastric cancer tumor suppressor acting through PPP3CA to dampen AKT/mTOR signaling and trigger autophagy, opposite to its breast cancer role.\",\n      \"evidence\": \"Loss- and gain-of-function studies in gastric cancer cell lines and in vivo, with AKT/mTOR western blots and autophagy assays\",\n      \"pmids\": [\"41214150\"],\n      \"confidence\": \"High\",\n      \"gaps\": [\n        \"Molecular basis for the tissue-specific reversal of oncogenic/suppressive role unexplained\",\n        \"Whether PPP3CA phosphatase activity is required for AKT/mTOR suppression not isolated\"\n      ]\n    },\n    {\n      \"year\": 2025,\n      \"claim\": \"Resolved the apparent paradox of autophagy initiation without productive flux by showing OR2T6 drives TFEB nuclear translocation and lysosomal gene shutdown.\",\n      \"evidence\": \"TFEB localization, lysosomal target gene expression, and lysosomal function assays in gastric cancer cells\",\n      \"pmids\": [\"41214150\"],\n      \"confidence\": \"Medium\",\n      \"gaps\": [\n        \"Mechanism by which TFEB nuclear translocation produces transcriptional inactivation rather than activation not explained\",\n        \"Link between PPP3CA/calcineurin activity and TFEB regulation not directly traced\",\n        \"Single lab without independent replication\"\n      ]\n    },\n    {\n      \"year\": null,\n      \"claim\": \"It remains unknown what ligand activates OR2T6 and what molecular switch determines whether it acts as an oncogene or tumor suppressor across tissues.\",\n      \"evidence\": \"\",\n      \"pmids\": [],\n      \"confidence\": \"Medium\",\n      \"gaps\": [\n        \"No endogenous or synthetic OR2T6 ligand identified\",\n        \"No structural model of the receptor or its PPP3CA interface\",\n        \"Tissue-specific determinants of opposing phenotypes uncharacterized\"\n      ]\n    }\n  ],\n  \"mechanism_profile\": {\n    \"molecular_activity\": [\n      {\"term_id\": \"GO:0060089\", \"supporting_discovery_ids\": [3]},\n      {\"term_id\": \"GO:0140096\", \"supporting_discovery_ids\": [2]}\n    ],\n    \"localization\": [\n      {\"term_id\": \"GO:0005886\", \"supporting_discovery_ids\": [3]}\n    ],\n    \"pathway\": [\n      {\"term_id\": \"R-HSA-162582\", \"supporting_discovery_ids\": [1, 3, 4]},\n      {\"term_id\": \"R-HSA-9612973\", \"supporting_discovery_ids\": [4, 5]},\n      {\"term_id\": \"R-HSA-1643685\", \"supporting_discovery_ids\": [0, 4]}\n    ],\n    \"complexes\": [],\n    \"partners\": [\"PPP3CA\"],\n    \"other_free_text\": []\n  }\n}","audit_flag":null,"evaluation":{"faith_supported":4,"faith_total":4,"faith_pct":100.0}}