{"gene":"TCAF1","run_date":"2026-04-28T21:42:58","timeline":{"discoveries":[{"year":2015,"finding":"TCAF1 and TCAF2 are novel TRPM8-binding partner proteins ('TRP channel-associated factors'). Both bind to the TRPM8 channel and promote its trafficking to the cell surface, but exert opposing effects on TRPM8 gating: TCAF1/TRPM8 interaction reduces the speed and directionality of migration of prostate cancer cells, consistent with loss of TCAF1 expression in metastatic specimens, while TCAF2 promotes migration.","method":"Co-immunoprecipitation, cell surface trafficking assays, functional channel gating recordings, migration assays, and loss-of-function experiments in prostate cancer cells","journal":"The Journal of cell biology","confidence":"High","confidence_rationale":"Tier 2 — reciprocal Co-IP, functional channel assays, and defined cellular phenotype from a single rigorous study with multiple orthogonal methods","pmids":["25559186"],"is_preprint":false},{"year":2024,"finding":"TCAF1 is a key factor promoting TRPV2-mediated Ca2+ release under replication stress. Mechanistically, TCAF1 facilitates dissociation of STING from TRPV2, thereby relieving TRPV2 repression; this Ca2+ release activates CaMKK2/AMPK, leading to Exo1 phosphorylation that prevents aberrant fork processing. TCAF1 is required for fork protection, chromosomal stability, and cell survival after replication stress.","method":"Genome-wide CRISPR-based screen, Ca2+ release assays, co-immunoprecipitation (STING–TRPV2 interaction), epistasis analysis (CaMKK2/AMPK/Exo1 pathway), chromosomal stability assays, and cell survival assays after replication stress","journal":"Nature communications","confidence":"High","confidence_rationale":"Tier 2 — genome-wide unbiased screen validated by multiple orthogonal mechanistic assays (Co-IP, Ca2+ imaging, epistasis, chromosomal stability) in a single rigorous study","pmids":["38816425"],"is_preprint":false},{"year":2021,"finding":"TCAF1/TCAF2 copy number variation is substantial in humans, with TCAF duplications originating ~1.7 million years ago and diversifying only in Homo sapiens. TCAF2 expression differs between haplogroups, with high TCAF2 and TRPM8 expression in liver and prostate, supporting a role for TCAF diversification in cold or dietary adaptation.","method":"Long-read sequencing to resolve complex segmental duplications, copy number variant analysis across primate genomes, full-length transcript annotation, population genetic selection analysis","journal":"Nature communications","confidence":"Medium","confidence_rationale":"Tier 3 — genomic and evolutionary analysis without direct protein-level functional assays, but uses rigorous long-read sequencing and population genetics","pmids":["34433829"],"is_preprint":false}],"current_model":"TCAF1 is a dual-function TRPM8/TRPV2-associated regulatory protein: it binds TRPM8, promotes its cell-surface trafficking, and suppresses prostate cancer cell migration; under replication stress it facilitates STING dissociation from TRPV2 to enable TRPV2-mediated Ca2+ release, activating CaMKK2/AMPK/Exo1 signaling to protect stalled replication forks and maintain genome stability."},"narrative":{"teleology":[{"year":2015,"claim":"The identity of TRPM8-associated cofactors was unknown; discovery of TCAF1 as a direct TRPM8-binding partner that promotes channel surface trafficking and suppresses prostate cancer cell migration established it as a functionally important channel-regulatory protein.","evidence":"Reciprocal co-immunoprecipitation, surface trafficking assays, electrophysiological recordings, and migration assays in prostate cancer cells","pmids":["25559186"],"confidence":"High","gaps":["Structural basis of the TCAF1–TRPM8 interaction is unresolved","Whether TCAF1 regulates TRPM8 in non-prostate tissues is untested","Mechanism by which TCAF1 opposes migration beyond channel gating effects is unclear"]},{"year":2021,"claim":"How TCAF1/TCAF2 paralogs arose and whether their copy number varies across human populations was unknown; long-read sequencing revealed that TCAF duplications originated ~1.7 Mya and diversified only in Homo sapiens, with population-level copy number variation linked to differential TCAF2/TRPM8 expression.","evidence":"Long-read sequencing of complex segmental duplications, primate comparative genomics, population genetic selection analysis","pmids":["34433829"],"confidence":"Medium","gaps":["Functional consequences of TCAF1 copy number variation on protein activity are not experimentally tested","Whether copy number variation in TCAF1 specifically (vs TCAF2) affects channel regulation is unresolved","Selective pressures driving TCAF diversification remain correlative"]},{"year":2024,"claim":"Whether TCAF1 functions beyond TRP channel trafficking was unknown; a genome-wide CRISPR screen revealed that TCAF1 promotes TRPV2-mediated Ca²⁺ release under replication stress by facilitating STING dissociation from TRPV2, activating a CaMKK2/AMPK/Exo1 pathway that protects stalled forks and maintains chromosomal stability.","evidence":"Genome-wide CRISPR screen, Ca²⁺ imaging, co-immunoprecipitation of STING–TRPV2, epistasis analysis of CaMKK2/AMPK/Exo1, chromosomal stability and cell survival assays","pmids":["38816425"],"confidence":"High","gaps":["Whether TCAF1 directly binds TRPV2 or acts indirectly through STING displacement is not resolved","Relative importance of TCAF1's TRPM8-regulatory versus TRPV2/replication-stress functions in vivo is unknown","Whether TCAF1-mediated fork protection operates in non-cancer cell contexts is untested"]},{"year":null,"claim":"Key unresolved questions include the structural basis of TCAF1 interactions with TRP channels, whether TCAF1's TRPM8-trafficking and TRPV2/replication-stress functions are coordinated or context-dependent, and the in vivo physiological consequence of TCAF1 loss.","evidence":"","pmids":[],"confidence":"Low","gaps":["No structural data exist for TCAF1 or any TCAF1–channel complex","No animal knockout or disease model has been reported","Whether TCAF1 regulates additional TRP family members beyond TRPM8 and TRPV2 is unexplored"]}],"mechanism_profile":{"molecular_activity":[{"term_id":"GO:0098772","term_label":"molecular function regulator activity","supporting_discovery_ids":[0,1]}],"localization":[{"term_id":"GO:0005886","term_label":"plasma membrane","supporting_discovery_ids":[0]}],"pathway":[{"term_id":"R-HSA-73894","term_label":"DNA Repair","supporting_discovery_ids":[1]}],"complexes":[],"partners":["TRPM8","TRPV2","STING"],"other_free_text":[]},"mechanistic_narrative":"TCAF1 is a TRP channel-associated regulatory protein that modulates the trafficking and activity of thermoTRP channels and protects genome stability under replication stress. TCAF1 binds TRPM8 and promotes its cell-surface trafficking in prostate epithelial cells, and the TCAF1–TRPM8 complex reduces prostate cancer cell migration speed and directionality, consistent with loss of TCAF1 expression in metastatic specimens [PMID:25559186]. Under replication stress, TCAF1 facilitates dissociation of STING from TRPV2, relieving TRPV2 repression and enabling Ca²⁺ release that activates a CaMKK2/AMPK/Exo1 signaling axis required for stalled replication fork protection and chromosomal stability [PMID:38816425]. TCAF1 and its paralog TCAF2 arose from segmental duplications ~1.7 million years ago and diversified exclusively in Homo sapiens, with copy number variation that may reflect adaptation to environmental pressures [PMID:34433829]."},"prefetch_data":{"uniprot":{"accession":"Q9Y4C2","full_name":"TRPM8 channel-associated factor 1","aliases":["TRP channel-associated factor 1"],"length_aa":921,"mass_kda":102.1,"function":"Positively regulates the plasma membrane cation channel TRPM8 activity. Involved in the recruitment of TRPM8 to the cell surface. 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Both bind to the TRPM8 channel and promote its trafficking to the cell surface, but exert opposing effects on TRPM8 gating: TCAF1/TRPM8 interaction reduces the speed and directionality of migration of prostate cancer cells, consistent with loss of TCAF1 expression in metastatic specimens, while TCAF2 promotes migration.\",\n      \"method\": \"Co-immunoprecipitation, cell surface trafficking assays, functional channel gating recordings, migration assays, and loss-of-function experiments in prostate cancer cells\",\n      \"journal\": \"The Journal of cell biology\",\n      \"confidence\": \"High\",\n      \"confidence_rationale\": \"Tier 2 — reciprocal Co-IP, functional channel assays, and defined cellular phenotype from a single rigorous study with multiple orthogonal methods\",\n      \"pmids\": [\"25559186\"],\n      \"is_preprint\": false\n    },\n    {\n      \"year\": 2024,\n      \"finding\": \"TCAF1 is a key factor promoting TRPV2-mediated Ca2+ release under replication stress. Mechanistically, TCAF1 facilitates dissociation of STING from TRPV2, thereby relieving TRPV2 repression; this Ca2+ release activates CaMKK2/AMPK, leading to Exo1 phosphorylation that prevents aberrant fork processing. TCAF1 is required for fork protection, chromosomal stability, and cell survival after replication stress.\",\n      \"method\": \"Genome-wide CRISPR-based screen, Ca2+ release assays, co-immunoprecipitation (STING–TRPV2 interaction), epistasis analysis (CaMKK2/AMPK/Exo1 pathway), chromosomal stability assays, and cell survival assays after replication stress\",\n      \"journal\": \"Nature communications\",\n      \"confidence\": \"High\",\n      \"confidence_rationale\": \"Tier 2 — genome-wide unbiased screen validated by multiple orthogonal mechanistic assays (Co-IP, Ca2+ imaging, epistasis, chromosomal stability) in a single rigorous study\",\n      \"pmids\": [\"38816425\"],\n      \"is_preprint\": false\n    },\n    {\n      \"year\": 2021,\n      \"finding\": \"TCAF1/TCAF2 copy number variation is substantial in humans, with TCAF duplications originating ~1.7 million years ago and diversifying only in Homo sapiens. TCAF2 expression differs between haplogroups, with high TCAF2 and TRPM8 expression in liver and prostate, supporting a role for TCAF diversification in cold or dietary adaptation.\",\n      \"method\": \"Long-read sequencing to resolve complex segmental duplications, copy number variant analysis across primate genomes, full-length transcript annotation, population genetic selection analysis\",\n      \"journal\": \"Nature communications\",\n      \"confidence\": \"Medium\",\n      \"confidence_rationale\": \"Tier 3 — genomic and evolutionary analysis without direct protein-level functional assays, but uses rigorous long-read sequencing and population genetics\",\n      \"pmids\": [\"34433829\"],\n      \"is_preprint\": false\n    }\n  ],\n  \"current_model\": \"TCAF1 is a dual-function TRPM8/TRPV2-associated regulatory protein: it binds TRPM8, promotes its cell-surface trafficking, and suppresses prostate cancer cell migration; under replication stress it facilitates STING dissociation from TRPV2 to enable TRPV2-mediated Ca2+ release, activating CaMKK2/AMPK/Exo1 signaling to protect stalled replication forks and maintain genome stability.\"\n}\n```","stage2_raw":"```json\n{\n  \"mechanistic_narrative\": \"TCAF1 is a TRP channel-associated factor that physically interacts with TRPM8 and TRPV2 to regulate their trafficking and activity in distinct cellular contexts. TCAF1 binds TRPM8 and promotes its cell-surface trafficking while suppressing channel gating, acting in opposition to TCAF2, which enhances TRPM8 activity; these opposing effects correspondingly modulate prostate cancer cell migration [PMID:25559186]. In the DNA damage response, TCAF1 facilitates TRPV2-mediated Ca²⁺ release from the ER by displacing STING from TRPV2 upon detection of cytosolic DNA, activating a CaMKK2/AMPK/Exo1 signaling axis that protects stressed replication forks and maintains genome stability [PMID:38816425].\",\n  \"teleology\": [\n    {\n      \"year\": 2015,\n      \"claim\": \"Establishing that TCAF1 is a direct binding partner and trafficking regulator of TRPM8 resolved how this cold-sensing channel reaches the plasma membrane and revealed that TCAF1 and TCAF2 exert opposing effects on TRPM8 gating and prostate cancer cell migration.\",\n      \"evidence\": \"Co-immunoprecipitation, cell-surface trafficking assays, patch-clamp electrophysiology, and migration assays in prostate cancer cells\",\n      \"pmids\": [\"25559186\"],\n      \"confidence\": \"High\",\n      \"gaps\": [\n        \"Structural basis of the TCAF1–TRPM8 interaction is undefined\",\n        \"Whether opposing TCAF1/TCAF2 regulation of TRPM8 occurs in non-cancer cell types is untested\",\n        \"Mechanism by which TCAF1 suppresses TRPM8 gating at the molecular level is unknown\"\n      ]\n    },\n    {\n      \"year\": 2024,\n      \"claim\": \"Identification of TCAF1 via a genome-wide screen as a promoter of replication fork protection revealed a second TRP channel axis: TCAF1 displaces STING from TRPV2 to permit ER Ca²⁺ release, activating CaMKK2/AMPK-dependent Exo1 phosphorylation and safeguarding genome stability under replication stress.\",\n      \"evidence\": \"Genome-wide CRISPR screen, Co-IP for STING–TRPV2 dissociation, Ca²⁺ imaging, replication fork protection assays, and chromosomal stability assays\",\n      \"pmids\": [\"38816425\"],\n      \"confidence\": \"High\",\n      \"gaps\": [\n        \"How TCAF1 mechanistically displaces STING from TRPV2 (direct competition vs. allosteric) is unresolved\",\n        \"Whether TCAF1-mediated fork protection operates through additional Ca²⁺-independent pathways has not been examined\",\n        \"In vivo relevance of TCAF1 loss for genome instability phenotypes (e.g., tumor models) is not established\"\n      ]\n    },\n    {\n      \"year\": null,\n      \"claim\": \"It remains unknown how TCAF1's dual roles as a TRP channel regulator (TRPM8 and TRPV2) are coordinated in the same cell, whether tissue-specific expression dictates pathway choice, and what structural features of TCAF1 mediate its distinct channel interactions.\",\n      \"evidence\": \"\",\n      \"pmids\": [],\n      \"confidence\": \"Low\",\n      \"gaps\": [\n        \"No structural model of TCAF1 or its channel-binding interfaces exists\",\n        \"Relative contribution of TRPM8 vs. TRPV2 regulation to TCAF1 function in normal physiology is unknown\",\n        \"Whether TCAF1 regulates additional TRP family members has not been explored\"\n      ]\n    }\n  ],\n  \"mechanism_profile\": {\n    \"molecular_activity\": [\n      {\"term_id\": \"GO:0098772\", \"supporting_discovery_ids\": [0, 1, 2]}\n    ],\n    \"localization\": [\n      {\"term_id\": \"GO:0005783\", \"supporting_discovery_ids\": [2]},\n      {\"term_id\": \"GO:0005886\", \"supporting_discovery_ids\": [0]}\n    ],\n    \"pathway\": [\n      {\"term_id\": \"GO:0009607\", \"supporting_discovery_ids\": []},\n      {\"term_id\": \"R-HSA-162582\", \"supporting_discovery_ids\": [1, 2]},\n      {\"term_id\": \"R-HSA-73894\", \"supporting_discovery_ids\": [2]}\n    ],\n    \"complexes\": [],\n    \"partners\": [\n      \"TRPM8\",\n      \"TRPV2\",\n      \"STING\",\n      \"TCAF2\"\n    ],\n    \"other_free_text\": []\n  }\n}\n```\n\n--- ROUND 2 (R2/R3, augmented corpus) ---\n\n```json\n{\n  \"mechanistic_narrative\": \"TCAF1 is a TRP channel-associated regulatory protein that modulates the trafficking and activity of thermoTRP channels and protects genome stability under replication stress. TCAF1 binds TRPM8 and promotes its cell-surface trafficking in prostate epithelial cells, and the TCAF1–TRPM8 complex reduces prostate cancer cell migration speed and directionality, consistent with loss of TCAF1 expression in metastatic specimens [PMID:25559186]. Under replication stress, TCAF1 facilitates dissociation of STING from TRPV2, relieving TRPV2 repression and enabling Ca²⁺ release that activates a CaMKK2/AMPK/Exo1 signaling axis required for stalled replication fork protection and chromosomal stability [PMID:38816425]. TCAF1 and its paralog TCAF2 arose from segmental duplications ~1.7 million years ago and diversified exclusively in Homo sapiens, with copy number variation that may reflect adaptation to environmental pressures [PMID:34433829].\",\n  \"teleology\": [\n    {\n      \"year\": 2015,\n      \"claim\": \"The identity of TRPM8-associated cofactors was unknown; discovery of TCAF1 as a direct TRPM8-binding partner that promotes channel surface trafficking and suppresses prostate cancer cell migration established it as a functionally important channel-regulatory protein.\",\n      \"evidence\": \"Reciprocal co-immunoprecipitation, surface trafficking assays, electrophysiological recordings, and migration assays in prostate cancer cells\",\n      \"pmids\": [\"25559186\"],\n      \"confidence\": \"High\",\n      \"gaps\": [\n        \"Structural basis of the TCAF1–TRPM8 interaction is unresolved\",\n        \"Whether TCAF1 regulates TRPM8 in non-prostate tissues is untested\",\n        \"Mechanism by which TCAF1 opposes migration beyond channel gating effects is unclear\"\n      ]\n    },\n    {\n      \"year\": 2021,\n      \"claim\": \"How TCAF1/TCAF2 paralogs arose and whether their copy number varies across human populations was unknown; long-read sequencing revealed that TCAF duplications originated ~1.7 Mya and diversified only in Homo sapiens, with population-level copy number variation linked to differential TCAF2/TRPM8 expression.\",\n      \"evidence\": \"Long-read sequencing of complex segmental duplications, primate comparative genomics, population genetic selection analysis\",\n      \"pmids\": [\"34433829\"],\n      \"confidence\": \"Medium\",\n      \"gaps\": [\n        \"Functional consequences of TCAF1 copy number variation on protein activity are not experimentally tested\",\n        \"Whether copy number variation in TCAF1 specifically (vs TCAF2) affects channel regulation is unresolved\",\n        \"Selective pressures driving TCAF diversification remain correlative\"\n      ]\n    },\n    {\n      \"year\": 2024,\n      \"claim\": \"Whether TCAF1 functions beyond TRP channel trafficking was unknown; a genome-wide CRISPR screen revealed that TCAF1 promotes TRPV2-mediated Ca²⁺ release under replication stress by facilitating STING dissociation from TRPV2, activating a CaMKK2/AMPK/Exo1 pathway that protects stalled forks and maintains chromosomal stability.\",\n      \"evidence\": \"Genome-wide CRISPR screen, Ca²⁺ imaging, co-immunoprecipitation of STING–TRPV2, epistasis analysis of CaMKK2/AMPK/Exo1, chromosomal stability and cell survival assays\",\n      \"pmids\": [\"38816425\"],\n      \"confidence\": \"High\",\n      \"gaps\": [\n        \"Whether TCAF1 directly binds TRPV2 or acts indirectly through STING displacement is not resolved\",\n        \"Relative importance of TCAF1's TRPM8-regulatory versus TRPV2/replication-stress functions in vivo is unknown\",\n        \"Whether TCAF1-mediated fork protection operates in non-cancer cell contexts is untested\"\n      ]\n    },\n    {\n      \"year\": null,\n      \"claim\": \"Key unresolved questions include the structural basis of TCAF1 interactions with TRP channels, whether TCAF1's TRPM8-trafficking and TRPV2/replication-stress functions are coordinated or context-dependent, and the in vivo physiological consequence of TCAF1 loss.\",\n      \"evidence\": \"\",\n      \"pmids\": [],\n      \"confidence\": \"Low\",\n      \"gaps\": [\n        \"No structural data exist for TCAF1 or any TCAF1–channel complex\",\n        \"No animal knockout or disease model has been reported\",\n        \"Whether TCAF1 regulates additional TRP family members beyond TRPM8 and TRPV2 is unexplored\"\n      ]\n    }\n  ],\n  \"mechanism_profile\": {\n    \"molecular_activity\": [\n      {\"term_id\": \"GO:0098772\", \"supporting_discovery_ids\": [0, 1]}\n    ],\n    \"localization\": [\n      {\"term_id\": \"GO:0005886\", \"supporting_discovery_ids\": [0]}\n    ],\n    \"pathway\": [\n      {\"term_id\": \"GO:0162582\", \"supporting_discovery_ids\": [0]},\n      {\"term_id\": \"R-HSA-73894\", \"supporting_discovery_ids\": [1]}\n    ],\n    \"complexes\": [],\n    \"partners\": [\"TRPM8\", \"TRPV2\", \"STING\"],\n    \"other_free_text\": []\n  }\n}\n```\n\nWait, I need to fix the pathway term. Let me check — \"R-HSA-162582\" is Signal Transduction. Let me correct that.\n\n```json\n{\n  \"mechanistic_narrative\": \"TCAF1 is a TRP channel-associated regulatory protein that modulates the trafficking and activity of thermoTRP channels and protects genome stability under replication stress. TCAF1 binds TRPM8 and promotes its cell-surface trafficking in prostate epithelial cells, and the TCAF1–TRPM8 complex reduces prostate cancer cell migration speed and directionality, consistent with loss of TCAF1 expression in metastatic specimens [PMID:25559186]. Under replication stress, TCAF1 facilitates dissociation of STING from TRPV2, relieving TRPV2 repression and enabling Ca²⁺ release that activates a CaMKK2/AMPK/Exo1 signaling axis required for stalled replication fork protection and chromosomal stability [PMID:38816425]. TCAF1 and its paralog TCAF2 arose from segmental duplications ~1.7 million years ago and diversified exclusively in Homo sapiens, with copy number variation that may reflect adaptation to environmental pressures [PMID:34433829].\",\n  \"teleology\": [\n    {\n      \"year\": 2015,\n      \"claim\": \"The identity of TRPM8-associated cofactors was unknown; discovery of TCAF1 as a direct TRPM8-binding partner that promotes channel surface trafficking and suppresses prostate cancer cell migration established it as a functionally important channel-regulatory protein.\",\n      \"evidence\": \"Reciprocal co-immunoprecipitation, surface trafficking assays, electrophysiological recordings, and migration assays in prostate cancer cells\",\n      \"pmids\": [\"25559186\"],\n      \"confidence\": \"High\",\n      \"gaps\": [\n        \"Structural basis of the TCAF1–TRPM8 interaction is unresolved\",\n        \"Whether TCAF1 regulates TRPM8 in non-prostate tissues is untested\",\n        \"Mechanism by which TCAF1 opposes migration beyond channel gating effects is unclear\"\n      ]\n    },\n    {\n      \"year\": 2021,\n      \"claim\": \"How TCAF1/TCAF2 paralogs arose and whether their copy number varies across human populations was unknown; long-read sequencing revealed that TCAF duplications originated ~1.7 Mya and diversified only in Homo sapiens, with population-level copy number variation linked to differential TCAF2/TRPM8 expression.\",\n      \"evidence\": \"Long-read sequencing of complex segmental duplications, primate comparative genomics, population genetic selection analysis\",\n      \"pmids\": [\"34433829\"],\n      \"confidence\": \"Medium\",\n      \"gaps\": [\n        \"Functional consequences of TCAF1 copy number variation on protein activity are not experimentally tested\",\n        \"Whether copy number variation in TCAF1 specifically (vs TCAF2) affects channel regulation is unresolved\",\n        \"Selective pressures driving TCAF diversification remain correlative\"\n      ]\n    },\n    {\n      \"year\": 2024,\n      \"claim\": \"Whether TCAF1 functions beyond TRP channel trafficking was unknown; a genome-wide CRISPR screen revealed that TCAF1 promotes TRPV2-mediated Ca²⁺ release under replication stress by facilitating STING dissociation from TRPV2, activating a CaMKK2/AMPK/Exo1 pathway that protects stalled forks and maintains chromosomal stability.\",\n      \"evidence\": \"Genome-wide CRISPR screen, Ca²⁺ imaging, co-immunoprecipitation of STING–TRPV2, epistasis analysis of CaMKK2/AMPK/Exo1, chromosomal stability and cell survival assays\",\n      \"pmids\": [\"38816425\"],\n      \"confidence\": \"High\",\n      \"gaps\": [\n        \"Whether TCAF1 directly binds TRPV2 or acts indirectly through STING displacement is not resolved\",\n        \"Relative importance of TCAF1's TRPM8-regulatory versus TRPV2/replication-stress functions in vivo is unknown\",\n        \"Whether TCAF1-mediated fork protection operates in non-cancer cell contexts is untested\"\n      ]\n    },\n    {\n      \"year\": null,\n      \"claim\": \"Key unresolved questions include the structural basis of TCAF1 interactions with TRP channels, whether TCAF1's TRPM8-trafficking and TRPV2/replication-stress functions are coordinated or context-dependent, and the in vivo physiological consequence of TCAF1 loss.\",\n      \"evidence\": \"\",\n      \"pmids\": [],\n      \"confidence\": \"Low\",\n      \"gaps\": [\n        \"No structural data exist for TCAF1 or any TCAF1–channel complex\",\n        \"No animal knockout or disease model has been reported\",\n        \"Whether TCAF1 regulates additional TRP family members beyond TRPM8 and TRPV2 is unexplored\"\n      ]\n    }\n  ],\n  \"mechanism_profile\": {\n    \"molecular_activity\": [\n      {\"term_id\": \"GO:0098772\", \"supporting_discovery_ids\": [0, 1]}\n    ],\n    \"localization\": [\n      {\"term_id\": \"GO:0005886\", \"supporting_discovery_ids\": [0]}\n    ],\n    \"pathway\": [\n      {\"term_id\": \"R-HSA-162582\", \"supporting_discovery_ids\": [0]},\n      {\"term_id\": \"R-HSA-73894\", \"supporting_discovery_ids\": [1]}\n    ],\n    \"complexes\": [],\n    \"partners\": [\"TRPM8\", \"TRPV2\", \"STING\"],\n    \"other_free_text\": []\n  }\n}\n```"}