{"gene":"TAFA2","run_date":"2026-06-10T10:51:54","timeline":{"discoveries":[{"year":2018,"finding":"TAFA2 deficiency in knockout mice causes severe neuronal reduction and increased apoptosis in the brain via downregulation of PI3K/Akt and MAPK/Erk signaling pathways, with reduced expression of CREB target genes (BDNF, c-fos, NF1) and CBP, indicating TAFA2 functions as a neurotrophic factor essential for neuronal survival.","method":"Knockout mouse model with behavioral tests (Morris water maze, novel object recognition), immunohistochemistry for apoptosis, and Western blot for pathway components","journal":"Acta biochimica et biophysica Sinica","confidence":"Medium","confidence_rationale":"Tier 2 / Moderate — clean KO with defined cellular phenotype and multiple pathway readouts, single lab","pmids":["30137205"],"is_preprint":false},{"year":2018,"finding":"TAFA2 promotes human skeletal (stromal) stem cell (hMSC) migration through activation of the Rac1-p38 signaling pathway, induces lamellipodia formation, and enhances hMSC proliferation without altering osteoblast or adipocyte differentiation. Interleukin-1β was identified as an upstream regulator of TAFA2 expression during fracture healing.","method":"In vitro trans-well migration assay, high-content image analysis, Rac1 activity assay, p38 pathway inhibition, in vivo closed femoral fracture mouse model, serum TAFA2 measurement in hip fracture patients","journal":"Stem cells (Dayton, Ohio)","confidence":"Medium","confidence_rationale":"Tier 2 / Moderate — defined cellular phenotype with pathway inhibition experiments, single lab, multiple orthogonal methods","pmids":["30485583"],"is_preprint":false},{"year":2023,"finding":"TAFA2 directly binds to ADGRL1 (latrophilin-1) through ADGRL1's lectin-like domain, and this interaction activates the cAMP/PKA/CREB/BCL2 signaling pathway to suppress neuronal apoptosis. Deletion of the lectin-like domain (ADGRL1ΔLec) or ADGRL1 knockout abolished TAFA2's anti-apoptotic effects.","method":"Co-immunoprecipitation, quantitative mass spectrometry-based proteomic analysis in V5 knockin mouse brain lysates, pull-down assays, ADGRL1 knockout, overexpression, and lectin-domain deletion mutant functional analysis, measurement of cAMP, p-PKA, p-CREB, and BCL2 levels","journal":"Life sciences","confidence":"High","confidence_rationale":"Tier 1-2 / Strong — receptor identified by Co-IP + MS, validated by pull-down, mechanistic pathway confirmed with KO and domain-deletion mutant, multiple orthogonal methods in one study","pmids":["37944639"],"is_preprint":false},{"year":2025,"finding":"Neuron-derived TAFA2 interacts with chemokine receptor CCR2 and promotes macrophage activation and liver injury. TAFA2 induced expression of inflammatory genes in wild-type macrophages but not in Ccr2 knockout macrophages. TAFA2 ablation or neuron-specific knockdown reduced liver ischaemia-reperfusion injury.","method":"FLAG-tagged TAFA2 co-immunoprecipitation to identify CCR2 interaction, RNA sequencing of macrophages, Ccr2 knockout macrophage experiments, in vivo TAFA2 ablation and neuron-specific knockdown mouse models, single-cell sequencing","journal":"Journal of hepatology","confidence":"Medium","confidence_rationale":"Tier 2 / Moderate — Co-IP for receptor identification, KO macrophage functional rescue, in vivo KD, single lab with multiple orthogonal methods","pmids":["40058705"],"is_preprint":false}],"current_model":"TAFA2 is a secreted neurokine that promotes neuronal survival by binding to the lectin-like domain of ADGRL1 to activate cAMP/PKA/CREB/BCL2 signaling, recruits CCR2+ macrophages via direct interaction with CCR2 to modulate neuroinflammatory and liver injury responses, and promotes skeletal stem cell migration through Rac1-p38 pathway activation downstream of IL-1β stimulation."},"narrative":{"mechanistic_narrative":"TAFA2 is a secreted neurokine that acts as a neurotrophic factor essential for neuronal survival and as a paracrine modulator of cell migration and inflammation [PMID:30137205, PMID:37944639]. In the brain, TAFA2 suppresses neuronal apoptosis by binding directly to the lectin-like domain of the adhesion GPCR ADGRL1 (latrophilin-1), activating cAMP/PKA/CREB/BCL2 signaling; deletion of the lectin domain or ADGRL1 knockout abolishes its anti-apoptotic effect [PMID:37944639]. Consistent with this pro-survival role, TAFA2 loss in knockout mice produces severe neuronal reduction and apoptosis accompanied by downregulation of PI3K/Akt and MAPK/Erk signaling and reduced CREB target gene expression [PMID:30137205]. Beyond the nervous system, TAFA2 drives human skeletal stem cell migration and proliferation through Rac1-p38 pathway activation, with IL-1β acting as an upstream inducer during fracture healing [PMID:30485583]. Neuron-derived TAFA2 also engages the chemokine receptor CCR2 to promote macrophage activation and aggravate liver ischaemia-reperfusion injury, an effect lost in Ccr2-deficient macrophages [PMID:40058705].","teleology":[{"year":2018,"claim":"Establishing whether TAFA2 has a non-redundant physiological role, loss-of-function in mice defined it as a neurotrophic factor required for neuronal survival.","evidence":"Knockout mouse with behavioral testing, apoptosis immunohistochemistry, and Western blot of survival pathway components","pmids":["30137205"],"confidence":"Medium","gaps":["Did not identify the receptor mediating the survival signal","Pathway readouts correlative without direct receptor linkage"]},{"year":2018,"claim":"Extending TAFA2's role beyond neurons, it was shown to drive skeletal stem cell migration and proliferation, linking it to tissue repair.","evidence":"In vitro migration assays, Rac1 activity assay, p38 inhibition, in vivo femoral fracture model, and patient serum measurement","pmids":["30485583"],"confidence":"Medium","gaps":["Receptor on skeletal stem cells not identified","Mechanism connecting IL-1β induction to TAFA2 secretion unresolved"]},{"year":2023,"claim":"Identifying the long-missing receptor, TAFA2 was shown to bind ADGRL1's lectin-like domain and signal through cAMP/PKA/CREB/BCL2 to block neuronal apoptosis.","evidence":"Co-IP plus quantitative mass spectrometry in V5 knockin brain lysates, pull-down, ADGRL1 knockout and lectin-domain deletion functional analysis","pmids":["37944639"],"confidence":"High","gaps":["Structural basis of the lectin-domain interaction not resolved","Relationship between ADGRL1 signaling and the earlier PI3K/Akt-MAPK readouts not reconciled"]},{"year":2025,"claim":"Revealing a pro-inflammatory function, neuron-derived TAFA2 was shown to engage CCR2 to activate macrophages and worsen liver injury.","evidence":"FLAG-tagged TAFA2 Co-IP identifying CCR2, macrophage RNA-seq, Ccr2 knockout rescue, in vivo ablation and neuron-specific knockdown, single-cell sequencing","pmids":["40058705"],"confidence":"Medium","gaps":["CCR2 binding shown by Co-IP without reciprocal structural validation","How a neuronal secreted factor reaches liver macrophages not fully defined"]},{"year":null,"claim":"It remains unresolved how TAFA2 selects among its distinct receptors (ADGRL1 versus CCR2) in different tissues and whether a single receptor mediates its skeletal stem cell effects.","evidence":"","pmids":[],"confidence":"Medium","gaps":["No receptor assigned for the skeletal stem cell Rac1-p38 response","Determinants of context-specific receptor engagement unknown"]}],"mechanism_profile":{"molecular_activity":[{"term_id":"GO:0048018","term_label":"receptor ligand activity","supporting_discovery_ids":[2,3]},{"term_id":"GO:0098772","term_label":"molecular function regulator activity","supporting_discovery_ids":[0,2]}],"localization":[{"term_id":"GO:0005576","term_label":"extracellular region","supporting_discovery_ids":[1,3]}],"pathway":[{"term_id":"R-HSA-162582","term_label":"Signal Transduction","supporting_discovery_ids":[2,3]},{"term_id":"R-HSA-168256","term_label":"Immune System","supporting_discovery_ids":[3]},{"term_id":"R-HSA-5357801","term_label":"Programmed Cell Death","supporting_discovery_ids":[0,2]}],"complexes":[],"partners":["ADGRL1","CCR2"],"other_free_text":[]}},"prefetch_data":{"uniprot":{"accession":"Q8N3H0","full_name":"Chemokine-like protein TAFA-2","aliases":[],"length_aa":131,"mass_kda":14.6,"function":"Has a role as neurotrophic factor involved in neuronal survival and neurobiological functions","subcellular_location":"Cytoplasm; Nucleus","url":"https://www.uniprot.org/uniprotkb/Q8N3H0/entry"},"depmap":{"release":"DepMap","has_data":true,"is_common_essential":false,"resolved_as":"","url":"https://depmap.org/portal/gene/TAFA2","classification":"Not Classified","n_dependent_lines":0,"n_total_lines":1208,"dependency_fraction":0.0},"opencell":{"profiled":false,"resolved_as":"","ensg_id":"","cell_line_id":"","localizations":[],"interactors":[],"url":"https://opencell.sf.czbiohub.org/search/TAFA2","total_profiled":1310},"omim":[{"mim_id":"617496","title":"FAMILY WITH SEQUENCE SIMILARITY 19, MEMBER A2, CC MOTIF CHEMOKINE-LIKE; FAM19A2","url":"https://www.omim.org/entry/617496"}],"hpa":{"profiled":true,"resolved_as":"","reliability":"","locations":[],"tissue_specificity":"Tissue enhanced","tissue_distribution":"Detected in many","driving_tissues":[{"tissue":"brain","ntpm":18.4}],"url":"https://www.proteinatlas.org/search/TAFA2"},"hgnc":{"alias_symbol":["TAFA-2"],"prev_symbol":["FAM19A2"]},"alphafold":{"accession":"Q8N3H0","domains":[{"cath_id":"-","chopping":"42-127","consensus_level":"medium","plddt":96.1336,"start":42,"end":127}],"viewer_url":"https://alphafold.ebi.ac.uk/entry/Q8N3H0","model_url":"https://alphafold.ebi.ac.uk/files/AF-Q8N3H0-F1-model_v6.cif","pae_url":"https://alphafold.ebi.ac.uk/files/AF-Q8N3H0-F1-predicted_aligned_error_v6.png","plddt_mean":88.31},"mouse_models":{"mgi_url":"https://www.informatics.jax.org/marker/summary?nomen=TAFA2","jax_strain_url":"https://www.jax.org/strain/search?query=TAFA2"},"sequence":{"accession":"Q8N3H0","fasta_url":"https://rest.uniprot.org/uniprotkb/Q8N3H0.fasta","uniprot_url":"https://www.uniprot.org/uniprotkb/Q8N3H0/entry","alphafold_viewer_url":"https://alphafold.ebi.ac.uk/entry/Q8N3H0"}},"corpus_meta":[{"pmid":"22464253","id":"PMC_22464253","title":"Identification of IRF8, TMEM39A, and IKZF3-ZPBP2 as susceptibility loci for systemic lupus erythematosus in a large-scale multiracial replication study.","date":"2012","source":"American journal of human genetics","url":"https://pubmed.ncbi.nlm.nih.gov/22464253","citation_count":156,"is_preprint":false},{"pmid":"16160854","id":"PMC_16160854","title":"Molecular analysis of a constitutional complex genome rearrangement with 11 breakpoints involving chromosomes 3, 11, 12, and 21 and a approximately 0.5-Mb submicroscopic deletion in a patient with mild mental retardation.","date":"2005","source":"Human genetics","url":"https://pubmed.ncbi.nlm.nih.gov/16160854","citation_count":32,"is_preprint":false},{"pmid":"35712659","id":"PMC_35712659","title":"Molecular Structure, Expression and Role of TAFA4 and its Receptor FPR1 in the Spinal Cord.","date":"2022","source":"Frontiers in cell and developmental 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Induces Skeletal (Stromal) Stem Cell Migration Through Activation of Rac1-p38 Signaling.","date":"2018","source":"Stem cells (Dayton, Ohio)","url":"https://pubmed.ncbi.nlm.nih.gov/30485583","citation_count":19,"is_preprint":false},{"pmid":"37944639","id":"PMC_37944639","title":"Neuronal survival factor TAFA2 suppresses apoptosis through binding to ADGRL1 and activating cAMP/PKA/CREB/BCL2 signaling pathway.","date":"2023","source":"Life sciences","url":"https://pubmed.ncbi.nlm.nih.gov/37944639","citation_count":15,"is_preprint":false},{"pmid":"35606283","id":"PMC_35606283","title":"A genome-wide association study on frequent exacerbation of asthma depending on smoking status.","date":"2022","source":"Respiratory medicine","url":"https://pubmed.ncbi.nlm.nih.gov/35606283","citation_count":10,"is_preprint":false},{"pmid":"40058705","id":"PMC_40058705","title":"Sour neuronal signalling attenuates macrophage-mediated liver injury.","date":"2025","source":"Journal of 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safety","url":"https://pubmed.ncbi.nlm.nih.gov/41719982","citation_count":0,"is_preprint":false}],"cost":{"stage1":{"model":"claude-sonnet-4-6","input_tokens":9038,"output_tokens":1224,"usd":0.022737,"stage1_stop_reason":"end_turn"},"stage2":{"model":"claude-opus-4-8","input_tokens":7861,"output_tokens":1901,"usd":0.043415,"stage2_stop_reason":"end_turn"},"total_usd":0.066152,"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\": \"TAFA2 deficiency in knockout mice causes severe neuronal reduction and increased apoptosis in the brain via downregulation of PI3K/Akt and MAPK/Erk signaling pathways, with reduced expression of CREB target genes (BDNF, c-fos, NF1) and CBP, indicating TAFA2 functions as a neurotrophic factor essential for neuronal survival.\",\n      \"method\": \"Knockout mouse model with behavioral tests (Morris water maze, novel object recognition), immunohistochemistry for apoptosis, and Western blot for pathway components\",\n      \"journal\": \"Acta biochimica et biophysica Sinica\",\n      \"confidence\": \"Medium\",\n      \"confidence_rationale\": \"Tier 2 / Moderate — clean KO with defined cellular phenotype and multiple pathway readouts, single lab\",\n      \"pmids\": [\"30137205\"],\n      \"is_preprint\": false\n    },\n    {\n      \"year\": 2018,\n      \"finding\": \"TAFA2 promotes human skeletal (stromal) stem cell (hMSC) migration through activation of the Rac1-p38 signaling pathway, induces lamellipodia formation, and enhances hMSC proliferation without altering osteoblast or adipocyte differentiation. Interleukin-1β was identified as an upstream regulator of TAFA2 expression during fracture healing.\",\n      \"method\": \"In vitro trans-well migration assay, high-content image analysis, Rac1 activity assay, p38 pathway inhibition, in vivo closed femoral fracture mouse model, serum TAFA2 measurement in hip fracture patients\",\n      \"journal\": \"Stem cells (Dayton, Ohio)\",\n      \"confidence\": \"Medium\",\n      \"confidence_rationale\": \"Tier 2 / Moderate — defined cellular phenotype with pathway inhibition experiments, single lab, multiple orthogonal methods\",\n      \"pmids\": [\"30485583\"],\n      \"is_preprint\": false\n    },\n    {\n      \"year\": 2023,\n      \"finding\": \"TAFA2 directly binds to ADGRL1 (latrophilin-1) through ADGRL1's lectin-like domain, and this interaction activates the cAMP/PKA/CREB/BCL2 signaling pathway to suppress neuronal apoptosis. Deletion of the lectin-like domain (ADGRL1ΔLec) or ADGRL1 knockout abolished TAFA2's anti-apoptotic effects.\",\n      \"method\": \"Co-immunoprecipitation, quantitative mass spectrometry-based proteomic analysis in V5 knockin mouse brain lysates, pull-down assays, ADGRL1 knockout, overexpression, and lectin-domain deletion mutant functional analysis, measurement of cAMP, p-PKA, p-CREB, and BCL2 levels\",\n      \"journal\": \"Life sciences\",\n      \"confidence\": \"High\",\n      \"confidence_rationale\": \"Tier 1-2 / Strong — receptor identified by Co-IP + MS, validated by pull-down, mechanistic pathway confirmed with KO and domain-deletion mutant, multiple orthogonal methods in one study\",\n      \"pmids\": [\"37944639\"],\n      \"is_preprint\": false\n    },\n    {\n      \"year\": 2025,\n      \"finding\": \"Neuron-derived TAFA2 interacts with chemokine receptor CCR2 and promotes macrophage activation and liver injury. TAFA2 induced expression of inflammatory genes in wild-type macrophages but not in Ccr2 knockout macrophages. TAFA2 ablation or neuron-specific knockdown reduced liver ischaemia-reperfusion injury.\",\n      \"method\": \"FLAG-tagged TAFA2 co-immunoprecipitation to identify CCR2 interaction, RNA sequencing of macrophages, Ccr2 knockout macrophage experiments, in vivo TAFA2 ablation and neuron-specific knockdown mouse models, single-cell sequencing\",\n      \"journal\": \"Journal of hepatology\",\n      \"confidence\": \"Medium\",\n      \"confidence_rationale\": \"Tier 2 / Moderate — Co-IP for receptor identification, KO macrophage functional rescue, in vivo KD, single lab with multiple orthogonal methods\",\n      \"pmids\": [\"40058705\"],\n      \"is_preprint\": false\n    }\n  ],\n  \"current_model\": \"TAFA2 is a secreted neurokine that promotes neuronal survival by binding to the lectin-like domain of ADGRL1 to activate cAMP/PKA/CREB/BCL2 signaling, recruits CCR2+ macrophages via direct interaction with CCR2 to modulate neuroinflammatory and liver injury responses, and promotes skeletal stem cell migration through Rac1-p38 pathway activation downstream of IL-1β stimulation.\"\n}\n```","stage2_raw":"{\n  \"mechanistic_narrative\": \"TAFA2 is a secreted neurokine that acts as a neurotrophic factor essential for neuronal survival and as a paracrine modulator of cell migration and inflammation [#0, #2]. In the brain, TAFA2 suppresses neuronal apoptosis by binding directly to the lectin-like domain of the adhesion GPCR ADGRL1 (latrophilin-1), activating cAMP/PKA/CREB/BCL2 signaling; deletion of the lectin domain or ADGRL1 knockout abolishes its anti-apoptotic effect [#2]. Consistent with this pro-survival role, TAFA2 loss in knockout mice produces severe neuronal reduction and apoptosis accompanied by downregulation of PI3K/Akt and MAPK/Erk signaling and reduced CREB target gene expression [#0]. Beyond the nervous system, TAFA2 drives human skeletal stem cell migration and proliferation through Rac1-p38 pathway activation, with IL-1\\u03b2 acting as an upstream inducer during fracture healing [#1]. Neuron-derived TAFA2 also engages the chemokine receptor CCR2 to promote macrophage activation and aggravate liver ischaemia-reperfusion injury, an effect lost in Ccr2-deficient macrophages [#3].\",\n  \"teleology\": [\n    {\n      \"year\": 2018,\n      \"claim\": \"Establishing whether TAFA2 has a non-redundant physiological role, loss-of-function in mice defined it as a neurotrophic factor required for neuronal survival.\",\n      \"evidence\": \"Knockout mouse with behavioral testing, apoptosis immunohistochemistry, and Western blot of survival pathway components\",\n      \"pmids\": [\"30137205\"],\n      \"confidence\": \"Medium\",\n      \"gaps\": [\"Did not identify the receptor mediating the survival signal\", \"Pathway readouts correlative without direct receptor linkage\"]\n    },\n    {\n      \"year\": 2018,\n      \"claim\": \"Extending TAFA2's role beyond neurons, it was shown to drive skeletal stem cell migration and proliferation, linking it to tissue repair.\",\n      \"evidence\": \"In vitro migration assays, Rac1 activity assay, p38 inhibition, in vivo femoral fracture model, and patient serum measurement\",\n      \"pmids\": [\"30485583\"],\n      \"confidence\": \"Medium\",\n      \"gaps\": [\"Receptor on skeletal stem cells not identified\", \"Mechanism connecting IL-1\\u03b2 induction to TAFA2 secretion unresolved\"]\n    },\n    {\n      \"year\": 2023,\n      \"claim\": \"Identifying the long-missing receptor, TAFA2 was shown to bind ADGRL1's lectin-like domain and signal through cAMP/PKA/CREB/BCL2 to block neuronal apoptosis.\",\n      \"evidence\": \"Co-IP plus quantitative mass spectrometry in V5 knockin brain lysates, pull-down, ADGRL1 knockout and lectin-domain deletion functional analysis\",\n      \"pmids\": [\"37944639\"],\n      \"confidence\": \"High\",\n      \"gaps\": [\"Structural basis of the lectin-domain interaction not resolved\", \"Relationship between ADGRL1 signaling and the earlier PI3K/Akt-MAPK readouts not reconciled\"]\n    },\n    {\n      \"year\": 2025,\n      \"claim\": \"Revealing a pro-inflammatory function, neuron-derived TAFA2 was shown to engage CCR2 to activate macrophages and worsen liver injury.\",\n      \"evidence\": \"FLAG-tagged TAFA2 Co-IP identifying CCR2, macrophage RNA-seq, Ccr2 knockout rescue, in vivo ablation and neuron-specific knockdown, single-cell sequencing\",\n      \"pmids\": [\"40058705\"],\n      \"confidence\": \"Medium\",\n      \"gaps\": [\"CCR2 binding shown by Co-IP without reciprocal structural validation\", \"How a neuronal secreted factor reaches liver macrophages not fully defined\"]\n    },\n    {\n      \"year\": null,\n      \"claim\": \"It remains unresolved how TAFA2 selects among its distinct receptors (ADGRL1 versus CCR2) in different tissues and whether a single receptor mediates its skeletal stem cell effects.\",\n      \"evidence\": \"\",\n      \"pmids\": [],\n      \"confidence\": \"Medium\",\n      \"gaps\": [\"No receptor assigned for the skeletal stem cell Rac1-p38 response\", \"Determinants of context-specific receptor engagement unknown\"]\n    }\n  ],\n  \"mechanism_profile\": {\n    \"molecular_activity\": [\n      {\"term_id\": \"GO:0048018\", \"supporting_discovery_ids\": [2, 3]},\n      {\"term_id\": \"GO:0098772\", \"supporting_discovery_ids\": [0, 2]}\n    ],\n    \"localization\": [\n      {\"term_id\": \"GO:0005576\", \"supporting_discovery_ids\": [1, 3]}\n    ],\n    \"pathway\": [\n      {\"term_id\": \"R-HSA-162582\", \"supporting_discovery_ids\": [2, 3]},\n      {\"term_id\": \"R-HSA-168256\", \"supporting_discovery_ids\": [3]},\n      {\"term_id\": \"R-HSA-5357801\", \"supporting_discovery_ids\": [0, 2]}\n    ],\n    \"complexes\": [],\n    \"partners\": [\"ADGRL1\", \"CCR2\"],\n    \"other_free_text\": []\n  }\n}","audit_flag":null,"evaluation":{"pairwise":"win","faith_supported":5,"faith_total":5,"faith_pct":100.0}}