{"gene":"AP3M1","run_date":"2026-06-09T22:02:43","timeline":{"discoveries":[{"year":2017,"finding":"AP3M1 acts as a component of the AP-3 complex, where AP3B1 serves as a rate-limiting step in complex assembly: depletion of AP3B1 induces decreased abundance of AP3M1, consistent with AP3B1 controlling the stoichiometry of AP3M1 within the complex. This interaction was experimentally confirmed at the protein level.","method":"Proteomics (CPTAC/TCGA datasets) combined with experimental confirmation of AP3B1–AP3M1 interaction and co-regulation","journal":"Cell systems","confidence":"Medium","confidence_rationale":"Tier 2 / Weak — single lab, experimental confirmation of complex interaction and rate-limiting assembly step, but abstract does not detail the specific orthogonal methods used for confirmation","pmids":["29032074"],"is_preprint":false}],"current_model":"AP3M1 is the mu-1 subunit of the AP-3 adaptor protein complex, where AP3B1 functions as a rate-limiting assembly factor whose depletion reduces AP3M1 protein abundance, indicating that AP3M1 stability and complex stoichiometry depend on AP3B1."},"narrative":{"mechanistic_narrative":"AP3M1 is a subunit of the AP-3 adaptor protein complex whose abundance is governed by the complex's assembly dynamics [PMID:29032074]. Within this complex, AP3B1 acts as a rate-limiting assembly factor: depletion of AP3B1 reduces AP3M1 protein abundance, indicating that AP3M1 stability and stoichiometry depend on co-regulation with AP3B1 [PMID:29032074]. Beyond this co-regulatory relationship within the AP-3 complex, no further mechanistic detail for AP3M1 has been characterized in the available corpus.","teleology":[{"year":2017,"claim":"It was unclear how AP3M1 abundance is controlled within the AP-3 complex; proteomic analysis with experimental confirmation showed AP3B1 is a rate-limiting assembly factor whose loss reduces AP3M1 levels, establishing that AP3M1 stoichiometry is co-regulated by AP3B1.","evidence":"Proteomics across CPTAC/TCGA datasets combined with experimental confirmation of the AP3B1–AP3M1 interaction and co-regulation","pmids":["29032074"],"confidence":"Medium","gaps":["Specific orthogonal methods confirming the interaction are not detailed","Cargo selectivity and vesicle-trafficking function of AP3M1 not addressed","Subcellular localization of AP3M1 not established in this finding"]},{"year":null,"claim":"The direct molecular activity, cargo-recognition role, and subcellular localization of AP3M1 within AP-3-mediated trafficking remain uncharacterized in the available corpus.","evidence":"","pmids":[],"confidence":"Medium","gaps":["No defined molecular function for AP3M1","No characterized localization","No identified cargo or trafficking pathway"]}],"mechanism_profile":{"molecular_activity":[],"localization":[],"pathway":[],"complexes":["AP-3 adaptor complex"],"partners":["AP3B1"],"other_free_text":[]}},"prefetch_data":{"uniprot":{"accession":"Q9Y2T2","full_name":"AP-3 complex subunit mu-1","aliases":["AP-3 adaptor complex mu3A subunit","Adaptor-related protein complex 3 subunit mu-1","Mu-adaptin 3A","Mu3A-adaptin"],"length_aa":418,"mass_kda":46.9,"function":"Part of the AP-3 complex, an adaptor-related complex which is not clathrin-associated. The complex is associated with the Golgi region as well as more peripheral structures. It facilitates the budding of vesicles from the Golgi membrane and may be directly involved in trafficking to lysosomes. In concert with the BLOC-1 complex, AP-3 is required to target cargos into vesicles assembled at cell bodies for delivery into neurites and nerve terminals","subcellular_location":"Golgi apparatus; Cytoplasmic vesicle membrane","url":"https://www.uniprot.org/uniprotkb/Q9Y2T2/entry"},"depmap":{"release":"DepMap","has_data":true,"is_common_essential":false,"resolved_as":"","url":"https://depmap.org/portal/gene/AP3M1","classification":"Not Classified","n_dependent_lines":16,"n_total_lines":1208,"dependency_fraction":0.013245033112582781},"opencell":{"profiled":false,"resolved_as":"","ensg_id":"","cell_line_id":"","localizations":[],"interactors":[],"url":"https://opencell.sf.czbiohub.org/search/AP3M1","total_profiled":1310},"omim":[{"mim_id":"610469","title":"ADAPTOR-RELATED PROTEIN COMPLEX 3, MU-2 SUBUNIT; AP3M2","url":"https://www.omim.org/entry/610469"},{"mim_id":"610366","title":"ADAPTOR-RELATED PROTEIN COMPLEX 3, MU-1 SUBUNIT; AP3M1","url":"https://www.omim.org/entry/610366"},{"mim_id":"607246","title":"ADAPTOR-RELATED PROTEIN COMPLEX 3, DELTA-1 SUBUNIT; AP3D1","url":"https://www.omim.org/entry/607246"},{"mim_id":"607042","title":"CLN3 LYSOSOMAL/ENDOSOMAL TRANSMEMBRANE PROTEIN, BATTENIN; CLN3","url":"https://www.omim.org/entry/607042"}],"hpa":{"profiled":true,"resolved_as":"","reliability":"","locations":[],"tissue_specificity":"Low tissue specificity","tissue_distribution":"Detected in all","driving_tissues":[],"url":"https://www.proteinatlas.org/search/AP3M1"},"hgnc":{"alias_symbol":[],"prev_symbol":[]},"alphafold":{"accession":"Q9Y2T2","domains":[{"cath_id":"3.30.450.60","chopping":"1-147","consensus_level":"high","plddt":91.135,"start":1,"end":147},{"cath_id":"2.60.40.1170","chopping":"177-268_387-406","consensus_level":"high","plddt":95.2331,"start":177,"end":406},{"cath_id":"2.60.40.1170","chopping":"273-379","consensus_level":"high","plddt":94.4603,"start":273,"end":379}],"viewer_url":"https://alphafold.ebi.ac.uk/entry/Q9Y2T2","model_url":"https://alphafold.ebi.ac.uk/files/AF-Q9Y2T2-F1-model_v6.cif","pae_url":"https://alphafold.ebi.ac.uk/files/AF-Q9Y2T2-F1-predicted_aligned_error_v6.png","plddt_mean":91.88},"mouse_models":{"mgi_url":"https://www.informatics.jax.org/marker/summary?nomen=AP3M1","jax_strain_url":"https://www.jax.org/strain/search?query=AP3M1"},"sequence":{"accession":"Q9Y2T2","fasta_url":"https://rest.uniprot.org/uniprotkb/Q9Y2T2.fasta","uniprot_url":"https://www.uniprot.org/uniprotkb/Q9Y2T2/entry","alphafold_viewer_url":"https://alphafold.ebi.ac.uk/entry/Q9Y2T2"}},"corpus_meta":[{"pmid":"29032074","id":"PMC_29032074","title":"Widespread Post-transcriptional Attenuation of Genomic Copy-Number Variation in Cancer.","date":"2017","source":"Cell systems","url":"https://pubmed.ncbi.nlm.nih.gov/29032074","citation_count":95,"is_preprint":false},{"pmid":"39149122","id":"PMC_39149122","title":"Identification of programmed cell death-related genes and diagnostic biomarkers in endometriosis using a machine learning and Mendelian randomization approach.","date":"2024","source":"Frontiers in endocrinology","url":"https://pubmed.ncbi.nlm.nih.gov/39149122","citation_count":15,"is_preprint":false},{"pmid":"19481122","id":"PMC_19481122","title":"Association analysis between schizophrenia and the AP-3 complex genes.","date":"2009","source":"Neuroscience research","url":"https://pubmed.ncbi.nlm.nih.gov/19481122","citation_count":9,"is_preprint":false},{"pmid":"17125464","id":"PMC_17125464","title":"Downregulation of genes encoding for subunits of adaptor complex-3 in cervical carcinomas.","date":"2006","source":"Biochemistry. Biokhimiia","url":"https://pubmed.ncbi.nlm.nih.gov/17125464","citation_count":9,"is_preprint":false},{"pmid":"36183948","id":"PMC_36183948","title":"Zhachong Shisanwei Pill resists ischemic stroke by lysosome pathway based on proteomics and bioinformatics.","date":"2022","source":"Journal of ethnopharmacology","url":"https://pubmed.ncbi.nlm.nih.gov/36183948","citation_count":8,"is_preprint":false},{"pmid":"37931855","id":"PMC_37931855","title":"Therapeutic targets for endometriosis: Genome-wide Mendelian randomization and colocalization analyses.","date":"2023","source":"Gene","url":"https://pubmed.ncbi.nlm.nih.gov/37931855","citation_count":5,"is_preprint":false},{"pmid":"41009665","id":"PMC_41009665","title":"Proteomic Screening for Cellular Targets of the Duck Enteritis Virus Protein VP26 Reveals That the Host Actin-Myosin II Network Regulates the Proliferation of the Virus.","date":"2025","source":"International journal of molecular sciences","url":"https://pubmed.ncbi.nlm.nih.gov/41009665","citation_count":0,"is_preprint":false},{"pmid":null,"id":"bio_10.1101_2024.08.02.24310874","title":"Genetics of Cardiac Aging Implicate Organ-Specific Variation","date":"2024-08-06","source":"bioRxiv","url":"https://doi.org/10.1101/2024.08.02.24310874","citation_count":0,"is_preprint":true}],"cost":{"stage1":{"model":"claude-sonnet-4-6","input_tokens":6422,"output_tokens":335,"usd":0.012146,"stage1_stop_reason":"end_turn"},"stage2":{"model":"claude-opus-4-8","input_tokens":6575,"output_tokens":817,"usd":0.02665,"stage2_stop_reason":"end_turn"},"total_usd":0.038796,"stage1_batch_id":"msgbatch_0179Z2pxRYBsXi2xADneafRw","stage2_batch_id":"msgbatch_01LaY9ZaVdgjWArcZo9eqQE5","note":"batch pricing = 50% of standard"},"stage1_raw":"```json\n{\n  \"discoveries\": [\n    {\n      \"year\": 2017,\n      \"finding\": \"AP3M1 acts as a component of the AP-3 complex, where AP3B1 serves as a rate-limiting step in complex assembly: depletion of AP3B1 induces decreased abundance of AP3M1, consistent with AP3B1 controlling the stoichiometry of AP3M1 within the complex. This interaction was experimentally confirmed at the protein level.\",\n      \"method\": \"Proteomics (CPTAC/TCGA datasets) combined with experimental confirmation of AP3B1–AP3M1 interaction and co-regulation\",\n      \"journal\": \"Cell systems\",\n      \"confidence\": \"Medium\",\n      \"confidence_rationale\": \"Tier 2 / Weak — single lab, experimental confirmation of complex interaction and rate-limiting assembly step, but abstract does not detail the specific orthogonal methods used for confirmation\",\n      \"pmids\": [\"29032074\"],\n      \"is_preprint\": false\n    }\n  ],\n  \"current_model\": \"AP3M1 is the mu-1 subunit of the AP-3 adaptor protein complex, where AP3B1 functions as a rate-limiting assembly factor whose depletion reduces AP3M1 protein abundance, indicating that AP3M1 stability and complex stoichiometry depend on AP3B1.\"\n}\n```","stage2_raw":"{\n  \"mechanistic_narrative\": \"AP3M1 is a subunit of the AP-3 adaptor protein complex whose abundance is governed by the complex's assembly dynamics [#0]. Within this complex, AP3B1 acts as a rate-limiting assembly factor: depletion of AP3B1 reduces AP3M1 protein abundance, indicating that AP3M1 stability and stoichiometry depend on co-regulation with AP3B1 [#0]. Beyond this co-regulatory relationship within the AP-3 complex, no further mechanistic detail for AP3M1 has been characterized in the available corpus.\",\n  \"teleology\": [\n    {\n      \"year\": 2017,\n      \"claim\": \"It was unclear how AP3M1 abundance is controlled within the AP-3 complex; proteomic analysis with experimental confirmation showed AP3B1 is a rate-limiting assembly factor whose loss reduces AP3M1 levels, establishing that AP3M1 stoichiometry is co-regulated by AP3B1.\",\n      \"evidence\": \"Proteomics across CPTAC/TCGA datasets combined with experimental confirmation of the AP3B1–AP3M1 interaction and co-regulation\",\n      \"pmids\": [\n        \"29032074\"\n      ],\n      \"confidence\": \"Medium\",\n      \"gaps\": [\n        \"Specific orthogonal methods confirming the interaction are not detailed\",\n        \"Cargo selectivity and vesicle-trafficking function of AP3M1 not addressed\",\n        \"Subcellular localization of AP3M1 not established in this finding\"\n      ]\n    },\n    {\n      \"year\": null,\n      \"claim\": \"The direct molecular activity, cargo-recognition role, and subcellular localization of AP3M1 within AP-3-mediated trafficking remain uncharacterized in the available corpus.\",\n      \"evidence\": \"\",\n      \"pmids\": [],\n      \"confidence\": \"Medium\",\n      \"gaps\": [\n        \"No defined molecular function for AP3M1\",\n        \"No characterized localization\",\n        \"No identified cargo or trafficking pathway\"\n      ]\n    }\n  ],\n  \"mechanism_profile\": {\n    \"molecular_activity\": [],\n    \"localization\": [],\n    \"pathway\": [],\n    \"complexes\": [\n      \"AP-3 adaptor complex\"\n    ],\n    \"partners\": [\n      \"AP3B1\"\n    ],\n    \"other_free_text\": []\n  }\n}","audit_flag":null,"evaluation":{"pairwise":"loss","faith_supported":1,"faith_total":2,"faith_pct":50.0}}