{"gene":"RFXANK","run_date":"2026-04-28T19:45:45","timeline":{"discoveries":[{"year":1999,"finding":"RFXANK (RFX-B) was identified as the smallest subunit of the trimeric RFX transcription factor complex; it contains three ankyrin repeats important for protein-protein interactions and complements the predominant bare lymphocyte syndrome (BLS) complementation group B, establishing it as the gene responsible for MHC class II transcriptional deficiency in that group.","method":"Protein purification of RFX complex, subunit sequencing, complementation assay in BLS cell lines","journal":"Immunity","confidence":"High","confidence_rationale":"Tier 2 — biochemical purification with sequence identification plus functional complementation in disease cell lines","pmids":["10072068"],"is_preprint":false},{"year":2001,"finding":"RFXANK ankyrin repeats mediate binding to two distinct partners simultaneously on opposite faces: RFXAP binds via two separate surfaces on the ankyrin groove, and CIITA binds the opposing face. A single point mutation in the ankyrin groove found in BLS patients (FZA patient) disrupts RFXAP binding, revealing the molecular mechanism of this immunodeficiency.","method":"Computational modeling of ankyrin repeats, site-directed alanine mutagenesis, in vitro and in vivo binding assays","journal":"Molecular and cellular biology","confidence":"High","confidence_rationale":"Tier 1-2 — mutagenesis combined with in vitro and in vivo binding studies, mechanistically pinpointing disease-causing residues","pmids":["11463838"],"is_preprint":false},{"year":2005,"finding":"Class IIa histone deacetylases HDAC4 and HDAC5 physically associate with RFXANK through its ankyrin repeats; through this interaction, HDAC4/5 repress MHC II promoter activation and endogenous HLA-DRA gene expression induced by CIITA. Phosphorylation of class II HDACs by CaMK causes CRM1-dependent nuclear export of HDAC/RFXANK complexes, relieving repression.","method":"Co-immunoprecipitation, yeast two-hybrid, transfection/reporter assays, CaMK phosphorylation assay, nuclear export assay","journal":"Molecular biology of the cell","confidence":"High","confidence_rationale":"Tier 2 — reciprocal co-IP, reporter assays, and kinase-dependent nuclear export, replicated with two independent labs (McKinsey and Wang papers)","pmids":["16236793","15964851"],"is_preprint":false},{"year":2005,"finding":"RFXANK interacts with HDAC4 via its ankyrin repeat domain; two RFXANK-binding sites were mapped on HDAC4 (residues 118-279 and 448-666). HDAC4 also interacted with CIITA. Consistent with these interactions, HDAC4 and homologs repress MHC II expression.","method":"Yeast two-hybrid screen, co-immunoprecipitation, reporter assays","journal":"The Journal of biological chemistry","confidence":"High","confidence_rationale":"Tier 2 — yeast two-hybrid plus reciprocal co-IP with domain mapping and functional reporter assay","pmids":["15964851"],"is_preprint":false},{"year":2000,"finding":"A founder 26-bp deletion mutation (752delG-25) in the RFXANK gene was identified in 17 of 20 North African BLS complementation group B patients, demonstrating that loss-of-function mutations in RFXANK abolish MHC class II expression and cause combined immunodeficiency.","method":"Mutation analysis, haplotype analysis for founder effect, functional complementation grouping","journal":"Immunogenetics","confidence":"Medium","confidence_rationale":"Tier 2 — genetic loss-of-function with defined immunological phenotype (MHC II absence), but primarily genetic/clinical rather than biochemical mechanism","pmids":["10803838"],"is_preprint":false},{"year":2011,"finding":"RFXANK deficiency due to a 26-bp founder deletion causes absence of MHC class II transcription, impairs antigen presentation to CD4+ T cells, and results in combined immunodeficiency; hematopoietic stem cell transplantation restores near-normal immune function, confirming the cell-autonomous hematopoietic origin of the defect.","method":"Genetic analysis, immunological phenotyping, hematopoietic stem cell transplantation outcomes in 35 patients","journal":"Blood","confidence":"Medium","confidence_rationale":"Tier 2 — large cohort with defined molecular lesion and functional immune reconstitution after HSCT, confirming pathway placement","pmids":["21908431"],"is_preprint":false}],"current_model":"RFXANK (RFX-B) is an ankyrin repeat-containing subunit of the trimeric RFX transcription factor complex that nucleates assembly of RFX by simultaneously binding RFXAP on one face and CIITA on the opposite face of its ankyrin repeats, thereby driving MHC class II gene transcription; it is also a signal-responsive regulator of antigen presentation because class IIa HDACs (HDAC4/5) bind its ankyrin repeats to repress MHC II expression, an interaction that is relieved by CaMK-mediated phosphorylation triggering CRM1-dependent nuclear export of the HDAC/RFXANK complex."},"narrative":{"teleology":[{"year":1999,"claim":"Identification of RFXANK as the smallest RFX complex subunit and the gene mutated in BLS group B established that a single ankyrin repeat-containing protein is required for MHC class II transcription.","evidence":"Biochemical purification of the RFX complex, subunit sequencing, and functional complementation of BLS cell lines","pmids":["10072068"],"confidence":"High","gaps":["How RFXANK ankyrin repeats engage individual partners was unknown","No structural model of the ankyrin repeat fold existed","Whether RFXANK has regulatory inputs beyond scaffolding was untested"]},{"year":2000,"claim":"Discovery of a 26-bp founder deletion in North African BLS patients confirmed that RFXANK loss of function is the predominant molecular cause of group B immunodeficiency and linked a specific allele to abolition of MHC class II expression.","evidence":"Mutation screening and haplotype analysis in 20 group B BLS patients","pmids":["10803838"],"confidence":"Medium","gaps":["Clinical study without biochemical reconstitution of the mutant protein","Long-term immunological consequences and transplant outcomes were not yet characterized","Whether the deletion produces a truncated protein or triggers nonsense-mediated decay was not resolved"]},{"year":2001,"claim":"Mutagenesis of RFXANK ankyrin repeats revealed that RFXAP and CIITA bind simultaneously on opposite faces, explaining how RFXANK nucleates enhanceosome assembly and why a single patient point mutation in the ankyrin groove causes disease by selectively disrupting RFXAP binding.","evidence":"Computational modeling of ankyrin repeats, alanine scanning mutagenesis, in vitro and in vivo protein interaction assays","pmids":["11463838"],"confidence":"High","gaps":["No crystal or cryo-EM structure of the ternary complex","Whether other transcription factors or coactivators contact the RFXANK scaffold was unexplored","Quantitative binding affinities for each face were not determined"]},{"year":2005,"claim":"Discovery that class IIa HDACs (HDAC4/5) bind RFXANK ankyrin repeats to repress MHC II transcription, and that CaMK phosphorylation triggers CRM1-dependent nuclear export of the HDAC/RFXANK complex, established RFXANK as a signal-responsive switch controlling antigen presentation.","evidence":"Reciprocal co-immunoprecipitation, yeast two-hybrid domain mapping, reporter assays, CaMK phosphorylation and nuclear export assays in two independent studies","pmids":["16236793","15964851"],"confidence":"High","gaps":["Whether HDAC4/5 binding and CIITA binding to RFXANK are mutually exclusive was not tested","Physiological signals upstream of CaMK that trigger this switch in antigen-presenting cells were not identified","In vivo validation in primary dendritic cells or macrophages was lacking"]},{"year":2011,"claim":"Demonstration that HSCT restores MHC class II expression and immune function in RFXANK-deficient patients confirmed the cell-autonomous hematopoietic origin of the defect and validated the pathway model in vivo.","evidence":"Clinical and immunological follow-up of 35 BLS patients after HSCT","pmids":["21908431"],"confidence":"Medium","gaps":["Clinical cohort study without molecular reconstitution experiments","Whether residual RFXANK-independent MHC II expression occurs in non-hematopoietic tissues was not addressed","Genotype–phenotype correlations for different RFXANK mutations remain limited"]},{"year":null,"claim":"No high-resolution structure of the RFX trimer or the RFXANK–HDAC complex exists, leaving unresolved how the competing interactions on the ankyrin repeat scaffold are coordinated and which physiological signals in antigen-presenting cells control the HDAC export switch.","evidence":"","pmids":[],"confidence":"High","gaps":["No crystal or cryo-EM structure of full RFX complex or RFXANK–HDAC interface","Upstream signaling pathways activating CaMK at MHC II loci in dendritic cells not defined","Whether RFXANK participates in transcription of non-MHC II target genes is unknown"]}],"mechanism_profile":{"molecular_activity":[{"term_id":"GO:0060090","term_label":"molecular adaptor activity","supporting_discovery_ids":[0,1]},{"term_id":"GO:0140110","term_label":"transcription regulator activity","supporting_discovery_ids":[0,1,2,3]}],"localization":[{"term_id":"GO:0005634","term_label":"nucleus","supporting_discovery_ids":[1,2]}],"pathway":[{"term_id":"R-HSA-74160","term_label":"Gene expression (Transcription)","supporting_discovery_ids":[0,1,2,3]},{"term_id":"R-HSA-168256","term_label":"Immune System","supporting_discovery_ids":[0,4,5]}],"complexes":["RFX complex"],"partners":["RFXAP","CIITA","HDAC4","HDAC5"],"other_free_text":[]},"mechanistic_narrative":"RFXANK (RFX-B) is the ankyrin repeat-containing subunit of the trimeric RFX transcription factor complex that drives MHC class II gene transcription by simultaneously engaging RFXAP and CIITA on opposite faces of its ankyrin repeats, thereby nucleating enhanceosome assembly on MHC II promoters [PMID:10072068, PMID:11463838]. Class IIa histone deacetylases HDAC4 and HDAC5 bind the same ankyrin repeat domain to repress MHC II expression; CaMK-mediated phosphorylation of these HDACs triggers CRM1-dependent nuclear export of HDAC/RFXANK complexes, relieving repression and enabling signal-responsive control of antigen presentation [PMID:16236793, PMID:15964851]. Loss-of-function mutations in RFXANK, including a 26-bp founder deletion prevalent in North African populations, abolish MHC class II transcription and cause bare lymphocyte syndrome complementation group B, a combined immunodeficiency correctable by hematopoietic stem cell transplantation [PMID:10072068, PMID:10803838, PMID:21908431]."},"prefetch_data":{"uniprot":{"accession":"O14593","full_name":"DNA-binding protein RFXANK","aliases":["Ankyrin repeat family A protein 1","Regulatory factor X subunit B","RFX-B","Regulatory factor X-associated ankyrin-containing protein"],"length_aa":260,"mass_kda":28.1,"function":"Activates transcription from class II MHC promoters. Activation requires the activity of the MHC class II transactivator/CIITA. May regulate other genes in the cell. RFX binds the X1 box of MHC-II promoters (PubMed:10072068, PubMed:10725724, PubMed:9806546). May also potentiate the activation of RAF1 (By similarity) Isoform 2 is not involved in the positive regulation of MHC class II genes","subcellular_location":"Cytoplasm; Nucleus","url":"https://www.uniprot.org/uniprotkb/O14593/entry"},"depmap":{"release":"DepMap","has_data":true,"is_common_essential":false,"resolved_as":"","url":"https://depmap.org/portal/gene/RFXANK","classification":"Not Classified","n_dependent_lines":9,"n_total_lines":1208,"dependency_fraction":0.0074503311258278145},"opencell":{"profiled":false,"resolved_as":"","ensg_id":"","cell_line_id":"","localizations":[],"interactors":[],"url":"https://opencell.sf.czbiohub.org/search/RFXANK","total_profiled":1310},"omim":[{"mim_id":"620817","title":"MHC CLASS II DEFICIENCY 4; MHC2D4","url":"https://www.omim.org/entry/620817"},{"mim_id":"620816","title":"MHC CLASS II DEFICIENCY 3; MHC2D3","url":"https://www.omim.org/entry/620816"},{"mim_id":"620815","title":"MHC CLASS II DEFICIENCY 2; MHC2D2","url":"https://www.omim.org/entry/620815"},{"mim_id":"605787","title":"ANKYRIN REPEAT-CONTAINING PROTEIN, FAMILY A, MEMBER 2; ANKRA2","url":"https://www.omim.org/entry/605787"},{"mim_id":"603200","title":"REGULATORY FACTOR X, ANKYRIN REPEAT-CONTAINING; RFXANK","url":"https://www.omim.org/entry/603200"}],"hpa":{"profiled":true,"resolved_as":"","reliability":"Enhanced","locations":[{"location":"Nucleoplasm","reliability":"Enhanced"}],"tissue_specificity":"Low tissue specificity","tissue_distribution":"Detected in all","driving_tissues":[],"url":"https://www.proteinatlas.org/search/RFXANK"},"hgnc":{"alias_symbol":["BLS","RFX-B","ANKRA1","F14150_1","MGC138628"],"prev_symbol":[]},"alphafold":{"accession":"O14593","domains":[],"viewer_url":"https://alphafold.ebi.ac.uk/entry/O14593","model_url":"https://alphafold.ebi.ac.uk/files/AF-O14593-F1-model_v6.cif","pae_url":"https://alphafold.ebi.ac.uk/files/AF-O14593-F1-predicted_aligned_error_v6.png","plddt_mean":78.06},"mouse_models":{"mgi_url":"https://www.informatics.jax.org/marker/summary?nomen=RFXANK","jax_strain_url":"https://www.jax.org/strain/search?query=RFXANK"},"sequence":{"accession":"O14593","fasta_url":"https://rest.uniprot.org/uniprotkb/O14593.fasta","uniprot_url":"https://www.uniprot.org/uniprotkb/O14593/entry","alphafold_viewer_url":"https://alphafold.ebi.ac.uk/entry/O14593"}},"corpus_meta":[{"pmid":"24008419","id":"PMC_24008419","title":"Infernal 1.1: 100-fold faster RNA homology searches.","date":"2013","source":"Bioinformatics (Oxford, 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A single point mutation in the ankyrin groove found in BLS patients (FZA patient) disrupts RFXAP binding, revealing the molecular mechanism of this immunodeficiency.\",\n      \"method\": \"Computational modeling of ankyrin repeats, site-directed alanine mutagenesis, in vitro and in vivo binding assays\",\n      \"journal\": \"Molecular and cellular biology\",\n      \"confidence\": \"High\",\n      \"confidence_rationale\": \"Tier 1-2 — mutagenesis combined with in vitro and in vivo binding studies, mechanistically pinpointing disease-causing residues\",\n      \"pmids\": [\"11463838\"],\n      \"is_preprint\": false\n    },\n    {\n      \"year\": 2005,\n      \"finding\": \"Class IIa histone deacetylases HDAC4 and HDAC5 physically associate with RFXANK through its ankyrin repeats; through this interaction, HDAC4/5 repress MHC II promoter activation and endogenous HLA-DRA gene expression induced by CIITA. Phosphorylation of class II HDACs by CaMK causes CRM1-dependent nuclear export of HDAC/RFXANK complexes, relieving repression.\",\n      \"method\": \"Co-immunoprecipitation, yeast two-hybrid, transfection/reporter assays, CaMK phosphorylation assay, nuclear export assay\",\n      \"journal\": \"Molecular biology of the cell\",\n      \"confidence\": \"High\",\n      \"confidence_rationale\": \"Tier 2 — reciprocal co-IP, reporter assays, and kinase-dependent nuclear export, replicated with two independent labs (McKinsey and Wang papers)\",\n      \"pmids\": [\"16236793\", \"15964851\"],\n      \"is_preprint\": false\n    },\n    {\n      \"year\": 2005,\n      \"finding\": \"RFXANK interacts with HDAC4 via its ankyrin repeat domain; two RFXANK-binding sites were mapped on HDAC4 (residues 118-279 and 448-666). HDAC4 also interacted with CIITA. Consistent with these interactions, HDAC4 and homologs repress MHC II expression.\",\n      \"method\": \"Yeast two-hybrid screen, co-immunoprecipitation, reporter assays\",\n      \"journal\": \"The Journal of biological chemistry\",\n      \"confidence\": \"High\",\n      \"confidence_rationale\": \"Tier 2 — yeast two-hybrid plus reciprocal co-IP with domain mapping and functional reporter assay\",\n      \"pmids\": [\"15964851\"],\n      \"is_preprint\": false\n    },\n    {\n      \"year\": 2000,\n      \"finding\": \"A founder 26-bp deletion mutation (752delG-25) in the RFXANK gene was identified in 17 of 20 North African BLS complementation group B patients, demonstrating that loss-of-function mutations in RFXANK abolish MHC class II expression and cause combined immunodeficiency.\",\n      \"method\": \"Mutation analysis, haplotype analysis for founder effect, functional complementation grouping\",\n      \"journal\": \"Immunogenetics\",\n      \"confidence\": \"Medium\",\n      \"confidence_rationale\": \"Tier 2 — genetic loss-of-function with defined immunological phenotype (MHC II absence), but primarily genetic/clinical rather than biochemical mechanism\",\n      \"pmids\": [\"10803838\"],\n      \"is_preprint\": false\n    },\n    {\n      \"year\": 2011,\n      \"finding\": \"RFXANK deficiency due to a 26-bp founder deletion causes absence of MHC class II transcription, impairs antigen presentation to CD4+ T cells, and results in combined immunodeficiency; hematopoietic stem cell transplantation restores near-normal immune function, confirming the cell-autonomous hematopoietic origin of the defect.\",\n      \"method\": \"Genetic analysis, immunological phenotyping, hematopoietic stem cell transplantation outcomes in 35 patients\",\n      \"journal\": \"Blood\",\n      \"confidence\": \"Medium\",\n      \"confidence_rationale\": \"Tier 2 — large cohort with defined molecular lesion and functional immune reconstitution after HSCT, confirming pathway placement\",\n      \"pmids\": [\"21908431\"],\n      \"is_preprint\": false\n    }\n  ],\n  \"current_model\": \"RFXANK (RFX-B) is an ankyrin repeat-containing subunit of the trimeric RFX transcription factor complex that nucleates assembly of RFX by simultaneously binding RFXAP on one face and CIITA on the opposite face of its ankyrin repeats, thereby driving MHC class II gene transcription; it is also a signal-responsive regulator of antigen presentation because class IIa HDACs (HDAC4/5) bind its ankyrin repeats to repress MHC II expression, an interaction that is relieved by CaMK-mediated phosphorylation triggering CRM1-dependent nuclear export of the HDAC/RFXANK complex.\"\n}\n```","stage2_raw":"```json\n{\n  \"mechanistic_narrative\": \"RFXANK (RFX-B) is the ankyrin repeat-containing subunit of the trimeric RFX transcription factor complex that drives MHC class II gene transcription by simultaneously engaging RFXAP and CIITA on opposite faces of its ankyrin repeats, thereby nucleating enhanceosome assembly on MHC II promoters [PMID:10072068, PMID:11463838]. Class IIa histone deacetylases HDAC4 and HDAC5 bind the same ankyrin repeat domain to repress MHC II expression; CaMK-mediated phosphorylation of these HDACs triggers CRM1-dependent nuclear export of HDAC/RFXANK complexes, relieving repression and enabling signal-responsive control of antigen presentation [PMID:16236793, PMID:15964851]. Loss-of-function mutations in RFXANK, including a 26-bp founder deletion prevalent in North African populations, abolish MHC class II transcription and cause bare lymphocyte syndrome complementation group B, a combined immunodeficiency correctable by hematopoietic stem cell transplantation [PMID:10072068, PMID:10803838, PMID:21908431].\",\n  \"teleology\": [\n    {\n      \"year\": 1999,\n      \"claim\": \"Identification of RFXANK as the smallest RFX complex subunit and the gene mutated in BLS group B established that a single ankyrin repeat-containing protein is required for MHC class II transcription.\",\n      \"evidence\": \"Biochemical purification of the RFX complex, subunit sequencing, and functional complementation of BLS cell lines\",\n      \"pmids\": [\"10072068\"],\n      \"confidence\": \"High\",\n      \"gaps\": [\n        \"How RFXANK ankyrin repeats engage individual partners was unknown\",\n        \"No structural model of the ankyrin repeat fold existed\",\n        \"Whether RFXANK has regulatory inputs beyond scaffolding was untested\"\n      ]\n    },\n    {\n      \"year\": 2000,\n      \"claim\": \"Discovery of a 26-bp founder deletion in North African BLS patients confirmed that RFXANK loss of function is the predominant molecular cause of group B immunodeficiency and linked a specific allele to abolition of MHC class II expression.\",\n      \"evidence\": \"Mutation screening and haplotype analysis in 20 group B BLS patients\",\n      \"pmids\": [\"10803838\"],\n      \"confidence\": \"Medium\",\n      \"gaps\": [\n        \"Clinical study without biochemical reconstitution of the mutant protein\",\n        \"Long-term immunological consequences and transplant outcomes were not yet characterized\",\n        \"Whether the deletion produces a truncated protein or triggers nonsense-mediated decay was not resolved\"\n      ]\n    },\n    {\n      \"year\": 2001,\n      \"claim\": \"Mutagenesis of RFXANK ankyrin repeats revealed that RFXAP and CIITA bind simultaneously on opposite faces, explaining how RFXANK nucleates enhanceosome assembly and why a single patient point mutation in the ankyrin groove causes disease by selectively disrupting RFXAP binding.\",\n      \"evidence\": \"Computational modeling of ankyrin repeats, alanine scanning mutagenesis, in vitro and in vivo protein interaction assays\",\n      \"pmids\": [\"11463838\"],\n      \"confidence\": \"High\",\n      \"gaps\": [\n        \"No crystal or cryo-EM structure of the ternary complex\",\n        \"Whether other transcription factors or coactivators contact the RFXANK scaffold was unexplored\",\n        \"Quantitative binding affinities for each face were not determined\"\n      ]\n    },\n    {\n      \"year\": 2005,\n      \"claim\": \"Discovery that class IIa HDACs (HDAC4/5) bind RFXANK ankyrin repeats to repress MHC II transcription, and that CaMK phosphorylation triggers CRM1-dependent nuclear export of the HDAC/RFXANK complex, established RFXANK as a signal-responsive switch controlling antigen presentation.\",\n      \"evidence\": \"Reciprocal co-immunoprecipitation, yeast two-hybrid domain mapping, reporter assays, CaMK phosphorylation and nuclear export assays in two independent studies\",\n      \"pmids\": [\"16236793\", \"15964851\"],\n      \"confidence\": \"High\",\n      \"gaps\": [\n        \"Whether HDAC4/5 binding and CIITA binding to RFXANK are mutually exclusive was not tested\",\n        \"Physiological signals upstream of CaMK that trigger this switch in antigen-presenting cells were not identified\",\n        \"In vivo validation in primary dendritic cells or macrophages was lacking\"\n      ]\n    },\n    {\n      \"year\": 2011,\n      \"claim\": \"Demonstration that HSCT restores MHC class II expression and immune function in RFXANK-deficient patients confirmed the cell-autonomous hematopoietic origin of the defect and validated the pathway model in vivo.\",\n      \"evidence\": \"Clinical and immunological follow-up of 35 BLS patients after HSCT\",\n      \"pmids\": [\"21908431\"],\n      \"confidence\": \"Medium\",\n      \"gaps\": [\n        \"Clinical cohort study without molecular reconstitution experiments\",\n        \"Whether residual RFXANK-independent MHC II expression occurs in non-hematopoietic tissues was not addressed\",\n        \"Genotype–phenotype correlations for different RFXANK mutations remain limited\"\n      ]\n    },\n    {\n      \"year\": null,\n      \"claim\": \"No high-resolution structure of the RFX trimer or the RFXANK–HDAC complex exists, leaving unresolved how the competing interactions on the ankyrin repeat scaffold are coordinated and which physiological signals in antigen-presenting cells control the HDAC export switch.\",\n      \"evidence\": \"\",\n      \"pmids\": [],\n      \"confidence\": \"High\",\n      \"gaps\": [\n        \"No crystal or cryo-EM structure of full RFX complex or RFXANK–HDAC interface\",\n        \"Upstream signaling pathways activating CaMK at MHC II loci in dendritic cells not defined\",\n        \"Whether RFXANK participates in transcription of non-MHC II target genes is unknown\"\n      ]\n    }\n  ],\n  \"mechanism_profile\": {\n    \"molecular_activity\": [\n      {\"term_id\": \"GO:0060090\", \"supporting_discovery_ids\": [0, 1]},\n      {\"term_id\": \"GO:0140110\", \"supporting_discovery_ids\": [0, 1, 2, 3]}\n    ],\n    \"localization\": [\n      {\"term_id\": \"GO:0005634\", \"supporting_discovery_ids\": [1, 2]}\n    ],\n    \"pathway\": [\n      {\"term_id\": \"R-HSA-74160\", \"supporting_discovery_ids\": [0, 1, 2, 3]},\n      {\"term_id\": \"R-HSA-168256\", \"supporting_discovery_ids\": [0, 4, 5]}\n    ],\n    \"complexes\": [\n      \"RFX complex\"\n    ],\n    \"partners\": [\n      \"RFXAP\",\n      \"CIITA\",\n      \"HDAC4\",\n      \"HDAC5\"\n    ],\n    \"other_free_text\": []\n  }\n}\n```"}