{"gene":"RSPH4A","run_date":"2026-04-28T20:42:06","timeline":{"discoveries":[{"year":2009,"finding":"RSPH4A encodes a protein component of the axonemal radial spoke head; loss-of-function mutations cause primary ciliary dyskinesia with central-microtubular-pair abnormalities (complete absence of central pair), establishing its structural role in maintaining normal motile cilia movement in 9+2-structure cilia and flagella.","method":"Whole-genome SNP linkage analysis, mutation identification in consanguineous PCD families, in situ hybridization of murine Rsph9, zebrafish knockdown/rescue experiments","journal":"American journal of human genetics","confidence":"High","confidence_rationale":"Tier 2 — genetic epistasis via knockdown/rescue in zebrafish, replicated across multiple families, foundational discovery paper with 267 citations","pmids":["19200523"],"is_preprint":false},{"year":2020,"finding":"Rsph4a is required for assembly of all three radial spoke heads (RS1, RS2, RS3) in the 96 nm axonemal repeat unit of mouse tracheal motile cilia; Rsph4a-deficient mice lack all triplet spoke heads, and Rsph4a contributes to planar beating of motile cilia in trachea, ependymal tissues, and oviduct.","method":"Cryo-electron tomography of Rsph4a knockout mouse tracheal cilia, ciliary movement observation, immunofluorescence analysis","journal":"PLoS genetics","confidence":"High","confidence_rationale":"Tier 1 — cryo-ET structural analysis combined with KO mouse model and functional ciliary movement assay; multiple orthogonal methods","pmids":["32203505"],"is_preprint":false},{"year":2021,"finding":"In human RSPH4A-/- respiratory cilia, the radial spoke heads of RS1 and RS2 (but not RS3) are missing, and additional structural defects occur in the arch domains adjacent to RS1 and RS2 heads; secondary heterogeneous defects appear in the central pair complex, distinguishing RSPH4A-/- from RSPH1-/- cilia.","method":"Cryo-electron tomography (cryo-ET) and subtomogram averaging of human patient nasal epithelial cilia collected noninvasively, compared to controls","journal":"Molecular biology of the cell","confidence":"High","confidence_rationale":"Tier 1 — native cryo-ET structure from patient samples with subtomogram averaging, directly revealing molecular-level structural defects","pmids":["33852348"],"is_preprint":false},{"year":2013,"finding":"A splice-site mutation (c.921+3_6delAAGT) in RSPH4A causes loss of function confirmed by quantitative ciliary ultrastructural analysis showing central apparatus defects, altered ciliary beat frequency and waveform, and abnormal transcript processing.","method":"Ciliary ultrastructural analysis by electron microscopy, ciliary beat frequency and waveform measurement, transcript analysis in PCD patients","journal":"Human mutation","confidence":"Medium","confidence_rationale":"Tier 2 — multiple orthogonal functional assays (EM ultrastructure, beat frequency, transcript) in a single cohort study","pmids":["23798057"],"is_preprint":false}],"current_model":"RSPH4A is a structural component of the axonemal radial spoke head that is essential for assembly of all three radial spoke heads (RS1, RS2, RS3) in the 96 nm repeat unit of motile cilia; loss of RSPH4A preferentially abolishes RS1 and RS2 heads in human cilia (with additional arch domain defects) and all three spoke heads in mice, disrupting planar ciliary beating and causing primary ciliary dyskinesia with central-pair complex abnormalities but without laterality defects."},"narrative":{"teleology":[{"year":2009,"claim":"The molecular basis of radial-spoke-head-related PCD was unknown; linkage analysis and zebrafish knockdown/rescue identified RSPH4A as a radial spoke head component whose loss causes PCD with central-pair defects, establishing the first genetic link between spoke head proteins and human ciliopathy.","evidence":"Whole-genome SNP linkage in consanguineous PCD families, mutation identification, zebrafish morpholino knockdown with rescue","pmids":["19200523"],"confidence":"High","gaps":["Which specific radial spokes (RS1, RS2, RS3) require RSPH4A was not resolved","Structural role at sub-nanometer resolution was not determined","Whether RSPH4A functions identically across species was untested"]},{"year":2013,"claim":"Whether RSPH4A mutations affect ciliary motility parameters beyond ultrastructure was unclear; quantitative analysis of a splice-site mutation demonstrated that RSPH4A loss alters ciliary beat frequency and waveform in addition to central apparatus ultrastructure, linking structural defects to functional motility impairment.","evidence":"Electron microscopy ultrastructural analysis, ciliary beat frequency and waveform measurement, transcript analysis in PCD patients","pmids":["23798057"],"confidence":"Medium","gaps":["Single cohort study; limited patient numbers for genotype-phenotype correlation","Mechanism by which spoke head loss alters beat waveform was not dissected","No direct structural visualization at molecular resolution"]},{"year":2020,"claim":"Whether RSPH4A is required for all three radial spoke heads or a subset was unresolved; cryo-electron tomography of Rsph4a-knockout mouse cilia revealed that all three spoke heads (RS1, RS2, RS3) are absent, establishing RSPH4A as a pan-spoke-head structural requirement in mouse motile cilia.","evidence":"Cryo-electron tomography of Rsph4a KO mouse tracheal cilia combined with ciliary movement observation and immunofluorescence","pmids":["32203505"],"confidence":"High","gaps":["Whether the pan-spoke-head requirement reflects direct structural incorporation or an assembly-factor role was not distinguished","Species-specific differences in RSPH4A dependency were not yet characterized"]},{"year":2021,"claim":"Whether RSPH4A loss produces the same structural defects in human and mouse cilia was unknown; cryo-ET of human RSPH4A-deficient cilia showed selective loss of RS1 and RS2 heads (but retention of RS3) with arch domain disruption and secondary central pair heterogeneity, revealing a species-specific spoke-head dependency distinct from the mouse phenotype.","evidence":"Cryo-electron tomography with subtomogram averaging of patient nasal epithelial cilia versus controls","pmids":["33852348"],"confidence":"High","gaps":["Molecular basis for why RS3 is spared in human but not mouse cilia is unknown","Direct protein–protein interactions of RSPH4A within each spoke head are not mapped","No atomic-resolution structure of the RSPH4A-containing spoke head complex exists"]},{"year":null,"claim":"The direct binding partners of RSPH4A within each radial spoke head, the basis for species-specific spoke-head dependency, and whether RSPH4A acts as a structural scaffold versus an assembly factor remain unresolved.","evidence":"","pmids":[],"confidence":"Low","gaps":["No reconstitution or crosslinking mass spectrometry defining RSPH4A's direct interaction network within the spoke head","No high-resolution structure showing RSPH4A positioning within the spoke head complex","Mechanism of species-divergent RS3 dependency is unexplained"]}],"mechanism_profile":{"molecular_activity":[{"term_id":"GO:0005198","term_label":"structural molecule activity","supporting_discovery_ids":[0,1,2]}],"localization":[{"term_id":"GO:0005929","term_label":"cilium","supporting_discovery_ids":[0,1,2,3]}],"pathway":[{"term_id":"R-HSA-1852241","term_label":"Organelle biogenesis and maintenance","supporting_discovery_ids":[0,1,2]}],"complexes":["radial spoke head"],"partners":[],"other_free_text":[]},"mechanistic_narrative":"RSPH4A is a structural component of the radial spoke head in 9+2 motile cilia, essential for the assembly and integrity of the radial spoke–central pair apparatus that governs planar ciliary beating. In mouse tracheal cilia, RSPH4A is required for assembly of all three radial spoke heads (RS1, RS2, RS3) within the 96 nm axonemal repeat unit, whereas in human respiratory cilia its loss selectively eliminates the RS1 and RS2 heads and disrupts adjacent arch domains, with secondary heterogeneous central pair complex defects [PMID:32203505, PMID:33852348]. Loss-of-function mutations in RSPH4A cause primary ciliary dyskinesia characterized by central microtubular pair abnormalities, altered ciliary beat frequency and waveform, and absence of laterality defects [PMID:19200523, PMID:23798057]."},"prefetch_data":{"uniprot":{"accession":"Q5TD94","full_name":"Radial spoke head protein 4 homolog A","aliases":["Radial spoke head-like protein 3"],"length_aa":716,"mass_kda":80.7,"function":"Component of the axonemal radial spoke head which plays an important role in ciliary motility (PubMed:19200523). Essential for triplet radial spokes (RS1, RS2 and RS3) head assembly in the motile cilia (By similarity)","subcellular_location":"Cytoplasm, cytoskeleton, cilium axoneme; Cell projection, cilium","url":"https://www.uniprot.org/uniprotkb/Q5TD94/entry"},"depmap":{"release":"DepMap","has_data":true,"is_common_essential":false,"resolved_as":"","url":"https://depmap.org/portal/gene/RSPH4A","classification":"Not Classified","n_dependent_lines":2,"n_total_lines":1208,"dependency_fraction":0.0016556291390728477},"opencell":{"profiled":false,"resolved_as":"","ensg_id":"","cell_line_id":"","localizations":[],"interactors":[],"url":"https://opencell.sf.czbiohub.org/search/RSPH4A","total_profiled":1310},"omim":[{"mim_id":"616481","title":"CILIARY DYSKINESIA, PRIMARY, 32; CILD32","url":"https://www.omim.org/entry/616481"},{"mim_id":"615876","title":"RADIAL SPOKE HEAD 3; RSPH3","url":"https://www.omim.org/entry/615876"},{"mim_id":"612650","title":"CILIARY DYSKINESIA, PRIMARY, 12; CILD12","url":"https://www.omim.org/entry/612650"},{"mim_id":"612649","title":"CILIARY DYSKINESIA, PRIMARY, 11; CILD11","url":"https://www.omim.org/entry/612649"},{"mim_id":"612648","title":"RADIAL SPOKE HEAD COMPONENT 9; RSPH9","url":"https://www.omim.org/entry/612648"}],"hpa":{"profiled":true,"resolved_as":"","reliability":"Approved","locations":[{"location":"Connecting piece","reliability":"Approved"},{"location":"Flagellar centriole","reliability":"Approved"},{"location":"Annulus","reliability":"Additional"}],"tissue_specificity":"Group enriched","tissue_distribution":"Detected in some","driving_tissues":[{"tissue":"choroid plexus","ntpm":22.0},{"tissue":"fallopian tube","ntpm":35.0}],"url":"https://www.proteinatlas.org/search/RSPH4A"},"hgnc":{"alias_symbol":["dJ412I7.1","FLJ37974","RSPH6B","CILD11"],"prev_symbol":["RSHL3"]},"alphafold":{"accession":"Q5TD94","domains":[{"cath_id":"-","chopping":"208-264","consensus_level":"high","plddt":86.596,"start":208,"end":264},{"cath_id":"-","chopping":"301-380_415-507_522-560_587-648","consensus_level":"medium","plddt":88.5861,"start":301,"end":648}],"viewer_url":"https://alphafold.ebi.ac.uk/entry/Q5TD94","model_url":"https://alphafold.ebi.ac.uk/files/AF-Q5TD94-F1-model_v6.cif","pae_url":"https://alphafold.ebi.ac.uk/files/AF-Q5TD94-F1-predicted_aligned_error_v6.png","plddt_mean":67.44},"mouse_models":{"mgi_url":"https://www.informatics.jax.org/marker/summary?nomen=RSPH4A","jax_strain_url":"https://www.jax.org/strain/search?query=RSPH4A"},"sequence":{"accession":"Q5TD94","fasta_url":"https://rest.uniprot.org/uniprotkb/Q5TD94.fasta","uniprot_url":"https://www.uniprot.org/uniprotkb/Q5TD94/entry","alphafold_viewer_url":"https://alphafold.ebi.ac.uk/entry/Q5TD94"}},"corpus_meta":[{"pmid":"19200523","id":"PMC_19200523","title":"Mutations in radial spoke head protein genes RSPH9 and RSPH4A cause primary ciliary dyskinesia with central-microtubular-pair abnormalities.","date":"2009","source":"American journal of human genetics","url":"https://pubmed.ncbi.nlm.nih.gov/19200523","citation_count":267,"is_preprint":false},{"pmid":"23798057","id":"PMC_23798057","title":"Founder mutation in RSPH4A identified in patients of Hispanic descent with primary ciliary dyskinesia.","date":"2013","source":"Human mutation","url":"https://pubmed.ncbi.nlm.nih.gov/23798057","citation_count":51,"is_preprint":false},{"pmid":"32203505","id":"PMC_32203505","title":"Rsph4a is essential for the triplet radial spoke head assembly of the mouse motile cilia.","date":"2020","source":"PLoS genetics","url":"https://pubmed.ncbi.nlm.nih.gov/32203505","citation_count":29,"is_preprint":false},{"pmid":"33670432","id":"PMC_33670432","title":"Primary Ciliary Dyskinesia Diagnostic Challenges: Understanding the Clinical Phenotype of the Puerto Rican RSPH4A Founder Mutation.","date":"2021","source":"Diagnostics (Basel, Switzerland)","url":"https://pubmed.ncbi.nlm.nih.gov/33670432","citation_count":17,"is_preprint":false},{"pmid":"33852348","id":"PMC_33852348","title":"Structural insights into the cause of human RSPH4A primary ciliary dyskinesia.","date":"2021","source":"Molecular biology of the cell","url":"https://pubmed.ncbi.nlm.nih.gov/33852348","citation_count":16,"is_preprint":false},{"pmid":"36768259","id":"PMC_36768259","title":"The RSPH4A Gene in Primary Ciliary Dyskinesia.","date":"2023","source":"International journal of molecular sciences","url":"https://pubmed.ncbi.nlm.nih.gov/36768259","citation_count":15,"is_preprint":false},{"pmid":"34513534","id":"PMC_34513534","title":"Primary Ciliary Dyskinesia: Ancestral Haplotypes Analysis of the RSPH4A Founder Mutation in Puerto Rico.","date":"2021","source":"Cureus","url":"https://pubmed.ncbi.nlm.nih.gov/34513534","citation_count":4,"is_preprint":false},{"pmid":"40429607","id":"PMC_40429607","title":"Assessing Olfactory Acuity in Primary Ciliary Dyskinesia with the RSPH4A Founder Mutation.","date":"2025","source":"Journal of clinical medicine","url":"https://pubmed.ncbi.nlm.nih.gov/40429607","citation_count":2,"is_preprint":false},{"pmid":"40262389","id":"PMC_40262389","title":"Primary ciliary dyskinesia in a Japanese woman caused by a novel RSPH4A variant.","date":"2025","source":"Respiratory investigation","url":"https://pubmed.ncbi.nlm.nih.gov/40262389","citation_count":1,"is_preprint":false},{"pmid":"38818043","id":"PMC_38818043","title":"A novel homozygous RSPH4A variant in a family with primary ciliary dyskinesia and literature review.","date":"2024","source":"Frontiers in genetics","url":"https://pubmed.ncbi.nlm.nih.gov/38818043","citation_count":1,"is_preprint":false},{"pmid":"40852414","id":"PMC_40852414","title":"Analysis of clinical and genetic features in an adolescent patient with primary ciliary dyskinesia induced by homozygous mutation in the RSPH4A gene: a case report.","date":"2025","source":"Frontiers in pediatrics","url":"https://pubmed.ncbi.nlm.nih.gov/40852414","citation_count":0,"is_preprint":false}],"cost":{"stage1":{"model":"claude-sonnet-4-6","input_tokens":6393,"output_tokens":1049,"usd":0.017457},"stage2":{"model":"claude-opus-4-6","input_tokens":4249,"output_tokens":1444,"usd":0.086017},"total_usd":0.103474,"stage1_batch_id":"msgbatch_011rkcQdVV1RaFq9XhcG6df6","stage2_batch_id":"msgbatch_01RzgrJafdF4EWHhj5mNi6dh","note":"batch pricing = 50% of standard"},"stage1_raw":"```json\n{\n  \"discoveries\": [\n    {\n      \"year\": 2009,\n      \"finding\": \"RSPH4A encodes a protein component of the axonemal radial spoke head; loss-of-function mutations cause primary ciliary dyskinesia with central-microtubular-pair abnormalities (complete absence of central pair), establishing its structural role in maintaining normal motile cilia movement in 9+2-structure cilia and flagella.\",\n      \"method\": \"Whole-genome SNP linkage analysis, mutation identification in consanguineous PCD families, in situ hybridization of murine Rsph9, zebrafish knockdown/rescue experiments\",\n      \"journal\": \"American journal of human genetics\",\n      \"confidence\": \"High\",\n      \"confidence_rationale\": \"Tier 2 — genetic epistasis via knockdown/rescue in zebrafish, replicated across multiple families, foundational discovery paper with 267 citations\",\n      \"pmids\": [\"19200523\"],\n      \"is_preprint\": false\n    },\n    {\n      \"year\": 2020,\n      \"finding\": \"Rsph4a is required for assembly of all three radial spoke heads (RS1, RS2, RS3) in the 96 nm axonemal repeat unit of mouse tracheal motile cilia; Rsph4a-deficient mice lack all triplet spoke heads, and Rsph4a contributes to planar beating of motile cilia in trachea, ependymal tissues, and oviduct.\",\n      \"method\": \"Cryo-electron tomography of Rsph4a knockout mouse tracheal cilia, ciliary movement observation, immunofluorescence analysis\",\n      \"journal\": \"PLoS genetics\",\n      \"confidence\": \"High\",\n      \"confidence_rationale\": \"Tier 1 — cryo-ET structural analysis combined with KO mouse model and functional ciliary movement assay; multiple orthogonal methods\",\n      \"pmids\": [\"32203505\"],\n      \"is_preprint\": false\n    },\n    {\n      \"year\": 2021,\n      \"finding\": \"In human RSPH4A-/- respiratory cilia, the radial spoke heads of RS1 and RS2 (but not RS3) are missing, and additional structural defects occur in the arch domains adjacent to RS1 and RS2 heads; secondary heterogeneous defects appear in the central pair complex, distinguishing RSPH4A-/- from RSPH1-/- cilia.\",\n      \"method\": \"Cryo-electron tomography (cryo-ET) and subtomogram averaging of human patient nasal epithelial cilia collected noninvasively, compared to controls\",\n      \"journal\": \"Molecular biology of the cell\",\n      \"confidence\": \"High\",\n      \"confidence_rationale\": \"Tier 1 — native cryo-ET structure from patient samples with subtomogram averaging, directly revealing molecular-level structural defects\",\n      \"pmids\": [\"33852348\"],\n      \"is_preprint\": false\n    },\n    {\n      \"year\": 2013,\n      \"finding\": \"A splice-site mutation (c.921+3_6delAAGT) in RSPH4A causes loss of function confirmed by quantitative ciliary ultrastructural analysis showing central apparatus defects, altered ciliary beat frequency and waveform, and abnormal transcript processing.\",\n      \"method\": \"Ciliary ultrastructural analysis by electron microscopy, ciliary beat frequency and waveform measurement, transcript analysis in PCD patients\",\n      \"journal\": \"Human mutation\",\n      \"confidence\": \"Medium\",\n      \"confidence_rationale\": \"Tier 2 — multiple orthogonal functional assays (EM ultrastructure, beat frequency, transcript) in a single cohort study\",\n      \"pmids\": [\"23798057\"],\n      \"is_preprint\": false\n    }\n  ],\n  \"current_model\": \"RSPH4A is a structural component of the axonemal radial spoke head that is essential for assembly of all three radial spoke heads (RS1, RS2, RS3) in the 96 nm repeat unit of motile cilia; loss of RSPH4A preferentially abolishes RS1 and RS2 heads in human cilia (with additional arch domain defects) and all three spoke heads in mice, disrupting planar ciliary beating and causing primary ciliary dyskinesia with central-pair complex abnormalities but without laterality defects.\"\n}\n```","stage2_raw":"```json\n{\n  \"mechanistic_narrative\": \"RSPH4A is a structural component of the radial spoke head in 9+2 motile cilia, essential for the assembly and integrity of the radial spoke–central pair apparatus that governs planar ciliary beating. In mouse tracheal cilia, RSPH4A is required for assembly of all three radial spoke heads (RS1, RS2, RS3) within the 96 nm axonemal repeat unit, whereas in human respiratory cilia its loss selectively eliminates the RS1 and RS2 heads and disrupts adjacent arch domains, with secondary heterogeneous central pair complex defects [PMID:32203505, PMID:33852348]. Loss-of-function mutations in RSPH4A cause primary ciliary dyskinesia characterized by central microtubular pair abnormalities, altered ciliary beat frequency and waveform, and absence of laterality defects [PMID:19200523, PMID:23798057].\",\n  \"teleology\": [\n    {\n      \"year\": 2009,\n      \"claim\": \"The molecular basis of radial-spoke-head-related PCD was unknown; linkage analysis and zebrafish knockdown/rescue identified RSPH4A as a radial spoke head component whose loss causes PCD with central-pair defects, establishing the first genetic link between spoke head proteins and human ciliopathy.\",\n      \"evidence\": \"Whole-genome SNP linkage in consanguineous PCD families, mutation identification, zebrafish morpholino knockdown with rescue\",\n      \"pmids\": [\"19200523\"],\n      \"confidence\": \"High\",\n      \"gaps\": [\n        \"Which specific radial spokes (RS1, RS2, RS3) require RSPH4A was not resolved\",\n        \"Structural role at sub-nanometer resolution was not determined\",\n        \"Whether RSPH4A functions identically across species was untested\"\n      ]\n    },\n    {\n      \"year\": 2013,\n      \"claim\": \"Whether RSPH4A mutations affect ciliary motility parameters beyond ultrastructure was unclear; quantitative analysis of a splice-site mutation demonstrated that RSPH4A loss alters ciliary beat frequency and waveform in addition to central apparatus ultrastructure, linking structural defects to functional motility impairment.\",\n      \"evidence\": \"Electron microscopy ultrastructural analysis, ciliary beat frequency and waveform measurement, transcript analysis in PCD patients\",\n      \"pmids\": [\"23798057\"],\n      \"confidence\": \"Medium\",\n      \"gaps\": [\n        \"Single cohort study; limited patient numbers for genotype-phenotype correlation\",\n        \"Mechanism by which spoke head loss alters beat waveform was not dissected\",\n        \"No direct structural visualization at molecular resolution\"\n      ]\n    },\n    {\n      \"year\": 2020,\n      \"claim\": \"Whether RSPH4A is required for all three radial spoke heads or a subset was unresolved; cryo-electron tomography of Rsph4a-knockout mouse cilia revealed that all three spoke heads (RS1, RS2, RS3) are absent, establishing RSPH4A as a pan-spoke-head structural requirement in mouse motile cilia.\",\n      \"evidence\": \"Cryo-electron tomography of Rsph4a KO mouse tracheal cilia combined with ciliary movement observation and immunofluorescence\",\n      \"pmids\": [\"32203505\"],\n      \"confidence\": \"High\",\n      \"gaps\": [\n        \"Whether the pan-spoke-head requirement reflects direct structural incorporation or an assembly-factor role was not distinguished\",\n        \"Species-specific differences in RSPH4A dependency were not yet characterized\"\n      ]\n    },\n    {\n      \"year\": 2021,\n      \"claim\": \"Whether RSPH4A loss produces the same structural defects in human and mouse cilia was unknown; cryo-ET of human RSPH4A-deficient cilia showed selective loss of RS1 and RS2 heads (but retention of RS3) with arch domain disruption and secondary central pair heterogeneity, revealing a species-specific spoke-head dependency distinct from the mouse phenotype.\",\n      \"evidence\": \"Cryo-electron tomography with subtomogram averaging of patient nasal epithelial cilia versus controls\",\n      \"pmids\": [\"33852348\"],\n      \"confidence\": \"High\",\n      \"gaps\": [\n        \"Molecular basis for why RS3 is spared in human but not mouse cilia is unknown\",\n        \"Direct protein–protein interactions of RSPH4A within each spoke head are not mapped\",\n        \"No atomic-resolution structure of the RSPH4A-containing spoke head complex exists\"\n      ]\n    },\n    {\n      \"year\": null,\n      \"claim\": \"The direct binding partners of RSPH4A within each radial spoke head, the basis for species-specific spoke-head dependency, and whether RSPH4A acts as a structural scaffold versus an assembly factor remain unresolved.\",\n      \"evidence\": \"\",\n      \"pmids\": [],\n      \"confidence\": \"Low\",\n      \"gaps\": [\n        \"No reconstitution or crosslinking mass spectrometry defining RSPH4A's direct interaction network within the spoke head\",\n        \"No high-resolution structure showing RSPH4A positioning within the spoke head complex\",\n        \"Mechanism of species-divergent RS3 dependency is unexplained\"\n      ]\n    }\n  ],\n  \"mechanism_profile\": {\n    \"molecular_activity\": [\n      {\"term_id\": \"GO:0005198\", \"supporting_discovery_ids\": [0, 1, 2]}\n    ],\n    \"localization\": [\n      {\"term_id\": \"GO:0005929\", \"supporting_discovery_ids\": [0, 1, 2, 3]}\n    ],\n    \"pathway\": [\n      {\"term_id\": \"R-HSA-1852241\", \"supporting_discovery_ids\": [0, 1, 2]}\n    ],\n    \"complexes\": [\"radial spoke head\"],\n    \"partners\": [],\n    \"other_free_text\": []\n  }\n}\n```"}