{"gene":"KIF3C","run_date":"2026-06-10T02:59:49","timeline":{"discoveries":[{"year":1998,"finding":"KIF3C forms a heteromeric kinesin complex with KIF3A (but not KIF3B) in rat brain, associates with a distinct population of membrane vesicles, and binds microtubules in a nucleotide-dependent manner, suggesting it functions as a vesicle-associated anterograde motor both independently and in association with KIF3A.","method":"Immunoprecipitation, sucrose density gradient sedimentation, subcellular fractionation, microtubule-binding assay, immunocytochemistry","journal":"Molecular biology of the cell","confidence":"High","confidence_rationale":"Tier 2 / Strong — reciprocal immunoprecipitation and biochemical fractionation replicated independently in two labs (PMID:9487132 and PMID:9450952) with multiple orthogonal methods","pmids":["9487132","9450952"],"is_preprint":false},{"year":1998,"finding":"KIF3C and KIF3B are 'variable' subunits that each associate with KIF3A but not with each other, indicating combinatorial heterodimer assembly within the KIF3 family.","method":"Immunoprecipitation from mouse brain; ligation-induced accumulation at proximal side of sciatic nerve indicating anterograde transport direction","journal":"Molecular biology of the cell","confidence":"High","confidence_rationale":"Tier 2 / Strong — independently confirmed by two labs (PMID:9450952, PMID:9487132) with reciprocal co-IP and nerve-ligation assay","pmids":["9450952","9487132"],"is_preprint":false},{"year":1998,"finding":"KIF3C localizes to the Golgi complex in spinal cord neurons and accumulates at the proximal side of ligated sciatic nerve, establishing it as an anterograde axonal motor.","method":"Double immunolabeling with anti-giantin, nerve ligation accumulation assay, immunocytochemistry","journal":"Molecular biology of the cell","confidence":"Medium","confidence_rationale":"Tier 2 / Moderate — direct localization experiment with functional implication (anterograde directionality), single lab","pmids":["9450952"],"is_preprint":false},{"year":2001,"finding":"Homozygous Kif3C knockout mice are viable, fertile, and develop normally, demonstrating that KIF3C is dispensable for normal neural development and behavior in mice.","method":"Homologous recombination knockout (two independent strains), phenotypic analysis","journal":"Molecular and cellular biology","confidence":"High","confidence_rationale":"Tier 2 / Strong — two independent knockout strains confirm the same negative phenotype, rigorous genetic loss-of-function","pmids":["11463814"],"is_preprint":false},{"year":2007,"finding":"FMRP acts as a molecular adaptor between RNA granules and KIF3C; KIF3C is a novel FMRP-interacting protein, and a KIF3C dominant-negative construct impedes distal transport of FMRP-containing RNA granules in dendrites.","method":"Co-immunoprecipitation of KIF3C with FMRP, time-lapse videomicroscopy of RNA granule dynamics with dominant-negative KIF3C expression","journal":"Human molecular genetics","confidence":"High","confidence_rationale":"Tier 2 / Moderate — reciprocal co-IP plus live imaging functional assay in the same study, single lab","pmids":["17881655"],"is_preprint":false},{"year":2013,"finding":"KIF3C preferentially binds to tyrosinated microtubules in the growth cone; its interaction with EB3 is necessary for localization at microtubule plus-ends. KIF3C depletion decreases microtubule catastrophe frequency, causing stable, overgrown, looped microtubules, and impairs axon outgrowth and regeneration after injury. KIF3C protein is locally translated in embryonic axons after injury.","method":"RNAi knockdown, KIF3C knockout mice, EB3 co-immunoprecipitation/interaction assay, live imaging of microtubule dynamics, in vitro and in vivo axon regeneration assays, local translation assay","journal":"The Journal of neuroscience","confidence":"High","confidence_rationale":"Tier 2 / Strong — multiple orthogonal methods (RNAi, KO mice, biochemical interaction, live microtubule dynamics, in vivo regeneration) in a single rigorous study","pmids":["23843507"],"is_preprint":false},{"year":2015,"finding":"Silencing KIF3C by shRNA in breast cancer cells inhibits epithelial-mesenchymal transition and metastasis by inhibiting TGF-β signaling and induces G2/M phase arrest suppressing proliferation.","method":"shRNA knockdown, flow cytometry cell cycle analysis, xenograft mouse model, Western blot for TGF-β pathway markers","journal":"Cancer letters","confidence":"Medium","confidence_rationale":"Tier 3 / Moderate — loss-of-function with defined cellular phenotype and pathway link, single lab, no mechanistic reconstitution","pmids":["26272184"],"is_preprint":false},{"year":2021,"finding":"METTL3-mediated m6A modification on KIF3C mRNA stabilizes it via IGF2BP1; miR-320d inhibits KIF3C expression by targeting METTL3, thereby reducing m6A-dependent KIF3C mRNA stabilization in prostate cancer cells.","method":"m6A modification assay, RIP, luciferase reporter, miR-320d overexpression, rescue experiments","journal":"Aging","confidence":"Medium","confidence_rationale":"Tier 3 / Moderate — multiple complementary assays establishing post-transcriptional regulation mechanism, single lab","pmids":["34537760"],"is_preprint":false},{"year":2024,"finding":"VASH2-induced tubulin detyrosination increases KIF3C binding to microtubules and enhances KIF3C-dependent endosomal recycling of EGFR, leading to prolonged activation of PI3K/Akt/mTOR signaling in lung squamous cell carcinoma.","method":"VASH2 knockdown/overexpression, tubulin detyrosination assay, co-immunoprecipitation, EGFR recycling assay, xenograft model with TCP inhibitor","journal":"Cell death & disease","confidence":"Medium","confidence_rationale":"Tier 2 / Moderate — multiple orthogonal methods linking tubulin modification to KIF3C-mediated cargo trafficking, single lab","pmids":["39443476"],"is_preprint":false},{"year":2023,"finding":"ZNF513 transcription factor binds KIF3C exon 1 and positively regulates KIF3C expression in gingival fibroblasts; the KIF3C p.R410H variant activates PI3K and KCNQ1 potassium channels. Double heterozygous mutations in ZNF513 and KIF3C together cause gingival hyperplasia in knock-in mice, whereas either mutation alone does not produce the phenotype.","method":"Chromatin immunoprecipitation/binding assay (ZNF513 to KIF3C exon 1), knock-in mouse model, in vitro functional assays, Western blot for PI3K/AKT/mTOR and Ras/Raf/MEK/ERK pathway markers","journal":"International journal of oral science","confidence":"Medium","confidence_rationale":"Tier 2 / Moderate — direct binding assay plus knock-in mouse genetic epistasis, single lab","pmids":["37752101"],"is_preprint":false},{"year":2024,"finding":"The KIF3AC heterodimer (KIF3A+KIF3C) and the Rab11 adaptor RCP are required for recycling of endocytosed β1-integrin back to the plasma membrane after focal adhesion disassembly; KIF3C associates with β1-integrin in an RCP-dependent manner only after FA disassembly. KIF3AC knockdown inhibits cell migration, RCP trafficking toward the leading edge, and polarized FA formation.","method":"Biochemical pulldown (KIF3C with β1-integrin), RNAi knockdown of KIF3C/KIF3A, live imaging of FA disassembly and integrin recycling, Rab11 endocytic compartment accumulation assay in mouse and human fibroblasts","journal":"bioRxiv","confidence":"Medium","confidence_rationale":"Tier 2 / Moderate — direct pulldown plus live imaging plus RNAi with defined phenotype, single lab, preprint not yet peer-reviewed","pmids":["bio_10.1101_2024.12.09.627580"],"is_preprint":true},{"year":2024,"finding":"KIF3C is required for proper cerebellar development: Kif3c-/- mice show reduced CGNP proliferation, cerebellar hypoplasia, and altered Bergmann glia density/patterning associated with reduced Hes1 expression, in a Hedgehog-independent but putative Notch-dependent manner.","method":"Kif3c germline knockout mouse analysis, quantification of CGNP proliferation, Hedgehog pathway reporter assay (no change detected), Hes1 expression measurement, Bergmann glia immunostaining","journal":"bioRxiv","confidence":"Medium","confidence_rationale":"Tier 2 / Moderate — genetic KO with defined cellular phenotype and pathway exclusion (HH-independent), single lab, preprint","pmids":["bio_10.1101_2024.12.02.626415"],"is_preprint":true}],"current_model":"KIF3C is a neuronally enriched kinesin-2 family anterograde motor that forms a heterodimer with KIF3A (but not KIF3B), associates with membrane vesicles and tyrosinated microtubules, transports FMRP-containing RNA granules in dendrites using FMRP as a molecular adaptor, regulates microtubule dynamics (catastrophe frequency) at axonal growth cones via interaction with EB3, participates in endosomal recycling of β1-integrin and EGFR in a KIF3AC/RCP-dependent manner to support cell migration, and is subject to post-transcriptional regulation by m6A modification (METTL3/IGF2BP1) and multiple miRNAs; in non-neural contexts, KIF3C activity is linked to PI3K/AKT/mTOR and TGF-β signaling, and its microtubule binding is enhanced by VASH2-mediated tubulin detyrosination."},"narrative":{"mechanistic_narrative":"KIF3C is a neuronally enriched kinesin-2 family motor that drives anterograde, microtubule-based transport and shapes microtubule dynamics in neurons [PMID:9487132, PMID:9450952]. It assembles combinatorially within the KIF3 family, forming a heterodimer with KIF3A but not with KIF3B, and associates with a distinct population of membrane vesicles and the Golgi complex while binding microtubules in a nucleotide-dependent manner [PMID:9487132, PMID:9450952]. As a transport motor it moves FMRP-containing RNA granules into dendrites using FMRP as a molecular adaptor [PMID:17881655], and the KIF3AC heterodimer together with the Rab11 adaptor RCP recycles endocytosed β1-integrin and EGFR cargo back to the plasma membrane to support cell migration [PMID:bio_10.1101_2024.12.09.627580, PMID:39443476]. Independently of cargo transport, KIF3C regulates microtubule plus-end dynamics at axonal growth cones: it preferentially binds tyrosinated microtubules, localizes to plus-ends via EB3, and promotes microtubule catastrophe, with KIF3C loss producing stable, overgrown, looped microtubules and impaired axon outgrowth and regeneration [PMID:23843507]. KIF3C microtubule binding is enhanced by VASH2-mediated tubulin detyrosination, which potentiates EGFR recycling and prolonged PI3K/Akt/mTOR signaling [PMID:39443476]. KIF3C expression is controlled post-transcriptionally by METTL3/IGF2BP1-dependent m6A mRNA stabilization (antagonized by miR-320d) [PMID:34537760] and transcriptionally by ZNF513 [PMID:37752101]. Germline Kif3c knockout mice are viable, fertile, and develop normally [PMID:11463814], though they show defective cerebellar development with reduced granule cell precursor proliferation [PMID:bio_10.1101_2024.12.02.626415].","teleology":[{"year":1998,"claim":"Established that KIF3C is a kinesin motor that assembles combinatorially with KIF3A (but not KIF3B) and functions as a vesicle-associated anterograde transporter, defining its core identity as a motor.","evidence":"Reciprocal immunoprecipitation, sucrose density sedimentation, subcellular fractionation, microtubule-binding assays, and nerve-ligation accumulation in rat and mouse brain","pmids":["9487132","9450952"],"confidence":"High","gaps":["Cargo specificity of the vesicle population not defined","Motility/directionality not directly measured at single-motor level"]},{"year":1998,"claim":"Localized KIF3C to the Golgi complex and demonstrated proximal accumulation upon nerve ligation, fixing its directional role as an anterograde axonal motor.","evidence":"Double immunolabeling with anti-giantin and nerve-ligation accumulation assay in spinal cord neurons","pmids":["9450952"],"confidence":"Medium","gaps":["Single-lab localization","Cargo carried during anterograde transport unidentified"]},{"year":2001,"claim":"Tested whether KIF3C is essential in vivo; knockout mice being viable and normal indicated functional redundancy rather than an indispensable role in neural development.","evidence":"Two independent homologous-recombination knockout strains with phenotypic analysis","pmids":["11463814"],"confidence":"High","gaps":["Redundant partners not identified at this stage","Subtle or context-specific phenotypes not assessed"]},{"year":2007,"claim":"Identified a specific cargo by showing FMRP acts as a molecular adaptor linking RNA granules to KIF3C, establishing KIF3C as a dendritic RNA-granule transporter.","evidence":"Reciprocal co-immunoprecipitation of KIF3C with FMRP and time-lapse imaging of granule transport with dominant-negative KIF3C","pmids":["17881655"],"confidence":"High","gaps":["Direct motor-adaptor binding interface not mapped","Single lab"]},{"year":2013,"claim":"Revealed a transport-independent function: KIF3C regulates microtubule catastrophe at growth cones via tyrosinated-microtubule and EB3 binding, controlling axon outgrowth and regeneration.","evidence":"RNAi, KIF3C knockout mice, EB3 interaction assays, live microtubule-dynamics imaging, in vivo regeneration assays, and local-translation assays","pmids":["23843507"],"confidence":"High","gaps":["Molecular mechanism by which KIF3C promotes catastrophe not resolved","Relationship between motor activity and catastrophe-promoting activity unclear"]},{"year":2015,"claim":"Extended KIF3C function to cancer cell biology, linking its activity to TGF-β-driven EMT, metastasis, and cell-cycle progression.","evidence":"shRNA knockdown, flow cytometry, xenograft model, and TGF-β pathway Western blots in breast cancer cells","pmids":["26272184"],"confidence":"Medium","gaps":["No mechanistic reconstitution linking KIF3C to TGF-β signaling","Single lab"]},{"year":2021,"claim":"Defined post-transcriptional control of KIF3C, showing m6A modification by METTL3/IGF2BP1 stabilizes its mRNA and is antagonized by miR-320d.","evidence":"m6A assays, RIP, luciferase reporters, and miR-320d rescue experiments in prostate cancer cells","pmids":["34537760"],"confidence":"Medium","gaps":["Downstream effector pathways of KIF3C in prostate cancer not detailed","Single lab"]},{"year":2023,"claim":"Identified transcriptional regulation of KIF3C by ZNF513 and a disease-associated variant, with genetic epistasis showing combined ZNF513/KIF3C mutation causes gingival hyperplasia.","evidence":"ChIP/binding assay, knock-in mouse genetic epistasis, and PI3K/AKT/mTOR and Ras/ERK pathway Western blots","pmids":["37752101"],"confidence":"Medium","gaps":["Mechanism by which p.R410H activates PI3K and KCNQ1 not resolved","Single lab"]},{"year":2024,"claim":"Linked tubulin detyrosination to KIF3C function, showing VASH2-mediated detyrosination enhances KIF3C microtubule binding and EGFR endosomal recycling to sustain PI3K/Akt/mTOR signaling.","evidence":"VASH2 knockdown/overexpression, detyrosination assays, co-IP, EGFR recycling assays, and xenograft with detyrosination inhibitor in lung squamous carcinoma","pmids":["39443476"],"confidence":"Medium","gaps":["Whether KIF3C directly motors EGFR-laden endosomes not shown","Single lab"]},{"year":2024,"claim":"Defined a KIF3AC/RCP cargo-recycling axis, showing the heterodimer recycles β1-integrin after focal adhesion disassembly to drive polarized cell migration.","evidence":"Biochemical pulldown, RNAi of KIF3C/KIF3A, and live imaging of FA disassembly and integrin recycling in fibroblasts (preprint)","pmids":["bio_10.1101_2024.12.09.627580"],"confidence":"Medium","gaps":["Not yet peer reviewed","Direct vs RCP-mediated integrin association not fully separated"]},{"year":2024,"claim":"Uncovered a developmental requirement for KIF3C in cerebellar growth via a Hedgehog-independent, putative Notch/Hes1 mechanism, contrasting with the originally normal-appearing knockout.","evidence":"Kif3c knockout cerebellar phenotyping, CGNP proliferation quantification, Hedgehog reporter (no change), and Hes1/Bergmann glia analysis (preprint)","pmids":["bio_10.1101_2024.12.02.626415"],"confidence":"Medium","gaps":["Notch dependence inferred, not directly demonstrated","Not yet peer reviewed"]},{"year":null,"claim":"How KIF3C's transport-motor activity and its microtubule-catastrophe-promoting activity are mechanistically coordinated, and which functions depend on the KIF3AC heterodimer versus KIF3C alone, remain unresolved.","evidence":"","pmids":[],"confidence":"Medium","gaps":["No structural model of the KIF3AC motor or its plus-end catastrophe mechanism","Unclear which in vivo cargoes require heterodimerization with KIF3A"]}],"mechanism_profile":{"molecular_activity":[{"term_id":"GO:0003774","term_label":"cytoskeletal motor activity","supporting_discovery_ids":[0,2]},{"term_id":"GO:0140657","term_label":"ATP-dependent activity","supporting_discovery_ids":[0]},{"term_id":"GO:0008092","term_label":"cytoskeletal protein binding","supporting_discovery_ids":[0,5]},{"term_id":"GO:0060090","term_label":"molecular adaptor activity","supporting_discovery_ids":[4]}],"localization":[{"term_id":"GO:0005794","term_label":"Golgi apparatus","supporting_discovery_ids":[2]},{"term_id":"GO:0031410","term_label":"cytoplasmic vesicle","supporting_discovery_ids":[0]},{"term_id":"GO:0005856","term_label":"cytoskeleton","supporting_discovery_ids":[5]},{"term_id":"GO:0005768","term_label":"endosome","supporting_discovery_ids":[10,8]}],"pathway":[{"term_id":"R-HSA-5653656","term_label":"Vesicle-mediated transport","supporting_discovery_ids":[0,4,10]},{"term_id":"R-HSA-9609507","term_label":"Protein localization","supporting_discovery_ids":[10,8]},{"term_id":"R-HSA-162582","term_label":"Signal Transduction","supporting_discovery_ids":[8,6]},{"term_id":"R-HSA-1266738","term_label":"Developmental Biology","supporting_discovery_ids":[5,11]}],"complexes":["KIF3AC heterodimer"],"partners":["KIF3A","FMRP","EB3","RCP","ITGB1","EGFR"],"other_free_text":[]}},"prefetch_data":{"uniprot":{"accession":"O14782","full_name":"Kinesin-like protein KIF3C","aliases":[],"length_aa":793,"mass_kda":89.5,"function":"Microtubule-based anterograde translocator for membranous organelles","subcellular_location":"Cytoplasm, cytoskeleton","url":"https://www.uniprot.org/uniprotkb/O14782/entry"},"depmap":{"release":"DepMap","has_data":true,"is_common_essential":false,"resolved_as":"","url":"https://depmap.org/portal/gene/KIF3C","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":[{"gene":"KIF3A","stoichiometry":10.0}],"url":"https://opencell.sf.czbiohub.org/search/KIF3C","total_profiled":1310},"omim":[{"mim_id":"612991","title":"ASXL TRANSCRIPTIONAL REGULATOR 2; ASXL2","url":"https://www.omim.org/entry/612991"},{"mim_id":"604683","title":"KINESIN FAMILY MEMBER 3A; KIF3A","url":"https://www.omim.org/entry/604683"},{"mim_id":"602845","title":"KINESIN FAMILY MEMBER 3C; KIF3C","url":"https://www.omim.org/entry/602845"},{"mim_id":"602109","title":"MATRILIN 3; MATN3","url":"https://www.omim.org/entry/602109"},{"mim_id":"309550","title":"FRAGILE X MESSENGER RIBONUCLEOPROTEIN 1; FMR1","url":"https://www.omim.org/entry/309550"}],"hpa":{"profiled":true,"resolved_as":"","reliability":"","locations":[],"tissue_specificity":"Tissue enriched","tissue_distribution":"Detected in many","driving_tissues":[{"tissue":"brain","ntpm":75.6}],"url":"https://www.proteinatlas.org/search/KIF3C"},"hgnc":{"alias_symbol":[],"prev_symbol":[]},"alphafold":{"accession":"O14782","domains":[{"cath_id":"3.40.850.10","chopping":"10-254_289-374","consensus_level":"high","plddt":88.216,"start":10,"end":374},{"cath_id":"-","chopping":"376-401_457-525","consensus_level":"medium","plddt":74.0577,"start":376,"end":525},{"cath_id":"-","chopping":"615-664","consensus_level":"medium","plddt":80.9624,"start":615,"end":664}],"viewer_url":"https://alphafold.ebi.ac.uk/entry/O14782","model_url":"https://alphafold.ebi.ac.uk/files/AF-O14782-F1-model_v6.cif","pae_url":"https://alphafold.ebi.ac.uk/files/AF-O14782-F1-predicted_aligned_error_v6.png","plddt_mean":69.81},"mouse_models":{"mgi_url":"https://www.informatics.jax.org/marker/summary?nomen=KIF3C","jax_strain_url":"https://www.jax.org/strain/search?query=KIF3C"},"sequence":{"accession":"O14782","fasta_url":"https://rest.uniprot.org/uniprotkb/O14782.fasta","uniprot_url":"https://www.uniprot.org/uniprotkb/O14782/entry","alphafold_viewer_url":"https://alphafold.ebi.ac.uk/entry/O14782"}},"corpus_meta":[{"pmid":"17881655","id":"PMC_17881655","title":"The fragile X mental retardation protein is a molecular adaptor between the neurospecific KIF3C kinesin and dendritic RNA granules.","date":"2007","source":"Human molecular genetics","url":"https://pubmed.ncbi.nlm.nih.gov/17881655","citation_count":103,"is_preprint":false},{"pmid":"9487132","id":"PMC_9487132","title":"KIF3C and KIF3A form a novel neuronal heteromeric kinesin that associates with membrane vesicles.","date":"1998","source":"Molecular biology of the cell","url":"https://pubmed.ncbi.nlm.nih.gov/9487132","citation_count":97,"is_preprint":false},{"pmid":"9450952","id":"PMC_9450952","title":"Characterization of the KIF3C neural kinesin-like motor from mouse.","date":"1998","source":"Molecular biology of the cell","url":"https://pubmed.ncbi.nlm.nih.gov/9450952","citation_count":89,"is_preprint":false},{"pmid":"23843507","id":"PMC_23843507","title":"The kinesin-2 family member KIF3C regulates microtubule dynamics and is required for axon growth and 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\"method\": \"Immunoprecipitation, sucrose density gradient sedimentation, subcellular fractionation, microtubule-binding assay, immunocytochemistry\",\n      \"journal\": \"Molecular biology of the cell\",\n      \"confidence\": \"High\",\n      \"confidence_rationale\": \"Tier 2 / Strong — reciprocal immunoprecipitation and biochemical fractionation replicated independently in two labs (PMID:9487132 and PMID:9450952) with multiple orthogonal methods\",\n      \"pmids\": [\"9487132\", \"9450952\"],\n      \"is_preprint\": false\n    },\n    {\n      \"year\": 1998,\n      \"finding\": \"KIF3C and KIF3B are 'variable' subunits that each associate with KIF3A but not with each other, indicating combinatorial heterodimer assembly within the KIF3 family.\",\n      \"method\": \"Immunoprecipitation from mouse brain; ligation-induced accumulation at proximal side of sciatic nerve indicating anterograde transport direction\",\n      \"journal\": \"Molecular biology of the cell\",\n      \"confidence\": \"High\",\n      \"confidence_rationale\": \"Tier 2 / Strong — independently confirmed by two labs (PMID:9450952, PMID:9487132) with reciprocal co-IP and nerve-ligation assay\",\n      \"pmids\": [\"9450952\", \"9487132\"],\n      \"is_preprint\": false\n    },\n    {\n      \"year\": 1998,\n      \"finding\": \"KIF3C localizes to the Golgi complex in spinal cord neurons and accumulates at the proximal side of ligated sciatic nerve, establishing it as an anterograde axonal motor.\",\n      \"method\": \"Double immunolabeling with anti-giantin, nerve ligation accumulation assay, immunocytochemistry\",\n      \"journal\": \"Molecular biology of the cell\",\n      \"confidence\": \"Medium\",\n      \"confidence_rationale\": \"Tier 2 / Moderate — direct localization experiment with functional implication (anterograde directionality), single lab\",\n      \"pmids\": [\"9450952\"],\n      \"is_preprint\": false\n    },\n    {\n      \"year\": 2001,\n      \"finding\": \"Homozygous Kif3C knockout mice are viable, fertile, and develop normally, demonstrating that KIF3C is dispensable for normal neural development and behavior in mice.\",\n      \"method\": \"Homologous recombination knockout (two independent strains), phenotypic analysis\",\n      \"journal\": \"Molecular and cellular biology\",\n      \"confidence\": \"High\",\n      \"confidence_rationale\": \"Tier 2 / Strong — two independent knockout strains confirm the same negative phenotype, rigorous genetic loss-of-function\",\n      \"pmids\": [\"11463814\"],\n      \"is_preprint\": false\n    },\n    {\n      \"year\": 2007,\n      \"finding\": \"FMRP acts as a molecular adaptor between RNA granules and KIF3C; KIF3C is a novel FMRP-interacting protein, and a KIF3C dominant-negative construct impedes distal transport of FMRP-containing RNA granules in dendrites.\",\n      \"method\": \"Co-immunoprecipitation of KIF3C with FMRP, time-lapse videomicroscopy of RNA granule dynamics with dominant-negative KIF3C expression\",\n      \"journal\": \"Human molecular genetics\",\n      \"confidence\": \"High\",\n      \"confidence_rationale\": \"Tier 2 / Moderate — reciprocal co-IP plus live imaging functional assay in the same study, single lab\",\n      \"pmids\": [\"17881655\"],\n      \"is_preprint\": false\n    },\n    {\n      \"year\": 2013,\n      \"finding\": \"KIF3C preferentially binds to tyrosinated microtubules in the growth cone; its interaction with EB3 is necessary for localization at microtubule plus-ends. KIF3C depletion decreases microtubule catastrophe frequency, causing stable, overgrown, looped microtubules, and impairs axon outgrowth and regeneration after injury. KIF3C protein is locally translated in embryonic axons after injury.\",\n      \"method\": \"RNAi knockdown, KIF3C knockout mice, EB3 co-immunoprecipitation/interaction assay, live imaging of microtubule dynamics, in vitro and in vivo axon regeneration assays, local translation assay\",\n      \"journal\": \"The Journal of neuroscience\",\n      \"confidence\": \"High\",\n      \"confidence_rationale\": \"Tier 2 / Strong — multiple orthogonal methods (RNAi, KO mice, biochemical interaction, live microtubule dynamics, in vivo regeneration) in a single rigorous study\",\n      \"pmids\": [\"23843507\"],\n      \"is_preprint\": false\n    },\n    {\n      \"year\": 2015,\n      \"finding\": \"Silencing KIF3C by shRNA in breast cancer cells inhibits epithelial-mesenchymal transition and metastasis by inhibiting TGF-β signaling and induces G2/M phase arrest suppressing proliferation.\",\n      \"method\": \"shRNA knockdown, flow cytometry cell cycle analysis, xenograft mouse model, Western blot for TGF-β pathway markers\",\n      \"journal\": \"Cancer letters\",\n      \"confidence\": \"Medium\",\n      \"confidence_rationale\": \"Tier 3 / Moderate — loss-of-function with defined cellular phenotype and pathway link, single lab, no mechanistic reconstitution\",\n      \"pmids\": [\"26272184\"],\n      \"is_preprint\": false\n    },\n    {\n      \"year\": 2021,\n      \"finding\": \"METTL3-mediated m6A modification on KIF3C mRNA stabilizes it via IGF2BP1; miR-320d inhibits KIF3C expression by targeting METTL3, thereby reducing m6A-dependent KIF3C mRNA stabilization in prostate cancer cells.\",\n      \"method\": \"m6A modification assay, RIP, luciferase reporter, miR-320d overexpression, rescue experiments\",\n      \"journal\": \"Aging\",\n      \"confidence\": \"Medium\",\n      \"confidence_rationale\": \"Tier 3 / Moderate — multiple complementary assays establishing post-transcriptional regulation mechanism, single lab\",\n      \"pmids\": [\"34537760\"],\n      \"is_preprint\": false\n    },\n    {\n      \"year\": 2024,\n      \"finding\": \"VASH2-induced tubulin detyrosination increases KIF3C binding to microtubules and enhances KIF3C-dependent endosomal recycling of EGFR, leading to prolonged activation of PI3K/Akt/mTOR signaling in lung squamous cell carcinoma.\",\n      \"method\": \"VASH2 knockdown/overexpression, tubulin detyrosination assay, co-immunoprecipitation, EGFR recycling assay, xenograft model with TCP inhibitor\",\n      \"journal\": \"Cell death & disease\",\n      \"confidence\": \"Medium\",\n      \"confidence_rationale\": \"Tier 2 / Moderate — multiple orthogonal methods linking tubulin modification to KIF3C-mediated cargo trafficking, single lab\",\n      \"pmids\": [\"39443476\"],\n      \"is_preprint\": false\n    },\n    {\n      \"year\": 2023,\n      \"finding\": \"ZNF513 transcription factor binds KIF3C exon 1 and positively regulates KIF3C expression in gingival fibroblasts; the KIF3C p.R410H variant activates PI3K and KCNQ1 potassium channels. Double heterozygous mutations in ZNF513 and KIF3C together cause gingival hyperplasia in knock-in mice, whereas either mutation alone does not produce the phenotype.\",\n      \"method\": \"Chromatin immunoprecipitation/binding assay (ZNF513 to KIF3C exon 1), knock-in mouse model, in vitro functional assays, Western blot for PI3K/AKT/mTOR and Ras/Raf/MEK/ERK pathway markers\",\n      \"journal\": \"International journal of oral science\",\n      \"confidence\": \"Medium\",\n      \"confidence_rationale\": \"Tier 2 / Moderate — direct binding assay plus knock-in mouse genetic epistasis, single lab\",\n      \"pmids\": [\"37752101\"],\n      \"is_preprint\": false\n    },\n    {\n      \"year\": 2024,\n      \"finding\": \"The KIF3AC heterodimer (KIF3A+KIF3C) and the Rab11 adaptor RCP are required for recycling of endocytosed β1-integrin back to the plasma membrane after focal adhesion disassembly; KIF3C associates with β1-integrin in an RCP-dependent manner only after FA disassembly. KIF3AC knockdown inhibits cell migration, RCP trafficking toward the leading edge, and polarized FA formation.\",\n      \"method\": \"Biochemical pulldown (KIF3C with β1-integrin), RNAi knockdown of KIF3C/KIF3A, live imaging of FA disassembly and integrin recycling, Rab11 endocytic compartment accumulation assay in mouse and human fibroblasts\",\n      \"journal\": \"bioRxiv\",\n      \"confidence\": \"Medium\",\n      \"confidence_rationale\": \"Tier 2 / Moderate — direct pulldown plus live imaging plus RNAi with defined phenotype, single lab, preprint not yet peer-reviewed\",\n      \"pmids\": [\"bio_10.1101_2024.12.09.627580\"],\n      \"is_preprint\": true\n    },\n    {\n      \"year\": 2024,\n      \"finding\": \"KIF3C is required for proper cerebellar development: Kif3c-/- mice show reduced CGNP proliferation, cerebellar hypoplasia, and altered Bergmann glia density/patterning associated with reduced Hes1 expression, in a Hedgehog-independent but putative Notch-dependent manner.\",\n      \"method\": \"Kif3c germline knockout mouse analysis, quantification of CGNP proliferation, Hedgehog pathway reporter assay (no change detected), Hes1 expression measurement, Bergmann glia immunostaining\",\n      \"journal\": \"bioRxiv\",\n      \"confidence\": \"Medium\",\n      \"confidence_rationale\": \"Tier 2 / Moderate — genetic KO with defined cellular phenotype and pathway exclusion (HH-independent), single lab, preprint\",\n      \"pmids\": [\"bio_10.1101_2024.12.02.626415\"],\n      \"is_preprint\": true\n    }\n  ],\n  \"current_model\": \"KIF3C is a neuronally enriched kinesin-2 family anterograde motor that forms a heterodimer with KIF3A (but not KIF3B), associates with membrane vesicles and tyrosinated microtubules, transports FMRP-containing RNA granules in dendrites using FMRP as a molecular adaptor, regulates microtubule dynamics (catastrophe frequency) at axonal growth cones via interaction with EB3, participates in endosomal recycling of β1-integrin and EGFR in a KIF3AC/RCP-dependent manner to support cell migration, and is subject to post-transcriptional regulation by m6A modification (METTL3/IGF2BP1) and multiple miRNAs; in non-neural contexts, KIF3C activity is linked to PI3K/AKT/mTOR and TGF-β signaling, and its microtubule binding is enhanced by VASH2-mediated tubulin detyrosination.\"\n}\n```","stage2_raw":"{\n  \"mechanistic_narrative\": \"KIF3C is a neuronally enriched kinesin-2 family motor that drives anterograde, microtubule-based transport and shapes microtubule dynamics in neurons [#0, #2]. It assembles combinatorially within the KIF3 family, forming a heterodimer with KIF3A but not with KIF3B, and associates with a distinct population of membrane vesicles and the Golgi complex while binding microtubules in a nucleotide-dependent manner [#0, #1, #2]. As a transport motor it moves FMRP-containing RNA granules into dendrites using FMRP as a molecular adaptor [#4], and the KIF3AC heterodimer together with the Rab11 adaptor RCP recycles endocytosed \\u03b21-integrin and EGFR cargo back to the plasma membrane to support cell migration [#10, #8]. Independently of cargo transport, KIF3C regulates microtubule plus-end dynamics at axonal growth cones: it preferentially binds tyrosinated microtubules, localizes to plus-ends via EB3, and promotes microtubule catastrophe, with KIF3C loss producing stable, overgrown, looped microtubules and impaired axon outgrowth and regeneration [#5]. KIF3C microtubule binding is enhanced by VASH2-mediated tubulin detyrosination, which potentiates EGFR recycling and prolonged PI3K/Akt/mTOR signaling [#8]. KIF3C expression is controlled post-transcriptionally by METTL3/IGF2BP1-dependent m6A mRNA stabilization (antagonized by miR-320d) [#7] and transcriptionally by ZNF513 [#9]. Germline Kif3c knockout mice are viable, fertile, and develop normally [#3], though they show defective cerebellar development with reduced granule cell precursor proliferation [#11].\",\n  \"teleology\": [\n    {\n      \"year\": 1998,\n      \"claim\": \"Established that KIF3C is a kinesin motor that assembles combinatorially with KIF3A (but not KIF3B) and functions as a vesicle-associated anterograde transporter, defining its core identity as a motor.\",\n      \"evidence\": \"Reciprocal immunoprecipitation, sucrose density sedimentation, subcellular fractionation, microtubule-binding assays, and nerve-ligation accumulation in rat and mouse brain\",\n      \"pmids\": [\"9487132\", \"9450952\"],\n      \"confidence\": \"High\",\n      \"gaps\": [\"Cargo specificity of the vesicle population not defined\", \"Motility/directionality not directly measured at single-motor level\"]\n    },\n    {\n      \"year\": 1998,\n      \"claim\": \"Localized KIF3C to the Golgi complex and demonstrated proximal accumulation upon nerve ligation, fixing its directional role as an anterograde axonal motor.\",\n      \"evidence\": \"Double immunolabeling with anti-giantin and nerve-ligation accumulation assay in spinal cord neurons\",\n      \"pmids\": [\"9450952\"],\n      \"confidence\": \"Medium\",\n      \"gaps\": [\"Single-lab localization\", \"Cargo carried during anterograde transport unidentified\"]\n    },\n    {\n      \"year\": 2001,\n      \"claim\": \"Tested whether KIF3C is essential in vivo; knockout mice being viable and normal indicated functional redundancy rather than an indispensable role in neural development.\",\n      \"evidence\": \"Two independent homologous-recombination knockout strains with phenotypic analysis\",\n      \"pmids\": [\"11463814\"],\n      \"confidence\": \"High\",\n      \"gaps\": [\"Redundant partners not identified at this stage\", \"Subtle or context-specific phenotypes not assessed\"]\n    },\n    {\n      \"year\": 2007,\n      \"claim\": \"Identified a specific cargo by showing FMRP acts as a molecular adaptor linking RNA granules to KIF3C, establishing KIF3C as a dendritic RNA-granule transporter.\",\n      \"evidence\": \"Reciprocal co-immunoprecipitation of KIF3C with FMRP and time-lapse imaging of granule transport with dominant-negative KIF3C\",\n      \"pmids\": [\"17881655\"],\n      \"confidence\": \"High\",\n      \"gaps\": [\"Direct motor-adaptor binding interface not mapped\", \"Single lab\"]\n    },\n    {\n      \"year\": 2013,\n      \"claim\": \"Revealed a transport-independent function: KIF3C regulates microtubule catastrophe at growth cones via tyrosinated-microtubule and EB3 binding, controlling axon outgrowth and regeneration.\",\n      \"evidence\": \"RNAi, KIF3C knockout mice, EB3 interaction assays, live microtubule-dynamics imaging, in vivo regeneration assays, and local-translation assays\",\n      \"pmids\": [\"23843507\"],\n      \"confidence\": \"High\",\n      \"gaps\": [\"Molecular mechanism by which KIF3C promotes catastrophe not resolved\", \"Relationship between motor activity and catastrophe-promoting activity unclear\"]\n    },\n    {\n      \"year\": 2015,\n      \"claim\": \"Extended KIF3C function to cancer cell biology, linking its activity to TGF-\\u03b2-driven EMT, metastasis, and cell-cycle progression.\",\n      \"evidence\": \"shRNA knockdown, flow cytometry, xenograft model, and TGF-\\u03b2 pathway Western blots in breast cancer cells\",\n      \"pmids\": [\"26272184\"],\n      \"confidence\": \"Medium\",\n      \"gaps\": [\"No mechanistic reconstitution linking KIF3C to TGF-\\u03b2 signaling\", \"Single lab\"]\n    },\n    {\n      \"year\": 2021,\n      \"claim\": \"Defined post-transcriptional control of KIF3C, showing m6A modification by METTL3/IGF2BP1 stabilizes its mRNA and is antagonized by miR-320d.\",\n      \"evidence\": \"m6A assays, RIP, luciferase reporters, and miR-320d rescue experiments in prostate cancer cells\",\n      \"pmids\": [\"34537760\"],\n      \"confidence\": \"Medium\",\n      \"gaps\": [\"Downstream effector pathways of KIF3C in prostate cancer not detailed\", \"Single lab\"]\n    },\n    {\n      \"year\": 2023,\n      \"claim\": \"Identified transcriptional regulation of KIF3C by ZNF513 and a disease-associated variant, with genetic epistasis showing combined ZNF513/KIF3C mutation causes gingival hyperplasia.\",\n      \"evidence\": \"ChIP/binding assay, knock-in mouse genetic epistasis, and PI3K/AKT/mTOR and Ras/ERK pathway Western blots\",\n      \"pmids\": [\"37752101\"],\n      \"confidence\": \"Medium\",\n      \"gaps\": [\"Mechanism by which p.R410H activates PI3K and KCNQ1 not resolved\", \"Single lab\"]\n    },\n    {\n      \"year\": 2024,\n      \"claim\": \"Linked tubulin detyrosination to KIF3C function, showing VASH2-mediated detyrosination enhances KIF3C microtubule binding and EGFR endosomal recycling to sustain PI3K/Akt/mTOR signaling.\",\n      \"evidence\": \"VASH2 knockdown/overexpression, detyrosination assays, co-IP, EGFR recycling assays, and xenograft with detyrosination inhibitor in lung squamous carcinoma\",\n      \"pmids\": [\"39443476\"],\n      \"confidence\": \"Medium\",\n      \"gaps\": [\"Whether KIF3C directly motors EGFR-laden endosomes not shown\", \"Single lab\"]\n    },\n    {\n      \"year\": 2024,\n      \"claim\": \"Defined a KIF3AC/RCP cargo-recycling axis, showing the heterodimer recycles \\u03b21-integrin after focal adhesion disassembly to drive polarized cell migration.\",\n      \"evidence\": \"Biochemical pulldown, RNAi of KIF3C/KIF3A, and live imaging of FA disassembly and integrin recycling in fibroblasts (preprint)\",\n      \"pmids\": [\"bio_10.1101_2024.12.09.627580\"],\n      \"confidence\": \"Medium\",\n      \"gaps\": [\"Not yet peer reviewed\", \"Direct vs RCP-mediated integrin association not fully separated\"]\n    },\n    {\n      \"year\": 2024,\n      \"claim\": \"Uncovered a developmental requirement for KIF3C in cerebellar growth via a Hedgehog-independent, putative Notch/Hes1 mechanism, contrasting with the originally normal-appearing knockout.\",\n      \"evidence\": \"Kif3c knockout cerebellar phenotyping, CGNP proliferation quantification, Hedgehog reporter (no change), and Hes1/Bergmann glia analysis (preprint)\",\n      \"pmids\": [\"bio_10.1101_2024.12.02.626415\"],\n      \"confidence\": \"Medium\",\n      \"gaps\": [\"Notch dependence inferred, not directly demonstrated\", \"Not yet peer reviewed\"]\n    },\n    {\n      \"year\": null,\n      \"claim\": \"How KIF3C's transport-motor activity and its microtubule-catastrophe-promoting activity are mechanistically coordinated, and which functions depend on the KIF3AC heterodimer versus KIF3C alone, remain unresolved.\",\n      \"evidence\": \"\",\n      \"pmids\": [],\n      \"confidence\": \"Medium\",\n      \"gaps\": [\"No structural model of the KIF3AC motor or its plus-end catastrophe mechanism\", \"Unclear which in vivo cargoes require heterodimerization with KIF3A\"]\n    }\n  ],\n  \"mechanism_profile\": {\n    \"molecular_activity\": [\n      {\"term_id\": \"GO:0003774\", \"supporting_discovery_ids\": [0, 2]},\n      {\"term_id\": \"GO:0140657\", \"supporting_discovery_ids\": [0]},\n      {\"term_id\": \"GO:0008092\", \"supporting_discovery_ids\": [0, 5]},\n      {\"term_id\": \"GO:0060090\", \"supporting_discovery_ids\": [4]}\n    ],\n    \"localization\": [\n      {\"term_id\": \"GO:0005794\", \"supporting_discovery_ids\": [2]},\n      {\"term_id\": \"GO:0031410\", \"supporting_discovery_ids\": [0]},\n      {\"term_id\": \"GO:0005856\", \"supporting_discovery_ids\": [5]},\n      {\"term_id\": \"GO:0005768\", \"supporting_discovery_ids\": [10, 8]}\n    ],\n    \"pathway\": [\n      {\"term_id\": \"R-HSA-5653656\", \"supporting_discovery_ids\": [0, 4, 10]},\n      {\"term_id\": \"R-HSA-9609507\", \"supporting_discovery_ids\": [10, 8]},\n      {\"term_id\": \"R-HSA-162582\", \"supporting_discovery_ids\": [8, 6]},\n      {\"term_id\": \"R-HSA-1266738\", \"supporting_discovery_ids\": [5, 11]}\n    ],\n    \"complexes\": [\"KIF3AC heterodimer\"],\n    \"partners\": [\"KIF3A\", \"FMRP\", \"EB3\", \"RCP\", \"ITGB1\", \"EGFR\"],\n    \"other_free_text\": []\n  }\n}","audit_flag":null,"evaluation":{"pairwise":"win","faith_supported":7,"faith_total":7,"faith_pct":100.0}}