{"gene":"KIF20A","run_date":"2026-06-10T02:59:49","timeline":{"discoveries":[{"year":2000,"finding":"KIF20A (Rab6-KIFL) was identified as a Rab6-binding kinesin via two-hybrid screen; it localizes to the spindle midzone in anaphase and to the cleavage furrow and midbody in telophase, and microinjection of anti-Rab6-KIFL antibodies causes binucleation due to failure of cleavage furrow formation, establishing a direct role in cytokinesis.","method":"Yeast two-hybrid screen, microinjection of inhibitory antibodies, time-lapse microscopy, immunofluorescence localization","journal":"The EMBO journal","confidence":"High","confidence_rationale":"Tier 2 / Strong — reciprocal binding assay plus direct loss-of-function (antibody injection) with defined cellular phenotype; replicated concept across multiple subsequent studies","pmids":["11060022"],"is_preprint":false},{"year":2004,"finding":"MKlp2 (KIF20A) is required for relocation of the Aurora B–INCENP chromosome passenger complex (CPC) from centromeres to the central spindle at the metaphase-to-anaphase transition; MKlp2 physically binds Aurora B and also binds the phosphatase Cdc14A, which can dephosphorylate INCENP to facilitate CPC relocation.","method":"siRNA depletion, co-immunoprecipitation, immunofluorescence microscopy","journal":"The Journal of cell biology","confidence":"High","confidence_rationale":"Tier 2 / Strong — reciprocal Co-IP showing direct binding, loss-of-function with defined localization phenotype, replicated by multiple subsequent studies","pmids":["15263015"],"is_preprint":false},{"year":2005,"finding":"KIF20A (RAB6KIFL) transports the scaffolding protein DLG5 as cargo; proteomics with anti-RAB6KIFL antibody identified DLG5 as a KIF20A cargo, and KIF20A knockdown displaced DLG5 from cytoplasmic membranes to the cytoplasm, demonstrating a membrane-trafficking function.","method":"Proteomics/pull-down with anti-RAB6KIFL antibody, siRNA knockdown, subcellular fractionation/immunolocalization","journal":"Cancer research","confidence":"Medium","confidence_rationale":"Tier 3 / Moderate — single lab, proteomics identification plus functional localization readout for the cargo","pmids":["15665285"],"is_preprint":false},{"year":2005,"finding":"KIF20A ATPase activity and microtubule-binding can be studied biochemically using recombinant protein from insect cells; Polo-like kinase 1 (Plk1) interaction with KIF20A was established using recombinant proteins in vitro.","method":"In vitro biochemical assays (microtubule binding, ATPase), recombinant protein expression in insect cells, in vitro Plk1 binding assay","journal":"Methods in enzymology","confidence":"Medium","confidence_rationale":"Tier 1 / Weak — in vitro reconstitution with purified proteins, single lab methods paper","pmids":["16473625"],"is_preprint":false},{"year":2010,"finding":"Mad2 binds MKlp2 (KIF20A) via a consensus Mad2-binding motif on MKlp2, preventing its loading onto the mitotic spindle and blocking CPC relocation from centromeres; an MKlp2 mutant refractory to Mad2 binding prematurely loads onto the spindle and mislocalizes Aurora B from the midbody, causing cytokinesis failure.","method":"Co-immunoprecipitation, site-directed mutagenesis of Mad2-binding motif, live-cell imaging, siRNA rescue experiments","journal":"The Journal of cell biology","confidence":"High","confidence_rationale":"Tier 2 / Strong — Co-IP plus mutagenesis plus defined loss-of-function phenotype, multiple orthogonal methods in one study","pmids":["21149564"],"is_preprint":false},{"year":2013,"finding":"MKlp2 requires myosin-II for its own localization to the equatorial cortex; this event is required to recruit Aurora B to the equatorial cortex, which in turn promotes focused RhoA accumulation and stable cleavage furrow ingression. An MKlp2 mutant defective in myosin-II binding fails to recruit Aurora B to the cortex and fails to maintain the ingressing furrow.","method":"Drug-induced monopolar cytokinesis assay, dominant-negative myosin-II, MKlp2 binding-mutant expression, immunofluorescence, live-cell imaging","journal":"PloS one","confidence":"High","confidence_rationale":"Tier 2 / Moderate — reciprocal co-localization, myosin-II binding mutant phenotype rescue, multiple functional readouts in single study","pmids":["23750214"],"is_preprint":false},{"year":2014,"finding":"Cdk1/cyclin B1 phosphorylates multiple sites in the MKlp2 stalk and C-terminal tail, inhibiting microtubule binding, bundling, oligomerization, and chromosome targeting of MKlp2 during early mitosis. Reversal of Cdk1 phosphorylation at anaphase onset promotes MKlp2–CPC complex formation and CPC relocation from chromosomes to the central spindle for cytokinesis.","method":"Identification of Cdk1 phosphorylation sites by mass spectrometry and mutagenesis, in vitro kinase assays, microtubule-binding/bundling assays, immunofluorescence, cell cycle analysis","journal":"Cell reports","confidence":"High","confidence_rationale":"Tier 1 / Strong — in vitro kinase assay plus mutagenesis plus functional rescue with defined cellular phenotypes, multiple orthogonal methods","pmids":["24656812"],"is_preprint":false},{"year":2014,"finding":"KIF20A promotes motility and invasiveness of pancreatic cancer cells by transporting the RNA-binding protein IGF2BP3 and its bound transcripts (including ARF6 and ARHGEF4 mRNAs) toward cell protrusions along microtubules; KIF20A knockdown inhibits IGF2BP3-containing stress granule accumulation in protrusions and suppresses local protein expression from these transcripts.","method":"siRNA knockdown, immunofluorescence, time-lapse microscopy, cell invasion/migration assays","journal":"Neoplasia (New York, N.Y.)","confidence":"Medium","confidence_rationale":"Tier 3 / Moderate — single lab, knockdown with defined cargo localization readout and functional consequence","pmids":["25499221"],"is_preprint":false},{"year":2015,"finding":"FOXM1 directly transcriptionally regulates KIF20A expression through a Forkhead response element (FHRE) in the KIF20A promoter; FOXM1 depletion reduces KIF20A expression, causes abnormal mitotic spindle morphology and chromosome alignment, and sensitizes breast cancer cells to paclitaxel-induced mitotic catastrophe.","method":"ChIP assay, promoter-luciferase reporter, siRNA knockdown, cell viability/senescence assays, spindle morphology by immunofluorescence","journal":"Oncogene","confidence":"High","confidence_rationale":"Tier 2 / Strong — ChIP plus luciferase reporter confirms direct transcriptional regulation; replicated in multiple cancer types by subsequent studies","pmids":["25961928"],"is_preprint":false},{"year":2016,"finding":"Aurora B phosphorylates MKlp2 at S878 within a lipid-association motif (LAM) in the C-terminal tail, acting as an inhibitory signal for abscission; B56-bound PP2A dephosphorylates MKlp2 S878 to promote abscission. A phospho-resistant S878A mutant of MKlp2 overrides Aurora B–mediated abscission blockade.","method":"Phospho-site mutagenesis (S878A), Aurora B kinase assay, PP2A phosphatase assay, live-cell imaging, abscission timing assays","journal":"Current biology : CB","confidence":"High","confidence_rationale":"Tier 1 / Strong — in vitro kinase/phosphatase assays with mutagenesis plus rescue in cells, multiple orthogonal methods","pmids":["27939310"],"is_preprint":false},{"year":2018,"finding":"KIF20A/MKLP2 interacts with RGS3 at the intercellular bridge of dividing neural progenitor cells (NPCs); KIF20A knockdown/knockout causes dislocation of RGS3 from the intercellular bridge, impairs Ephrin-B–RGS cell fate signaling, and shifts NPCs from proliferative to differentiative divisions, resulting in thinner cortex and ventriculomegaly without substantial cytokinesis defect.","method":"Co-immunoprecipitation, immunofluorescence, in utero electroporation knockdown, germline and inducible conditional KO mice, live imaging","journal":"Nature communications","confidence":"High","confidence_rationale":"Tier 2 / Strong — Co-IP plus genetic KO (germline and inducible) with multiple defined phenotypic readouts in vivo","pmids":["30006548"],"is_preprint":false},{"year":2018,"finding":"Loss of function of KIF20A (R182W ATPase-defective mutation identified in congenital cardiomyopathy patients) prevents efficient transport of Aurora B as part of the CPC: Aurora B remains trapped on chromatin and fails to translocate to the spindle midzone during cytokinesis.","method":"Patient compound heterozygous mutations, functional ATPase assay, immunofluorescence of Aurora B localization in patient-derived cells, zebrafish translational-blocking morpholino model","journal":"PLoS genetics","confidence":"High","confidence_rationale":"Tier 1 / Strong — ATPase-defective mutation with direct functional readout (Aurora B mislocalization) and in vivo zebrafish confirmation","pmids":["29357359"],"is_preprint":false},{"year":2020,"finding":"MKLP2 (KIF20A) is a processive, plus-end-directed motor that can transport the CPC along microtubules in vitro; strong suppression of MKLP2 motor activity via a P-loop mutant disrupts CPC accumulation at both the spindle midzone and equatorial cortex, whereas partial inhibition with Paprotrain mainly affects equatorial cortex localization.","method":"In vitro single-molecule motility assays with purified MKLP2 and CPC, P-loop ATPase mutant expression, Paprotrain inhibitor, live-cell imaging","journal":"Current biology : CB","confidence":"High","confidence_rationale":"Tier 1 / Strong — direct in vitro reconstitution of processive transport with purified proteins plus mutagenesis plus cell-based rescue, multiple orthogonal methods","pmids":["32502404"],"is_preprint":false},{"year":2020,"finding":"The INCENP RRKKRR motif is required for both centromeric CPC localization in metaphase and MKLP2-dependent CPC transport in anaphase; MKLP2 and DNA bind competitively to this motif, and INCENP T59 phosphorylation acts as a switch that prevents MKLP2 binding in metaphase. CPC binding to MKLP2 promotes the microtubule-dependent ATPase activity of MKLP2 in anaphase.","method":"Crystal structure of survivin–H3pT3 complex, mutagenesis of INCENP RRKKRR motif, ATPase assays, immunofluorescence, competitive binding assays","journal":"The Journal of cell biology","confidence":"High","confidence_rationale":"Tier 1 / Strong — crystal structure plus mutagenesis plus in vitro ATPase assay, multiple orthogonal methods in one rigorous study","pmids":["32356865"],"is_preprint":false},{"year":2020,"finding":"SEPT7 interacts with KIF20A at the intercellular bridge of dividing NPCs; SEPT7 knockdown displaces KIF20A from the midbody, causing early neuronal differentiation. NPC-specific inducible knockout of Sept7 causes early cell cycle exit and precocious differentiation without noticeable cytokinesis defect.","method":"Co-immunoprecipitation, immunofluorescence, in utero electroporation knockdown, inducible conditional KO mice","journal":"Cerebral cortex (New York, N.Y. : 1991)","confidence":"High","confidence_rationale":"Tier 2 / Strong — Co-IP plus genetic knockout with defined cellular phenotype","pmids":["31813992"],"is_preprint":false},{"year":2022,"finding":"MKLP2 facilitates chromosome congression in prometaphase by promoting error correction of syntelic kinetochore-microtubule attachments; MKLP2 inhibition results in elevated Aurora kinase activity, phosphorylation of HEC1-Ser55, and aneuploidy.","method":"Live imaging with fluorescent histones, MKLP2 small-molecule inhibitor (MKLP2i), siRNA, flow cytometry for aneuploidy","journal":"Journal of cell science","confidence":"Medium","confidence_rationale":"Tier 2 / Moderate — live imaging plus inhibitor/siRNA with defined molecular readouts, single lab","pmids":["35638575"],"is_preprint":false},{"year":2022,"finding":"KIF20A promotes castration-resistant prostate cancer (CRPC) progression through its role in Golgi-driven secretory vesicle fission and trafficking; KIF20A expression causes secretion of autocrine factors that activate androgen receptor signaling, and pharmacologic disruption of vesicle biogenesis blocks KIF20A-driven castration-resistant proliferation.","method":"Stable KIF20A overexpression, conditioned media transfer assays, Paprotrain inhibitor, androgen receptor reporter assays, in vivo xenograft, vesicle biogenesis inhibitors","journal":"Oncogene","confidence":"Medium","confidence_rationale":"Tier 2 / Moderate — conditioned media + pharmacologic vesicle disruption + in vivo validation, single lab","pmids":["35418689"],"is_preprint":false},{"year":2022,"finding":"The C-terminal tail of MKlp2 (CTM peptides) selectively binds PI(3)P-containing membranes over other negatively charged lipids, and this interaction depends critically on residue S21; this selective phosphoinositide binding provides a mechanism for MKlp2 tethering to the plasma membrane at the intercellular bridge during abscission.","method":"Quartz crystal microbalance-dissipation (QCM-D), atomic force microscopy force spectroscopy, synthetic peptide mutagenesis on model lipid membranes","journal":"The journal of physical chemistry. B","confidence":"Medium","confidence_rationale":"Tier 1 / Weak — rigorous biophysical in vitro assays with mutagenesis, single lab, model membranes only","pmids":["35316051"],"is_preprint":false},{"year":2023,"finding":"High-resolution crystal and cryo-EM structures of the KIF20A motor domain reveal an unusually long L6 insertion that integrates into the core of the motor domain, dramatically affecting allostery and ATPase activity. The neck linker is four times longer than in kinesin-1, and the extended neck linker is required for motor activity. These structural features explain the low processivity/motility of KIF20A compared to other kinesins.","method":"X-ray crystallography (nucleotide-free motor domain), cryo-EM (microtubule-bound structure), ATPase activity assays, mutagenesis of L6 insertion and neck linker","journal":"Open biology","confidence":"High","confidence_rationale":"Tier 1 / Strong — high-resolution crystal and cryo-EM structures with functional validation (ATPase assays and mutagenesis) in one study","pmids":["37726093"],"is_preprint":false},{"year":2023,"finding":"KIF20A physically interacts with BTRC (β-TrCP1), a substrate recognition subunit of SCFβ-TrCP E3 ubiquitin ligase; via this interaction, KIF20A reduces BTRC-mediated CDC25A poly-ubiquitination and enhances CDC25A protein stability.","method":"GST pull-down, co-immunoprecipitation, in vitro ubiquitination assay, cycloheximide chase assay","journal":"Journal of ginseng research","confidence":"Medium","confidence_rationale":"Tier 2 / Moderate — reciprocal Co-IP plus pull-down plus in vitro ubiquitination assay, single lab","pmids":["38223825"],"is_preprint":false},{"year":2024,"finding":"KIF20A inhibits FBXW7-mediated ubiquitination and degradation of c-Myc by competitively inhibiting the FBXW7–c-Myc interaction; KIF20A overexpression thereby stabilizes c-Myc, promotes glycolysis, and enhances tumor proliferation. KIF20A downregulation reduces c-Myc levels and suppresses MMR expression.","method":"KIF20A liver-specific knockout mouse, co-immunoprecipitation, c-Myc splicing mutant constructs, ubiquitination assays, immunohistochemistry of patient cohort","journal":"Cancer letters","confidence":"Medium","confidence_rationale":"Tier 2 / Moderate — Co-IP plus conditional KO mouse plus mechanistic mutant validation, single lab","pmids":["38971490"],"is_preprint":false},{"year":2024,"finding":"KIF20A inhibits DHX9 proteasomal degradation by blocking TRIM21-mediated K48-linked polyubiquitination at DHX9-K755; elevated DHX9 stabilizes SOX2 mRNA, upregulating SOX2 to promote cancer stem cell maintenance and ferroptosis resistance in OSCC.","method":"Co-immunoprecipitation, ubiquitination assay (K48-linkage specific), co-localization, SOX2 mRNA stability assay, loss-of-function/gain-of-function in vitro and in vivo","journal":"Cell death & disease","confidence":"Medium","confidence_rationale":"Tier 2 / Moderate — Co-IP plus site-specific ubiquitination assay plus functional rescue, single lab","pmids":["41672965"],"is_preprint":false},{"year":2025,"finding":"KIF20A maximal enrichment at antiparallel microtubule overlaps of the spindle midzone requires PRC1-crosslinked microtubules and cooperation with KIF4A: KIF20A delivers the CPC from non-overlapping microtubules to the midzone, while KIF4A retains the CPC at PRC1-crosslinked overlaps. Conditional depletion of KIF4A confirms it is required for CPC localization at the spindle midzone in anaphase.","method":"In vitro reconstitution with purified proteins, conditional KIF4A depletion in mitotic cells, live-cell imaging, immunofluorescence","journal":"bioRxiv","confidence":"Medium","confidence_rationale":"Tier 1 / Weak — in vitro reconstitution plus cell depletion; preprint, not yet peer-reviewed","pmids":[],"is_preprint":true},{"year":2025,"finding":"KIF20A cooperates with Myosin II to regulate actomyosin and branched actin dynamics, facilitating fission of transport intermediates at early endosomes; KIF20A inhibition causes enlargement of early and late endosomes, impairs Transferrin trafficking, and mislocalizes β1-Integrin from the plasma membrane.","method":"KIF20A inhibitor (Paprotrain), live-cell endosome imaging, Transferrin trafficking assay, β1-Integrin localization, Myosin II co-localization and functional assays","journal":"bioRxiv","confidence":"Low","confidence_rationale":"Tier 3 / Weak — preprint, single lab, inhibitor-based phenotypic assays without mechanistic reconstitution of the motor-myosin cooperation","pmids":[],"is_preprint":true},{"year":2026,"finding":"SYMPK interacts with KIF20A and NUMA1 during meiotic metaphase I in oocytes, as revealed by immunoprecipitation-mass spectrometry; SYMPK is required for proper localization of KIF20A and NUMA1 to the acentrosomal spindle, and SYMPK-deficient oocytes show disorganized spindle architecture and metaphase I arrest.","method":"Oocyte-specific Sympk knockout mice, immunoprecipitation-mass spectrometry, immunofluorescence, chromosome spread analysis","journal":"Journal of genetics and genomics","confidence":"Medium","confidence_rationale":"Tier 2 / Moderate — IP-MS plus genetic KO with defined localization phenotype, single lab","pmids":["41520922"],"is_preprint":false},{"year":2019,"finding":"KIF20A localizes to microtubules in spermatogenic cells and co-localizes with the spindle midzone and midbody; KIF20A inhibition (Paprotrain) leads to defects in central spindle assembly and cytokinetic abscission in male meiosis, increased aneuploidy, and impaired acrosome formation and maturation during spermatogenesis.","method":"Immunofluorescence localization, Paprotrain inhibitor treatment, flow cytometry for ploidy, acrosome staining","journal":"Biochimica et biophysica acta. Molecular cell research","confidence":"Medium","confidence_rationale":"Tier 2 / Weak — direct localization experiments plus inhibitor-based functional readouts, single lab","pmids":["31884069"],"is_preprint":false},{"year":2020,"finding":"Transcription factor GATA2 directly binds the KIF20A promoter and transcriptionally activates KIF20A in HBV-related hepatocellular carcinoma; HBx protein indirectly upregulates KIF20A via GATA2. GATA2 overexpression promotes HepG2.2.15 cell growth and inhibits apoptosis via KIF20A.","method":"ChIP assay, luciferase reporter assay, siRNA knockdown, overexpression, CCK-8 and flow cytometry","journal":"Frontiers in cellular and infection microbiology","confidence":"Medium","confidence_rationale":"Tier 2 / Moderate — ChIP plus luciferase reporter confirm direct promoter binding, functional rescue, single lab","pmids":["39624268"],"is_preprint":false},{"year":2026,"finding":"Lactate-driven histone H3K18 lactylation (H3K18la) directly activates transcription of KIF20A; KIF20A in turn stabilizes c-Myc protein, enhancing PD-L1 expression and suppressing cytotoxic T cell function, constituting a metabolic-epigenetic immune evasion axis. Glycolysis inhibition reduces H3K18la-driven KIF20A upregulation and synergizes with anti-PD-1 therapy.","method":"ChIP-sequencing, ChIP-PCR, dual-luciferase reporter, HCC-CD8+ T cell co-cultures, gene knockdown/overexpression, mouse xenograft and orthotopic models, pan-lysine and H3K18la immunohistochemistry in patient cohorts","journal":"Cancer biology & medicine","confidence":"Medium","confidence_rationale":"Tier 2 / Moderate — ChIP-seq plus reporter assay plus functional in vivo models, single lab, multiple orthogonal methods","pmids":["41937416"],"is_preprint":false},{"year":2022,"finding":"Auxin-inducible acute degradation of endogenous Mklp2 in MDCK cells causes delayed relocation of CPC component Aurora-B to the spindle midzone during anaphase and leads to cytokinesis failure and binucleation; these phenotypes are rescued by re-expression of Mklp2, confirming specificity.","method":"AID (auxin-inducible degron) tag on endogenous MKLP2, live-cell imaging, immunofluorescence, rescue by re-expression","journal":"Biology of the cell","confidence":"Medium","confidence_rationale":"Tier 2 / Moderate — acute conditional degradation with rescue, clean temporal control, single lab","pmids":["40490973"],"is_preprint":false},{"year":2026,"finding":"KIF20A physically interacts with DEPDC1 in liposarcoma cells as shown by co-immunoprecipitation; KIF20A knockdown partially reverses DEPDC1-driven proliferation, migration, and invasion, and attenuates PI3K/AKT/mTOR signaling activation.","method":"Co-immunoprecipitation, siRNA knockdown, CCK-8/invasion assays, western blot of PI3K/AKT/mTOR pathway","journal":"Frontiers in endocrinology","confidence":"Low","confidence_rationale":"Tier 3 / Weak — single Co-IP plus knockdown functional readout, single lab, no mechanistic detail on how interaction affects motor function","pmids":["40600015"],"is_preprint":false},{"year":2026,"finding":"KIF20A physically interacts with CLIP1 and enhances its protein stability in cervical cancer cells; CLIP1 silencing reverses the oncogenic effects of KIF20A overexpression.","method":"Co-immunoprecipitation, siRNA knockdown, protein stability assays, proliferation/migration/invasion functional assays, in vivo xenograft","journal":"Scientific reports","confidence":"Low","confidence_rationale":"Tier 3 / Weak — single Co-IP plus rescue experiment, single lab, mechanism of stability enhancement not biochemically detailed","pmids":["41776329"],"is_preprint":false},{"year":2026,"finding":"Transcription factor ATF2 binds directly to the KIF20A promoter and activates its transcription in prostate cancer, as validated by ChIP and dual-luciferase reporter assays.","method":"ChIP assay, dual-luciferase reporter, qRT-PCR, western blot, KIF20A knockdown functional assays","journal":"Frontiers in bioscience (Landmark edition)","confidence":"Medium","confidence_rationale":"Tier 2 / Weak — ChIP plus luciferase reporter establish direct promoter binding, single lab","pmids":["42216528"],"is_preprint":false}],"current_model":"KIF20A (MKLP2/RAB6KIFL) is a kinesin-6 family motor with a structurally atypical motor domain (extended L6 loop, long neck linker) that confers low processivity; it acts as a processive plus-end-directed microtubule motor that transports the Aurora B–containing chromosomal passenger complex (CPC) from anaphase chromosomes to the central spindle midzone and equatorial cortex, a process that is temporally gated by Cdk1 phosphorylation (inhibitory in early mitosis, relieved at anaphase) and spatially coordinated with KIF4A at PRC1-crosslinked antiparallel overlaps; at the cortex MKlp2 requires myosin-II for docking and recruits Aurora B to drive RhoA-dependent cleavage furrow ingression; abscission timing is further controlled by Aurora B phosphorylation of MKlp2-S878 in its lipid-association motif (inhibitory) opposed by B56-PP2A (permissive), while its Mad2-binding motif prevents premature spindle loading during the spindle assembly checkpoint; beyond cytokinesis, KIF20A also transports cargo such as DLG5, IGF2BP3-containing RNA granules, and vesicle intermediates at endosomes in cooperation with Myosin II, and—through Golgi-dependent secretory pathways—drives autocrine AR signaling in prostate cancer; in neural progenitors KIF20A interacts with RGS3 and SEPT7 at the intercellular bridge to regulate cell fate signaling independent of spindle orientation; non-mitotic functions include stabilizing c-Myc (by blocking FBXW7-mediated ubiquitination), stabilizing DHX9/SOX2 via inhibiting TRIM21 ubiquitination, and stabilizing CDC25A via BTRC sequestration; its expression is transcriptionally controlled by FOXM1, GATA2, ATF2, FOXK1, and IRF6, and epigenetically by H3K18 lactylation."},"narrative":{"mechanistic_narrative":"KIF20A (MKLP2/Rab6-KIFL) is a plus-end-directed kinesin-6 motor that drives cytokinesis by transporting the Aurora B chromosomal passenger complex (CPC) from anaphase chromosomes to the central spindle midzone and equatorial cortex [PMID:11060022, PMID:15263015, PMID:32502404]. Its structurally atypical motor domain — an unusually long L6 insertion and a neck linker four times longer than kinesin-1 — accounts for its low processivity yet supports the processive CPC transport demonstrated in single-molecule reconstitution [PMID:32502404, PMID:37726093]. CPC handoff is tightly gated: Cdk1/cyclin B1 phosphorylates the MKlp2 stalk and tail to block microtubule binding and chromosome targeting in early mitosis, and this inhibition is relieved at anaphase onset [PMID:24656812], while a Mad2-binding motif prevents premature spindle loading during the checkpoint [PMID:21149564]. CPC engagement is mediated through the INCENP RRKKRR motif, whose binding to MKlp2 is switched by INCENP T59 phosphorylation and stimulates the microtubule-dependent ATPase of the motor [PMID:32356865]. At the equatorial cortex MKlp2 requires myosin-II for docking and there recruits Aurora B to focus RhoA accumulation and stabilize furrow ingression [PMID:23750214], and abscission timing is set by Aurora B phosphorylation of MKlp2-S878 within a lipid-association motif, opposed by B56-PP2A, with the C-terminal tail selectively binding PI(3)P membranes for tethering at the intercellular bridge [PMID:27939310, PMID:35316051]. Compound heterozygous ATPase-defective mutation (R182W) causes congenital cardiomyopathy by trapping Aurora B on chromatin [PMID:29357359]. Beyond mitosis, KIF20A transports membrane and RNA-granule cargo including DLG5 and IGF2BP3-bound transcripts [PMID:15665285, PMID:25499221], regulates neural progenitor cell fate through RGS3 and SEPT7 at the intercellular bridge [PMID:30006548, PMID:31813992], and in cancer stabilizes oncoproteins by antagonizing E3 ligase–mediated ubiquitination — blocking FBXW7–c-Myc, TRIM21–DHX9, and BTRC–CDC25A degradation [PMID:38223825, PMID:38971490, PMID:41672965]. Its expression is driven by multiple transcription factors (FOXM1, GATA2, ATF2) and by H3K18 lactylation [PMID:25961928, PMID:39624268, PMID:42216528, PMID:41937416].","teleology":[{"year":2000,"claim":"Established KIF20A as a Rab6-binding kinesin physically required for cleavage furrow formation, defining cytokinesis as its founding function.","evidence":"Yeast two-hybrid, inhibitory antibody microinjection, and time-lapse imaging localizing it to midzone, furrow, and midbody","pmids":["11060022"],"confidence":"High","gaps":["Did not define the molecular cargo at the furrow","Motor activity not directly measured"]},{"year":2004,"claim":"Identified the key cytokinetic cargo, showing MKlp2 binds and relocates the Aurora B–INCENP CPC from centromeres to the central spindle at the metaphase-to-anaphase transition.","evidence":"siRNA depletion, co-immunoprecipitation with Aurora B and Cdc14A, immunofluorescence","pmids":["15263015"],"confidence":"High","gaps":["Did not demonstrate direct motor-driven transport in vitro","Temporal gating mechanism not resolved"]},{"year":2005,"claim":"Extended KIF20A function beyond CPC transport to membrane trafficking by identifying DLG5 as a transported cargo.","evidence":"Anti-RAB6KIFL proteomics, siRNA knockdown, and subcellular localization of DLG5","pmids":["15665285"],"confidence":"Medium","gaps":["Single lab","Direct motor-cargo binding not biochemically reconstituted"]},{"year":2010,"claim":"Defined how spindle loading is temporally restricted, showing a Mad2-binding motif prevents premature MKlp2 spindle loading during the checkpoint.","evidence":"Co-IP, Mad2-motif mutagenesis, live imaging, and siRNA rescue","pmids":["21149564"],"confidence":"High","gaps":["Relationship to Cdk1 gating not integrated"]},{"year":2014,"claim":"Revealed the master cell-cycle switch: Cdk1/cyclin B1 phosphorylation inhibits MKlp2 microtubule binding and chromosome targeting until anaphase, when dephosphorylation licenses CPC relocation.","evidence":"Mass spectrometry phosphosite mapping, in vitro kinase assays, microtubule-binding/bundling assays, and cellular rescue","pmids":["24656812"],"confidence":"High","gaps":["Identity of the anaphase phosphatase not resolved here"]},{"year":2014,"claim":"Showed an interphase cargo-transport role in cancer cell migration via delivery of IGF2BP3-bound mRNA granules to protrusions.","evidence":"siRNA knockdown, immunofluorescence, time-lapse, and invasion assays in pancreatic cancer cells","pmids":["25499221"],"confidence":"Medium","gaps":["Single lab","Direct motor–IGF2BP3 binding not reconstituted"]},{"year":2013,"claim":"Dissected cortical CPC delivery, showing MKlp2 needs myosin-II for equatorial cortex docking and there recruits Aurora B to focus RhoA and stabilize the furrow.","evidence":"Monopolar cytokinesis assay, dominant-negative myosin-II, binding-mutant rescue, live imaging","pmids":["23750214"],"confidence":"High","gaps":["Myosin-II binding interface not mapped at residue level"]},{"year":2016,"claim":"Identified the abscission-timing switch: Aurora B phosphorylation of MKlp2-S878 in a lipid-association motif blocks abscission and is reversed by B56-PP2A.","evidence":"S878A mutagenesis, Aurora B kinase and PP2A phosphatase assays, abscission-timing live imaging","pmids":["27939310"],"confidence":"High","gaps":["How S878 phosphorylation alters membrane association left to later biophysics"]},{"year":2018,"claim":"Uncovered a spindle-independent neurodevelopmental role, with MKLP2–RGS3 interaction at the intercellular bridge controlling neural progenitor cell-fate signaling.","evidence":"Co-IP, in utero electroporation, germline and inducible conditional KO mice, live imaging","pmids":["30006548"],"confidence":"High","gaps":["Mechanism linking bridge localization to Ephrin-B/RGS signaling output incomplete"]},{"year":2018,"claim":"Linked KIF20A directly to human disease, demonstrating an ATPase-defective R182W mutation traps Aurora B on chromatin and causes congenital cardiomyopathy.","evidence":"Patient compound heterozygous mutations, ATPase assay, patient-cell Aurora B localization, zebrafish morpholino","pmids":["29357359"],"confidence":"High","gaps":["Tissue specificity of the cardiac phenotype not fully explained"]},{"year":2020,"claim":"Provided direct proof that MKLP2 is a processive plus-end motor that transports the CPC, and partitioned midzone versus cortical delivery by degree of motor inhibition.","evidence":"Single-molecule in vitro motility with purified MKLP2 and CPC, P-loop mutant, Paprotrain, live imaging","pmids":["32502404"],"confidence":"High","gaps":["Spatial cues distinguishing midzone vs cortex destinations not defined"]},{"year":2020,"claim":"Defined the molecular CPC–motor handoff, showing the INCENP RRKKRR motif binds MKLP2 competitively with DNA, gated by INCENP T59 phosphorylation, and that CPC binding stimulates MKLP2 ATPase.","evidence":"Crystal structure, RRKKRR mutagenesis, ATPase and competitive binding assays","pmids":["32356865"],"confidence":"High","gaps":["Kinase/phosphatase controlling INCENP T59 not identified here"]},{"year":2020,"claim":"Added a second intercellular-bridge partner, SEPT7, required to retain KIF20A at the midbody and restrain precocious neuronal differentiation.","evidence":"Co-IP, in utero electroporation, inducible conditional Sept7 KO mice","pmids":["31813992"],"confidence":"High","gaps":["Interplay of SEPT7 and RGS3 at the bridge not resolved"]},{"year":2022,"claim":"Revealed an earlier-mitosis role in chromosome congression via error correction of syntelic attachments, separable from cytokinesis.","evidence":"Live imaging, MKLP2 small-molecule inhibitor, siRNA, aneuploidy flow cytometry","pmids":["35638575"],"confidence":"Medium","gaps":["Single lab","Mechanism connecting motor to Aurora kinase activity at kinetochores unclear"]},{"year":2022,"claim":"Connected KIF20A to secretory-pathway-driven oncogenic signaling, with Golgi vesicle fission supporting autocrine androgen receptor activation in castration-resistant prostate cancer.","evidence":"Overexpression, conditioned-media transfer, Paprotrain, AR reporter, xenografts, vesicle-biogenesis inhibitors","pmids":["35418689"],"confidence":"Medium","gaps":["Single lab","Identity of secreted autocrine factors not defined"]},{"year":2022,"claim":"Provided the biophysical basis for membrane tethering, showing the MKlp2 C-terminal tail selectively binds PI(3)P membranes dependent on S21.","evidence":"QCM-D, AFM force spectroscopy, peptide mutagenesis on model membranes","pmids":["35316051"],"confidence":"Medium","gaps":["Model membranes only","S21-dependent tethering not validated in cells"]},{"year":2023,"claim":"Provided the structural explanation for KIF20A's low processivity, showing a long L6 insertion that integrates into the motor core and an extended neck linker required for motility.","evidence":"X-ray crystallography, microtubule-bound cryo-EM, ATPase assays, 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cytokinesis.\",\n      \"method\": \"Yeast two-hybrid screen, microinjection of inhibitory antibodies, time-lapse microscopy, immunofluorescence localization\",\n      \"journal\": \"The EMBO journal\",\n      \"confidence\": \"High\",\n      \"confidence_rationale\": \"Tier 2 / Strong — reciprocal binding assay plus direct loss-of-function (antibody injection) with defined cellular phenotype; replicated concept across multiple subsequent studies\",\n      \"pmids\": [\"11060022\"],\n      \"is_preprint\": false\n    },\n    {\n      \"year\": 2004,\n      \"finding\": \"MKlp2 (KIF20A) is required for relocation of the Aurora B–INCENP chromosome passenger complex (CPC) from centromeres to the central spindle at the metaphase-to-anaphase transition; MKlp2 physically binds Aurora B and also binds the phosphatase Cdc14A, which can dephosphorylate INCENP to facilitate CPC relocation.\",\n      \"method\": \"siRNA depletion, co-immunoprecipitation, immunofluorescence microscopy\",\n      \"journal\": \"The Journal of cell biology\",\n      \"confidence\": \"High\",\n      \"confidence_rationale\": \"Tier 2 / Strong — reciprocal Co-IP showing direct binding, loss-of-function with defined localization phenotype, replicated by multiple subsequent studies\",\n      \"pmids\": [\"15263015\"],\n      \"is_preprint\": false\n    },\n    {\n      \"year\": 2005,\n      \"finding\": \"KIF20A (RAB6KIFL) transports the scaffolding protein DLG5 as cargo; proteomics with anti-RAB6KIFL antibody identified DLG5 as a KIF20A cargo, and KIF20A knockdown displaced DLG5 from cytoplasmic membranes to the cytoplasm, demonstrating a membrane-trafficking function.\",\n      \"method\": \"Proteomics/pull-down with anti-RAB6KIFL antibody, siRNA knockdown, subcellular fractionation/immunolocalization\",\n      \"journal\": \"Cancer research\",\n      \"confidence\": \"Medium\",\n      \"confidence_rationale\": \"Tier 3 / Moderate — single lab, proteomics identification plus functional localization readout for the cargo\",\n      \"pmids\": [\"15665285\"],\n      \"is_preprint\": false\n    },\n    {\n      \"year\": 2005,\n      \"finding\": \"KIF20A ATPase activity and microtubule-binding can be studied biochemically using recombinant protein from insect cells; Polo-like kinase 1 (Plk1) interaction with KIF20A was established using recombinant proteins in vitro.\",\n      \"method\": \"In vitro biochemical assays (microtubule binding, ATPase), recombinant protein expression in insect cells, in vitro Plk1 binding assay\",\n      \"journal\": \"Methods in enzymology\",\n      \"confidence\": \"Medium\",\n      \"confidence_rationale\": \"Tier 1 / Weak — in vitro reconstitution with purified proteins, single lab methods paper\",\n      \"pmids\": [\"16473625\"],\n      \"is_preprint\": false\n    },\n    {\n      \"year\": 2010,\n      \"finding\": \"Mad2 binds MKlp2 (KIF20A) via a consensus Mad2-binding motif on MKlp2, preventing its loading onto the mitotic spindle and blocking CPC relocation from centromeres; an MKlp2 mutant refractory to Mad2 binding prematurely loads onto the spindle and mislocalizes Aurora B from the midbody, causing cytokinesis failure.\",\n      \"method\": \"Co-immunoprecipitation, site-directed mutagenesis of Mad2-binding motif, live-cell imaging, siRNA rescue experiments\",\n      \"journal\": \"The Journal of cell biology\",\n      \"confidence\": \"High\",\n      \"confidence_rationale\": \"Tier 2 / Strong — Co-IP plus mutagenesis plus defined loss-of-function phenotype, multiple orthogonal methods in one study\",\n      \"pmids\": [\"21149564\"],\n      \"is_preprint\": false\n    },\n    {\n      \"year\": 2013,\n      \"finding\": \"MKlp2 requires myosin-II for its own localization to the equatorial cortex; this event is required to recruit Aurora B to the equatorial cortex, which in turn promotes focused RhoA accumulation and stable cleavage furrow ingression. An MKlp2 mutant defective in myosin-II binding fails to recruit Aurora B to the cortex and fails to maintain the ingressing furrow.\",\n      \"method\": \"Drug-induced monopolar cytokinesis assay, dominant-negative myosin-II, MKlp2 binding-mutant expression, immunofluorescence, live-cell imaging\",\n      \"journal\": \"PloS one\",\n      \"confidence\": \"High\",\n      \"confidence_rationale\": \"Tier 2 / Moderate — reciprocal co-localization, myosin-II binding mutant phenotype rescue, multiple functional readouts in single study\",\n      \"pmids\": [\"23750214\"],\n      \"is_preprint\": false\n    },\n    {\n      \"year\": 2014,\n      \"finding\": \"Cdk1/cyclin B1 phosphorylates multiple sites in the MKlp2 stalk and C-terminal tail, inhibiting microtubule binding, bundling, oligomerization, and chromosome targeting of MKlp2 during early mitosis. Reversal of Cdk1 phosphorylation at anaphase onset promotes MKlp2–CPC complex formation and CPC relocation from chromosomes to the central spindle for cytokinesis.\",\n      \"method\": \"Identification of Cdk1 phosphorylation sites by mass spectrometry and mutagenesis, in vitro kinase assays, microtubule-binding/bundling assays, immunofluorescence, cell cycle analysis\",\n      \"journal\": \"Cell reports\",\n      \"confidence\": \"High\",\n      \"confidence_rationale\": \"Tier 1 / Strong — in vitro kinase assay plus mutagenesis plus functional rescue with defined cellular phenotypes, multiple orthogonal methods\",\n      \"pmids\": [\"24656812\"],\n      \"is_preprint\": false\n    },\n    {\n      \"year\": 2014,\n      \"finding\": \"KIF20A promotes motility and invasiveness of pancreatic cancer cells by transporting the RNA-binding protein IGF2BP3 and its bound transcripts (including ARF6 and ARHGEF4 mRNAs) toward cell protrusions along microtubules; KIF20A knockdown inhibits IGF2BP3-containing stress granule accumulation in protrusions and suppresses local protein expression from these transcripts.\",\n      \"method\": \"siRNA knockdown, immunofluorescence, time-lapse microscopy, cell invasion/migration assays\",\n      \"journal\": \"Neoplasia (New York, N.Y.)\",\n      \"confidence\": \"Medium\",\n      \"confidence_rationale\": \"Tier 3 / Moderate — single lab, knockdown with defined cargo localization readout and functional consequence\",\n      \"pmids\": [\"25499221\"],\n      \"is_preprint\": false\n    },\n    {\n      \"year\": 2015,\n      \"finding\": \"FOXM1 directly transcriptionally regulates KIF20A expression through a Forkhead response element (FHRE) in the KIF20A promoter; FOXM1 depletion reduces KIF20A expression, causes abnormal mitotic spindle morphology and chromosome alignment, and sensitizes breast cancer cells to paclitaxel-induced mitotic catastrophe.\",\n      \"method\": \"ChIP assay, promoter-luciferase reporter, siRNA knockdown, cell viability/senescence assays, spindle morphology by immunofluorescence\",\n      \"journal\": \"Oncogene\",\n      \"confidence\": \"High\",\n      \"confidence_rationale\": \"Tier 2 / Strong — ChIP plus luciferase reporter confirms direct transcriptional regulation; replicated in multiple cancer types by subsequent studies\",\n      \"pmids\": [\"25961928\"],\n      \"is_preprint\": false\n    },\n    {\n      \"year\": 2016,\n      \"finding\": \"Aurora B phosphorylates MKlp2 at S878 within a lipid-association motif (LAM) in the C-terminal tail, acting as an inhibitory signal for abscission; B56-bound PP2A dephosphorylates MKlp2 S878 to promote abscission. A phospho-resistant S878A mutant of MKlp2 overrides Aurora B–mediated abscission blockade.\",\n      \"method\": \"Phospho-site mutagenesis (S878A), Aurora B kinase assay, PP2A phosphatase assay, live-cell imaging, abscission timing assays\",\n      \"journal\": \"Current biology : CB\",\n      \"confidence\": \"High\",\n      \"confidence_rationale\": \"Tier 1 / Strong — in vitro kinase/phosphatase assays with mutagenesis plus rescue in cells, multiple orthogonal methods\",\n      \"pmids\": [\"27939310\"],\n      \"is_preprint\": false\n    },\n    {\n      \"year\": 2018,\n      \"finding\": \"KIF20A/MKLP2 interacts with RGS3 at the intercellular bridge of dividing neural progenitor cells (NPCs); KIF20A knockdown/knockout causes dislocation of RGS3 from the intercellular bridge, impairs Ephrin-B–RGS cell fate signaling, and shifts NPCs from proliferative to differentiative divisions, resulting in thinner cortex and ventriculomegaly without substantial cytokinesis defect.\",\n      \"method\": \"Co-immunoprecipitation, immunofluorescence, in utero electroporation knockdown, germline and inducible conditional KO mice, live imaging\",\n      \"journal\": \"Nature communications\",\n      \"confidence\": \"High\",\n      \"confidence_rationale\": \"Tier 2 / Strong — Co-IP plus genetic KO (germline and inducible) with multiple defined phenotypic readouts in vivo\",\n      \"pmids\": [\"30006548\"],\n      \"is_preprint\": false\n    },\n    {\n      \"year\": 2018,\n      \"finding\": \"Loss of function of KIF20A (R182W ATPase-defective mutation identified in congenital cardiomyopathy patients) prevents efficient transport of Aurora B as part of the CPC: Aurora B remains trapped on chromatin and fails to translocate to the spindle midzone during cytokinesis.\",\n      \"method\": \"Patient compound heterozygous mutations, functional ATPase assay, immunofluorescence of Aurora B localization in patient-derived cells, zebrafish translational-blocking morpholino model\",\n      \"journal\": \"PLoS genetics\",\n      \"confidence\": \"High\",\n      \"confidence_rationale\": \"Tier 1 / Strong — ATPase-defective mutation with direct functional readout (Aurora B mislocalization) and in vivo zebrafish confirmation\",\n      \"pmids\": [\"29357359\"],\n      \"is_preprint\": false\n    },\n    {\n      \"year\": 2020,\n      \"finding\": \"MKLP2 (KIF20A) is a processive, plus-end-directed motor that can transport the CPC along microtubules in vitro; strong suppression of MKLP2 motor activity via a P-loop mutant disrupts CPC accumulation at both the spindle midzone and equatorial cortex, whereas partial inhibition with Paprotrain mainly affects equatorial cortex localization.\",\n      \"method\": \"In vitro single-molecule motility assays with purified MKLP2 and CPC, P-loop ATPase mutant expression, Paprotrain inhibitor, live-cell imaging\",\n      \"journal\": \"Current biology : CB\",\n      \"confidence\": \"High\",\n      \"confidence_rationale\": \"Tier 1 / Strong — direct in vitro reconstitution of processive transport with purified proteins plus mutagenesis plus cell-based rescue, multiple orthogonal methods\",\n      \"pmids\": [\"32502404\"],\n      \"is_preprint\": false\n    },\n    {\n      \"year\": 2020,\n      \"finding\": \"The INCENP RRKKRR motif is required for both centromeric CPC localization in metaphase and MKLP2-dependent CPC transport in anaphase; MKLP2 and DNA bind competitively to this motif, and INCENP T59 phosphorylation acts as a switch that prevents MKLP2 binding in metaphase. CPC binding to MKLP2 promotes the microtubule-dependent ATPase activity of MKLP2 in anaphase.\",\n      \"method\": \"Crystal structure of survivin–H3pT3 complex, mutagenesis of INCENP RRKKRR motif, ATPase assays, immunofluorescence, competitive binding assays\",\n      \"journal\": \"The Journal of cell biology\",\n      \"confidence\": \"High\",\n      \"confidence_rationale\": \"Tier 1 / Strong — crystal structure plus mutagenesis plus in vitro ATPase assay, multiple orthogonal methods in one rigorous study\",\n      \"pmids\": [\"32356865\"],\n      \"is_preprint\": false\n    },\n    {\n      \"year\": 2020,\n      \"finding\": \"SEPT7 interacts with KIF20A at the intercellular bridge of dividing NPCs; SEPT7 knockdown displaces KIF20A from the midbody, causing early neuronal differentiation. NPC-specific inducible knockout of Sept7 causes early cell cycle exit and precocious differentiation without noticeable cytokinesis defect.\",\n      \"method\": \"Co-immunoprecipitation, immunofluorescence, in utero electroporation knockdown, inducible conditional KO mice\",\n      \"journal\": \"Cerebral cortex (New York, N.Y. : 1991)\",\n      \"confidence\": \"High\",\n      \"confidence_rationale\": \"Tier 2 / Strong — Co-IP plus genetic knockout with defined cellular phenotype\",\n      \"pmids\": [\"31813992\"],\n      \"is_preprint\": false\n    },\n    {\n      \"year\": 2022,\n      \"finding\": \"MKLP2 facilitates chromosome congression in prometaphase by promoting error correction of syntelic kinetochore-microtubule attachments; MKLP2 inhibition results in elevated Aurora kinase activity, phosphorylation of HEC1-Ser55, and aneuploidy.\",\n      \"method\": \"Live imaging with fluorescent histones, MKLP2 small-molecule inhibitor (MKLP2i), siRNA, flow cytometry for aneuploidy\",\n      \"journal\": \"Journal of cell science\",\n      \"confidence\": \"Medium\",\n      \"confidence_rationale\": \"Tier 2 / Moderate — live imaging plus inhibitor/siRNA with defined molecular readouts, single lab\",\n      \"pmids\": [\"35638575\"],\n      \"is_preprint\": false\n    },\n    {\n      \"year\": 2022,\n      \"finding\": \"KIF20A promotes castration-resistant prostate cancer (CRPC) progression through its role in Golgi-driven secretory vesicle fission and trafficking; KIF20A expression causes secretion of autocrine factors that activate androgen receptor signaling, and pharmacologic disruption of vesicle biogenesis blocks KIF20A-driven castration-resistant proliferation.\",\n      \"method\": \"Stable KIF20A overexpression, conditioned media transfer assays, Paprotrain inhibitor, androgen receptor reporter assays, in vivo xenograft, vesicle biogenesis inhibitors\",\n      \"journal\": \"Oncogene\",\n      \"confidence\": \"Medium\",\n      \"confidence_rationale\": \"Tier 2 / Moderate — conditioned media + pharmacologic vesicle disruption + in vivo validation, single lab\",\n      \"pmids\": [\"35418689\"],\n      \"is_preprint\": false\n    },\n    {\n      \"year\": 2022,\n      \"finding\": \"The C-terminal tail of MKlp2 (CTM peptides) selectively binds PI(3)P-containing membranes over other negatively charged lipids, and this interaction depends critically on residue S21; this selective phosphoinositide binding provides a mechanism for MKlp2 tethering to the plasma membrane at the intercellular bridge during abscission.\",\n      \"method\": \"Quartz crystal microbalance-dissipation (QCM-D), atomic force microscopy force spectroscopy, synthetic peptide mutagenesis on model lipid membranes\",\n      \"journal\": \"The journal of physical chemistry. B\",\n      \"confidence\": \"Medium\",\n      \"confidence_rationale\": \"Tier 1 / Weak — rigorous biophysical in vitro assays with mutagenesis, single lab, model membranes only\",\n      \"pmids\": [\"35316051\"],\n      \"is_preprint\": false\n    },\n    {\n      \"year\": 2023,\n      \"finding\": \"High-resolution crystal and cryo-EM structures of the KIF20A motor domain reveal an unusually long L6 insertion that integrates into the core of the motor domain, dramatically affecting allostery and ATPase activity. The neck linker is four times longer than in kinesin-1, and the extended neck linker is required for motor activity. These structural features explain the low processivity/motility of KIF20A compared to other kinesins.\",\n      \"method\": \"X-ray crystallography (nucleotide-free motor domain), cryo-EM (microtubule-bound structure), ATPase activity assays, mutagenesis of L6 insertion and neck linker\",\n      \"journal\": \"Open biology\",\n      \"confidence\": \"High\",\n      \"confidence_rationale\": \"Tier 1 / Strong — high-resolution crystal and cryo-EM structures with functional validation (ATPase assays and mutagenesis) in one study\",\n      \"pmids\": [\"37726093\"],\n      \"is_preprint\": false\n    },\n    {\n      \"year\": 2023,\n      \"finding\": \"KIF20A physically interacts with BTRC (β-TrCP1), a substrate recognition subunit of SCFβ-TrCP E3 ubiquitin ligase; via this interaction, KIF20A reduces BTRC-mediated CDC25A poly-ubiquitination and enhances CDC25A protein stability.\",\n      \"method\": \"GST pull-down, co-immunoprecipitation, in vitro ubiquitination assay, cycloheximide chase assay\",\n      \"journal\": \"Journal of ginseng research\",\n      \"confidence\": \"Medium\",\n      \"confidence_rationale\": \"Tier 2 / Moderate — reciprocal Co-IP plus pull-down plus in vitro ubiquitination assay, single lab\",\n      \"pmids\": [\"38223825\"],\n      \"is_preprint\": false\n    },\n    {\n      \"year\": 2024,\n      \"finding\": \"KIF20A inhibits FBXW7-mediated ubiquitination and degradation of c-Myc by competitively inhibiting the FBXW7–c-Myc interaction; KIF20A overexpression thereby stabilizes c-Myc, promotes glycolysis, and enhances tumor proliferation. KIF20A downregulation reduces c-Myc levels and suppresses MMR expression.\",\n      \"method\": \"KIF20A liver-specific knockout mouse, co-immunoprecipitation, c-Myc splicing mutant constructs, ubiquitination assays, immunohistochemistry of patient cohort\",\n      \"journal\": \"Cancer letters\",\n      \"confidence\": \"Medium\",\n      \"confidence_rationale\": \"Tier 2 / Moderate — Co-IP plus conditional KO mouse plus mechanistic mutant validation, single lab\",\n      \"pmids\": [\"38971490\"],\n      \"is_preprint\": false\n    },\n    {\n      \"year\": 2024,\n      \"finding\": \"KIF20A inhibits DHX9 proteasomal degradation by blocking TRIM21-mediated K48-linked polyubiquitination at DHX9-K755; elevated DHX9 stabilizes SOX2 mRNA, upregulating SOX2 to promote cancer stem cell maintenance and ferroptosis resistance in OSCC.\",\n      \"method\": \"Co-immunoprecipitation, ubiquitination assay (K48-linkage specific), co-localization, SOX2 mRNA stability assay, loss-of-function/gain-of-function in vitro and in vivo\",\n      \"journal\": \"Cell death & disease\",\n      \"confidence\": \"Medium\",\n      \"confidence_rationale\": \"Tier 2 / Moderate — Co-IP plus site-specific ubiquitination assay plus functional rescue, single lab\",\n      \"pmids\": [\"41672965\"],\n      \"is_preprint\": false\n    },\n    {\n      \"year\": 2025,\n      \"finding\": \"KIF20A maximal enrichment at antiparallel microtubule overlaps of the spindle midzone requires PRC1-crosslinked microtubules and cooperation with KIF4A: KIF20A delivers the CPC from non-overlapping microtubules to the midzone, while KIF4A retains the CPC at PRC1-crosslinked overlaps. Conditional depletion of KIF4A confirms it is required for CPC localization at the spindle midzone in anaphase.\",\n      \"method\": \"In vitro reconstitution with purified proteins, conditional KIF4A depletion in mitotic cells, live-cell imaging, immunofluorescence\",\n      \"journal\": \"bioRxiv\",\n      \"confidence\": \"Medium\",\n      \"confidence_rationale\": \"Tier 1 / Weak — in vitro reconstitution plus cell depletion; preprint, not yet peer-reviewed\",\n      \"pmids\": [],\n      \"is_preprint\": true\n    },\n    {\n      \"year\": 2025,\n      \"finding\": \"KIF20A cooperates with Myosin II to regulate actomyosin and branched actin dynamics, facilitating fission of transport intermediates at early endosomes; KIF20A inhibition causes enlargement of early and late endosomes, impairs Transferrin trafficking, and mislocalizes β1-Integrin from the plasma membrane.\",\n      \"method\": \"KIF20A inhibitor (Paprotrain), live-cell endosome imaging, Transferrin trafficking assay, β1-Integrin localization, Myosin II co-localization and functional assays\",\n      \"journal\": \"bioRxiv\",\n      \"confidence\": \"Low\",\n      \"confidence_rationale\": \"Tier 3 / Weak — preprint, single lab, inhibitor-based phenotypic assays without mechanistic reconstitution of the motor-myosin cooperation\",\n      \"pmids\": [],\n      \"is_preprint\": true\n    },\n    {\n      \"year\": 2026,\n      \"finding\": \"SYMPK interacts with KIF20A and NUMA1 during meiotic metaphase I in oocytes, as revealed by immunoprecipitation-mass spectrometry; SYMPK is required for proper localization of KIF20A and NUMA1 to the acentrosomal spindle, and SYMPK-deficient oocytes show disorganized spindle architecture and metaphase I arrest.\",\n      \"method\": \"Oocyte-specific Sympk knockout mice, immunoprecipitation-mass spectrometry, immunofluorescence, chromosome spread analysis\",\n      \"journal\": \"Journal of genetics and genomics\",\n      \"confidence\": \"Medium\",\n      \"confidence_rationale\": \"Tier 2 / Moderate — IP-MS plus genetic KO with defined localization phenotype, single lab\",\n      \"pmids\": [\"41520922\"],\n      \"is_preprint\": false\n    },\n    {\n      \"year\": 2019,\n      \"finding\": \"KIF20A localizes to microtubules in spermatogenic cells and co-localizes with the spindle midzone and midbody; KIF20A inhibition (Paprotrain) leads to defects in central spindle assembly and cytokinetic abscission in male meiosis, increased aneuploidy, and impaired acrosome formation and maturation during spermatogenesis.\",\n      \"method\": \"Immunofluorescence localization, Paprotrain inhibitor treatment, flow cytometry for ploidy, acrosome staining\",\n      \"journal\": \"Biochimica et biophysica acta. Molecular cell research\",\n      \"confidence\": \"Medium\",\n      \"confidence_rationale\": \"Tier 2 / Weak — direct localization experiments plus inhibitor-based functional readouts, single lab\",\n      \"pmids\": [\"31884069\"],\n      \"is_preprint\": false\n    },\n    {\n      \"year\": 2020,\n      \"finding\": \"Transcription factor GATA2 directly binds the KIF20A promoter and transcriptionally activates KIF20A in HBV-related hepatocellular carcinoma; HBx protein indirectly upregulates KIF20A via GATA2. GATA2 overexpression promotes HepG2.2.15 cell growth and inhibits apoptosis via KIF20A.\",\n      \"method\": \"ChIP assay, luciferase reporter assay, siRNA knockdown, overexpression, CCK-8 and flow cytometry\",\n      \"journal\": \"Frontiers in cellular and infection microbiology\",\n      \"confidence\": \"Medium\",\n      \"confidence_rationale\": \"Tier 2 / Moderate — ChIP plus luciferase reporter confirm direct promoter binding, functional rescue, single lab\",\n      \"pmids\": [\"39624268\"],\n      \"is_preprint\": false\n    },\n    {\n      \"year\": 2026,\n      \"finding\": \"Lactate-driven histone H3K18 lactylation (H3K18la) directly activates transcription of KIF20A; KIF20A in turn stabilizes c-Myc protein, enhancing PD-L1 expression and suppressing cytotoxic T cell function, constituting a metabolic-epigenetic immune evasion axis. Glycolysis inhibition reduces H3K18la-driven KIF20A upregulation and synergizes with anti-PD-1 therapy.\",\n      \"method\": \"ChIP-sequencing, ChIP-PCR, dual-luciferase reporter, HCC-CD8+ T cell co-cultures, gene knockdown/overexpression, mouse xenograft and orthotopic models, pan-lysine and H3K18la immunohistochemistry in patient cohorts\",\n      \"journal\": \"Cancer biology & medicine\",\n      \"confidence\": \"Medium\",\n      \"confidence_rationale\": \"Tier 2 / Moderate — ChIP-seq plus reporter assay plus functional in vivo models, single lab, multiple orthogonal methods\",\n      \"pmids\": [\"41937416\"],\n      \"is_preprint\": false\n    },\n    {\n      \"year\": 2022,\n      \"finding\": \"Auxin-inducible acute degradation of endogenous Mklp2 in MDCK cells causes delayed relocation of CPC component Aurora-B to the spindle midzone during anaphase and leads to cytokinesis failure and binucleation; these phenotypes are rescued by re-expression of Mklp2, confirming specificity.\",\n      \"method\": \"AID (auxin-inducible degron) tag on endogenous MKLP2, live-cell imaging, immunofluorescence, rescue by re-expression\",\n      \"journal\": \"Biology of the cell\",\n      \"confidence\": \"Medium\",\n      \"confidence_rationale\": \"Tier 2 / Moderate — acute conditional degradation with rescue, clean temporal control, single lab\",\n      \"pmids\": [\"40490973\"],\n      \"is_preprint\": false\n    },\n    {\n      \"year\": 2026,\n      \"finding\": \"KIF20A physically interacts with DEPDC1 in liposarcoma cells as shown by co-immunoprecipitation; KIF20A knockdown partially reverses DEPDC1-driven proliferation, migration, and invasion, and attenuates PI3K/AKT/mTOR signaling activation.\",\n      \"method\": \"Co-immunoprecipitation, siRNA knockdown, CCK-8/invasion assays, western blot of PI3K/AKT/mTOR pathway\",\n      \"journal\": \"Frontiers in endocrinology\",\n      \"confidence\": \"Low\",\n      \"confidence_rationale\": \"Tier 3 / Weak — single Co-IP plus knockdown functional readout, single lab, no mechanistic detail on how interaction affects motor function\",\n      \"pmids\": [\"40600015\"],\n      \"is_preprint\": false\n    },\n    {\n      \"year\": 2026,\n      \"finding\": \"KIF20A physically interacts with CLIP1 and enhances its protein stability in cervical cancer cells; CLIP1 silencing reverses the oncogenic effects of KIF20A overexpression.\",\n      \"method\": \"Co-immunoprecipitation, siRNA knockdown, protein stability assays, proliferation/migration/invasion functional assays, in vivo xenograft\",\n      \"journal\": \"Scientific reports\",\n      \"confidence\": \"Low\",\n      \"confidence_rationale\": \"Tier 3 / Weak — single Co-IP plus rescue experiment, single lab, mechanism of stability enhancement not biochemically detailed\",\n      \"pmids\": [\"41776329\"],\n      \"is_preprint\": false\n    },\n    {\n      \"year\": 2026,\n      \"finding\": \"Transcription factor ATF2 binds directly to the KIF20A promoter and activates its transcription in prostate cancer, as validated by ChIP and dual-luciferase reporter assays.\",\n      \"method\": \"ChIP assay, dual-luciferase reporter, qRT-PCR, western blot, KIF20A knockdown functional assays\",\n      \"journal\": \"Frontiers in bioscience (Landmark edition)\",\n      \"confidence\": \"Medium\",\n      \"confidence_rationale\": \"Tier 2 / Weak — ChIP plus luciferase reporter establish direct promoter binding, single lab\",\n      \"pmids\": [\"42216528\"],\n      \"is_preprint\": false\n    }\n  ],\n  \"current_model\": \"KIF20A (MKLP2/RAB6KIFL) is a kinesin-6 family motor with a structurally atypical motor domain (extended L6 loop, long neck linker) that confers low processivity; it acts as a processive plus-end-directed microtubule motor that transports the Aurora B–containing chromosomal passenger complex (CPC) from anaphase chromosomes to the central spindle midzone and equatorial cortex, a process that is temporally gated by Cdk1 phosphorylation (inhibitory in early mitosis, relieved at anaphase) and spatially coordinated with KIF4A at PRC1-crosslinked antiparallel overlaps; at the cortex MKlp2 requires myosin-II for docking and recruits Aurora B to drive RhoA-dependent cleavage furrow ingression; abscission timing is further controlled by Aurora B phosphorylation of MKlp2-S878 in its lipid-association motif (inhibitory) opposed by B56-PP2A (permissive), while its Mad2-binding motif prevents premature spindle loading during the spindle assembly checkpoint; beyond cytokinesis, KIF20A also transports cargo such as DLG5, IGF2BP3-containing RNA granules, and vesicle intermediates at endosomes in cooperation with Myosin II, and—through Golgi-dependent secretory pathways—drives autocrine AR signaling in prostate cancer; in neural progenitors KIF20A interacts with RGS3 and SEPT7 at the intercellular bridge to regulate cell fate signaling independent of spindle orientation; non-mitotic functions include stabilizing c-Myc (by blocking FBXW7-mediated ubiquitination), stabilizing DHX9/SOX2 via inhibiting TRIM21 ubiquitination, and stabilizing CDC25A via BTRC sequestration; its expression is transcriptionally controlled by FOXM1, GATA2, ATF2, FOXK1, and IRF6, and epigenetically by H3K18 lactylation.\"\n}\n```","stage2_raw":"{\n  \"mechanistic_narrative\": \"KIF20A (MKLP2/Rab6-KIFL) is a plus-end-directed kinesin-6 motor that drives cytokinesis by transporting the Aurora B chromosomal passenger complex (CPC) from anaphase chromosomes to the central spindle midzone and equatorial cortex [#0, #1, #12]. Its structurally atypical motor domain — an unusually long L6 insertion and a neck linker four times longer than kinesin-1 — accounts for its low processivity yet supports the processive CPC transport demonstrated in single-molecule reconstitution [#12, #18]. CPC handoff is tightly gated: Cdk1/cyclin B1 phosphorylates the MKlp2 stalk and tail to block microtubule binding and chromosome targeting in early mitosis, and this inhibition is relieved at anaphase onset [#6], while a Mad2-binding motif prevents premature spindle loading during the checkpoint [#4]. CPC engagement is mediated through the INCENP RRKKRR motif, whose binding to MKlp2 is switched by INCENP T59 phosphorylation and stimulates the microtubule-dependent ATPase of the motor [#13]. At the equatorial cortex MKlp2 requires myosin-II for docking and there recruits Aurora B to focus RhoA accumulation and stabilize furrow ingression [#5], and abscission timing is set by Aurora B phosphorylation of MKlp2-S878 within a lipid-association motif, opposed by B56-PP2A, with the C-terminal tail selectively binding PI(3)P membranes for tethering at the intercellular bridge [#9, #17]. Compound heterozygous ATPase-defective mutation (R182W) causes congenital cardiomyopathy by trapping Aurora B on chromatin [#11]. Beyond mitosis, KIF20A transports membrane and RNA-granule cargo including DLG5 and IGF2BP3-bound transcripts [#2, #7], regulates neural progenitor cell fate through RGS3 and SEPT7 at the intercellular bridge [#10, #14], and in cancer stabilizes oncoproteins by antagonizing E3 ligase–mediated ubiquitination — blocking FBXW7–c-Myc, TRIM21–DHX9, and BTRC–CDC25A degradation [#19, #20, #21]. Its expression is driven by multiple transcription factors (FOXM1, GATA2, ATF2) and by H3K18 lactylation [#8, #26, #31, #27].\",\n  \"teleology\": [\n    {\n      \"year\": 2000,\n      \"claim\": \"Established KIF20A as a Rab6-binding kinesin physically required for cleavage furrow formation, defining cytokinesis as its founding function.\",\n      \"evidence\": \"Yeast two-hybrid, inhibitory antibody microinjection, and time-lapse imaging localizing it to midzone, furrow, and midbody\",\n      \"pmids\": [\"11060022\"],\n      \"confidence\": \"High\",\n      \"gaps\": [\"Did not define the molecular cargo at the furrow\", \"Motor activity not directly measured\"]\n    },\n    {\n      \"year\": 2004,\n      \"claim\": \"Identified the key cytokinetic cargo, showing MKlp2 binds and relocates the Aurora B–INCENP CPC from centromeres to the central spindle at the metaphase-to-anaphase transition.\",\n      \"evidence\": \"siRNA depletion, co-immunoprecipitation with Aurora B and Cdc14A, immunofluorescence\",\n      \"pmids\": [\"15263015\"],\n      \"confidence\": \"High\",\n      \"gaps\": [\"Did not demonstrate direct motor-driven transport in vitro\", \"Temporal gating mechanism not resolved\"]\n    },\n    {\n      \"year\": 2005,\n      \"claim\": \"Extended KIF20A function beyond CPC transport to membrane trafficking by identifying DLG5 as a transported cargo.\",\n      \"evidence\": \"Anti-RAB6KIFL proteomics, siRNA knockdown, and subcellular localization of DLG5\",\n      \"pmids\": [\"15665285\"],\n      \"confidence\": \"Medium\",\n      \"gaps\": [\"Single lab\", \"Direct motor-cargo binding not biochemically reconstituted\"]\n    },\n    {\n      \"year\": 2010,\n      \"claim\": \"Defined how spindle loading is temporally restricted, showing a Mad2-binding motif prevents premature MKlp2 spindle loading during the checkpoint.\",\n      \"evidence\": \"Co-IP, Mad2-motif mutagenesis, live imaging, and siRNA rescue\",\n      \"pmids\": [\"21149564\"],\n      \"confidence\": \"High\",\n      \"gaps\": [\"Relationship to Cdk1 gating not integrated\"]\n    },\n    {\n      \"year\": 2014,\n      \"claim\": \"Revealed the master cell-cycle switch: Cdk1/cyclin B1 phosphorylation inhibits MKlp2 microtubule binding and chromosome targeting until anaphase, when dephosphorylation licenses CPC relocation.\",\n      \"evidence\": \"Mass spectrometry phosphosite mapping, in vitro kinase assays, microtubule-binding/bundling assays, and cellular rescue\",\n      \"pmids\": [\"24656812\"],\n      \"confidence\": \"High\",\n      \"gaps\": [\"Identity of the anaphase phosphatase not resolved here\"]\n    },\n    {\n      \"year\": 2014,\n      \"claim\": \"Showed an interphase cargo-transport role in cancer cell migration via delivery of IGF2BP3-bound mRNA granules to protrusions.\",\n      \"evidence\": \"siRNA knockdown, immunofluorescence, time-lapse, and invasion assays in pancreatic cancer cells\",\n      \"pmids\": [\"25499221\"],\n      \"confidence\": \"Medium\",\n      \"gaps\": [\"Single lab\", \"Direct motor–IGF2BP3 binding not reconstituted\"]\n    },\n    {\n      \"year\": 2013,\n      \"claim\": \"Dissected cortical CPC delivery, showing MKlp2 needs myosin-II for equatorial cortex docking and there recruits Aurora B to focus RhoA and stabilize the furrow.\",\n      \"evidence\": \"Monopolar cytokinesis assay, dominant-negative myosin-II, binding-mutant rescue, live imaging\",\n      \"pmids\": [\"23750214\"],\n      \"confidence\": \"High\",\n      \"gaps\": [\"Myosin-II binding interface not mapped at residue level\"]\n    },\n    {\n      \"year\": 2016,\n      \"claim\": \"Identified the abscission-timing switch: Aurora B phosphorylation of MKlp2-S878 in a lipid-association motif blocks abscission and is reversed by B56-PP2A.\",\n      \"evidence\": \"S878A mutagenesis, Aurora B kinase and PP2A phosphatase assays, abscission-timing live imaging\",\n      \"pmids\": [\"27939310\"],\n      \"confidence\": \"High\",\n      \"gaps\": [\"How S878 phosphorylation alters membrane association left to later biophysics\"]\n    },\n    {\n      \"year\": 2018,\n      \"claim\": \"Uncovered a spindle-independent neurodevelopmental role, with MKLP2–RGS3 interaction at the intercellular bridge controlling neural progenitor cell-fate signaling.\",\n      \"evidence\": \"Co-IP, in utero electroporation, germline and inducible conditional KO mice, live imaging\",\n      \"pmids\": [\"30006548\"],\n      \"confidence\": \"High\",\n      \"gaps\": [\"Mechanism linking bridge localization to Ephrin-B/RGS signaling output incomplete\"]\n    },\n    {\n      \"year\": 2018,\n      \"claim\": \"Linked KIF20A directly to human disease, demonstrating an ATPase-defective R182W mutation traps Aurora B on chromatin and causes congenital cardiomyopathy.\",\n      \"evidence\": \"Patient compound heterozygous mutations, ATPase assay, patient-cell Aurora B localization, zebrafish morpholino\",\n      \"pmids\": [\"29357359\"],\n      \"confidence\": \"High\",\n      \"gaps\": [\"Tissue specificity of the cardiac phenotype not fully explained\"]\n    },\n    {\n      \"year\": 2020,\n      \"claim\": \"Provided direct proof that MKLP2 is a processive plus-end motor that transports the CPC, and partitioned midzone versus cortical delivery by degree of motor inhibition.\",\n      \"evidence\": \"Single-molecule in vitro motility with purified MKLP2 and CPC, P-loop mutant, Paprotrain, live imaging\",\n      \"pmids\": [\"32502404\"],\n      \"confidence\": \"High\",\n      \"gaps\": [\"Spatial cues distinguishing midzone vs cortex destinations not defined\"]\n    },\n    {\n      \"year\": 2020,\n      \"claim\": \"Defined the molecular CPC–motor handoff, showing the INCENP RRKKRR motif binds MKLP2 competitively with DNA, gated by INCENP T59 phosphorylation, and that CPC binding stimulates MKLP2 ATPase.\",\n      \"evidence\": \"Crystal structure, RRKKRR mutagenesis, ATPase and competitive binding assays\",\n      \"pmids\": [\"32356865\"],\n      \"confidence\": \"High\",\n      \"gaps\": [\"Kinase/phosphatase controlling INCENP T59 not identified here\"]\n    },\n    {\n      \"year\": 2020,\n      \"claim\": \"Added a second intercellular-bridge partner, SEPT7, required to retain KIF20A at the midbody and restrain precocious neuronal differentiation.\",\n      \"evidence\": \"Co-IP, in utero electroporation, inducible conditional Sept7 KO mice\",\n      \"pmids\": [\"31813992\"],\n      \"confidence\": \"High\",\n      \"gaps\": [\"Interplay of SEPT7 and RGS3 at the bridge not resolved\"]\n    },\n    {\n      \"year\": 2022,\n      \"claim\": \"Revealed an earlier-mitosis role in chromosome congression via error correction of syntelic attachments, separable from cytokinesis.\",\n      \"evidence\": \"Live imaging, MKLP2 small-molecule inhibitor, siRNA, aneuploidy flow cytometry\",\n      \"pmids\": [\"35638575\"],\n      \"confidence\": \"Medium\",\n      \"gaps\": [\"Single lab\", \"Mechanism connecting motor to Aurora kinase activity at kinetochores unclear\"]\n    },\n    {\n      \"year\": 2022,\n      \"claim\": \"Connected KIF20A to secretory-pathway-driven oncogenic signaling, with Golgi vesicle fission supporting autocrine androgen receptor activation in castration-resistant prostate cancer.\",\n      \"evidence\": \"Overexpression, conditioned-media transfer, Paprotrain, AR reporter, xenografts, vesicle-biogenesis inhibitors\",\n      \"pmids\": [\"35418689\"],\n      \"confidence\": \"Medium\",\n      \"gaps\": [\"Single lab\", \"Identity of secreted autocrine factors not defined\"]\n    },\n    {\n      \"year\": 2022,\n      \"claim\": \"Provided the biophysical basis for membrane tethering, showing the MKlp2 C-terminal tail selectively binds PI(3)P membranes dependent on S21.\",\n      \"evidence\": \"QCM-D, AFM force spectroscopy, peptide mutagenesis on model membranes\",\n      \"pmids\": [\"35316051\"],\n      \"confidence\": \"Medium\",\n      \"gaps\": [\"Model membranes only\", \"S21-dependent tethering not validated in cells\"]\n    },\n    {\n      \"year\": 2023,\n      \"claim\": \"Provided the structural explanation for KIF20A's low processivity, showing a long L6 insertion that integrates into the motor core and an extended neck linker required for motility.\",\n      \"evidence\": \"X-ray crystallography, microtubule-bound cryo-EM, ATPase assays, L6/neck-linker mutagenesis\",\n      \"pmids\": [\"37726093\"],\n      \"confidence\": \"High\",\n      \"gaps\": [\"Structure of the CPC-bound transporting complex not resolved\"]\n    },\n    {\n      \"year\": 2023,\n      \"claim\": \"Defined a non-motor oncogenic mechanism, showing KIF20A binds BTRC to reduce CDC25A ubiquitination and stabilize it.\",\n      \"evidence\": \"GST pull-down, Co-IP, in vitro ubiquitination, cycloheximide chase\",\n      \"pmids\": [\"38223825\"],\n      \"confidence\": \"Medium\",\n      \"gaps\": [\"Single lab\", \"Whether motor activity is required not addressed\"]\n    },\n    {\n      \"year\": 2024,\n      \"claim\": \"Broadened the protein-stabilization paradigm, showing KIF20A competitively blocks FBXW7–c-Myc binding to stabilize c-Myc and drive glycolysis and tumor growth.\",\n      \"evidence\": \"Liver-specific KO mouse, Co-IP, c-Myc splicing mutants, ubiquitination assays, patient IHC\",\n      \"pmids\": [\"38971490\"],\n      \"confidence\": \"Medium\",\n      \"gaps\": [\"Single lab\", \"Structural basis of FBXW7 competition undefined\"]\n    },\n    {\n      \"year\": 2024,\n      \"claim\": \"Added a third E3-antagonism mechanism, showing KIF20A blocks TRIM21-mediated K48 ubiquitination of DHX9 to stabilize SOX2 mRNA and cancer stemness.\",\n      \"evidence\": \"Co-IP, K48-linkage ubiquitination assay, SOX2 mRNA stability, in vitro/in vivo functional rescue\",\n      \"pmids\": [\"41672965\"],\n      \"confidence\": \"Medium\",\n      \"gaps\": [\"Single lab\", \"Generality of TRIM21 antagonism unclear\"]\n    },\n    {\n      \"year\": 2020,\n      \"claim\": \"Identified GATA2 as a direct transcriptional activator of KIF20A in HBV-related hepatocellular carcinoma, linking viral oncogenesis to KIF20A expression.\",\n      \"evidence\": \"ChIP, luciferase reporter, siRNA, overexpression, viability/apoptosis assays\",\n      \"pmids\": [\"39624268\"],\n      \"confidence\": \"Medium\",\n      \"gaps\": [\"Single lab\", \"Direct downstream KIF20A effectors in this context not mapped\"]\n    },\n    {\n      \"year\": 2025,\n      \"claim\": \"Refined midzone targeting, showing KIF20A delivers CPC from non-overlapping microtubules while PRC1-crosslinked KIF4A retains it at antiparallel overlaps.\",\n      \"evidence\": \"In vitro reconstitution with purified proteins, conditional KIF4A depletion, live imaging (preprint)\",\n      \"pmids\": [],\n      \"confidence\": \"Medium\",\n      \"gaps\": [\"Preprint, not peer-reviewed\", \"Handoff stoichiometry between KIF20A and KIF4A undefined\"]\n    },\n    {\n      \"year\": 2026,\n      \"claim\": \"Connected KIF20A to a metabolic-epigenetic immune-evasion axis, where H3K18 lactylation activates KIF20A transcription and KIF20A stabilizes c-Myc to raise PD-L1 and suppress T cells.\",\n      \"evidence\": \"ChIP-seq, reporter assays, CD8+ T cell co-cultures, xenograft/orthotopic models, patient IHC\",\n      \"pmids\": [\"41937416\"],\n      \"confidence\": \"Medium\",\n      \"gaps\": [\"Single lab\", \"Specific H3K18la-occupied promoter element not finely mapped\"]\n    },\n    {\n      \"year\": null,\n      \"claim\": \"How the diverse non-mitotic activities (E3-ligase antagonism, RNA-granule and endosomal transport, neural cell-fate signaling) depend on or are separable from canonical motor and CPC-transport functions remains unresolved.\",\n      \"evidence\": \"\",\n      \"pmids\": [],\n      \"confidence\": \"Medium\",\n      \"gaps\": [\"No unified model linking motor activity to stabilization functions\", \"Several interactions rest on single Co-IPs without reciprocal validation\", \"Tissue-specific regulation of distinct functions undefined\"]\n    }\n  ],\n  \"mechanism_profile\": {\n    \"molecular_activity\": [\n      {\"term_id\": \"GO:0003774\", \"supporting_discovery_ids\": [12, 18, 0]},\n      {\"term_id\": \"GO:0140657\", \"supporting_discovery_ids\": [3, 13, 18, 11]},\n      {\"term_id\": \"GO:0008092\", \"supporting_discovery_ids\": [6, 12, 18]},\n      {\"term_id\": \"GO:0008289\", \"supporting_discovery_ids\": [17, 9]},\n      {\"term_id\": \"GO:0140313\", \"supporting_discovery_ids\": [20, 21, 19]}\n    ],\n    \"localization\": [\n      {\"term_id\": \"GO:0005819\", \"supporting_discovery_ids\": [0, 1, 12, 28]},\n      {\"term_id\": \"GO:0005856\", \"supporting_discovery_ids\": [12, 18, 25]},\n      {\"term_id\": \"GO:0005794\", \"supporting_discovery_ids\": [16]},\n      {\"term_id\": \"GO:0005768\", \"supporting_discovery_ids\": [23]},\n      {\"term_id\": \"GO:0005886\", \"supporting_discovery_ids\": [5, 17]}\n    ],\n    \"pathway\": [\n      {\"term_id\": \"R-HSA-1640170\", \"supporting_discovery_ids\": [0, 1, 6, 12, 28]},\n      {\"term_id\": \"R-HSA-1852241\", \"supporting_discovery_ids\": [0, 5]},\n      {\"term_id\": \"R-HSA-5653656\", \"supporting_discovery_ids\": [2, 7, 16, 23]},\n      {\"term_id\": \"R-HSA-1643685\", \"supporting_discovery_ids\": [11, 16, 20, 27]},\n      {\"term_id\": \"R-HSA-1266738\", \"supporting_discovery_ids\": [10, 14]}\n    ],\n    \"complexes\": [\n      \"chromosomal passenger complex (CPC)\"\n    ],\n    \"partners\": [\n      \"AURKB\",\n      \"INCENP\",\n      \"MAD2\",\n      \"RAB6\",\n      \"RGS3\",\n      \"SEPT7\",\n      \"BTRC\",\n      \"KIF4A\"\n    ],\n    \"other_free_text\": []\n  }\n}","audit_flag":null,"evaluation":{"pairwise":"win","faith_supported":8,"faith_total":8,"faith_pct":100.0}}