Affinage

Showing KIF2C — MCAK is a alias.

KIF2C

Kinesin-like protein KIF2C · UniProt Q99661

Length
725 aa
Mass
81.3 kDa
Annotated
2026-06-10
100 papers in source corpus 52 papers cited in narrative 51 extracted findings
Cross-family judge vs UniProt: tie faithfulness: 8/8 claims corpus-supported (100%)

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

KIF2C (MCAK) is a kinesin-13 microtubule depolymerase that catalytically removes tubulin dimers from microtubule ends to control microtubule dynamics during mitosis and beyond (PMID:12620232). It accelerates tubulin dissociation ~100-fold by assembling at protofilament ends as an ATP-hydrolyzing complex (PMID:12620232), and targets ends efficiently by first undergoing ATP-independent one-dimensional lattice diffusion before catalysis (PMID:16672973). Its enzymatic cycle is built from defined elements: the kinesin-13-specific KVD motif of loop 2 senses the tubulin interdimer interface so that the conformational change on tubulin binding—not ATP hydrolysis—drives tubulin release (PMID:26055718), while α4-helix residues and the C-terminal domain/neck confer microtubule-end recognition and robust depolymerization (PMID:27733589, PMID:17093055). MCAK exists in an autoinhibited closed/compact conformation in which the C-terminus engages the motor domains, an interaction allosterically displaced upon microtubule binding to extend the molecule at ends (PMID:25915621, PMID:30578316). In cells, its principal mitotic function is error correction of kinetochore-microtubule attachments rather than chromosome translocation: centromere-localized MCAK promotes microtubule turnover to coordinate directional switching and to resolve syntelic, merotelic, and lateral attachments (PMID:14699064, PMID:18039936, PMID:23891108). This activity is gated by a phosphorylation network—Aurora B phosphorylates S196 to open the molecule and inhibit depolymerization and to drive its centromeric targeting (PMID:14972678, PMID:14960279, PMID:24291095), Aurora A regulates pole activity via S196/S719 (PMID:18434591), PLK1 phosphorylates S715 to activate it (PMID:26206521), and Cdk1 phosphorylates T537 to abolish end recognition (PMID:29230353)—and by binding partners that target or modulate it, including EB1/EB3 and TIP150 for plus-end accumulation (PMID:17968321, PMID:19543227), hSgo2 for centromere recruitment (PMID:17485487, PMID:20889715), and Kif18b/EB3 for cooperative plus-end depolymerizing networks (PMID:21820309, PMID:35502670). Its conformation and activity are further constrained by inhibitors GTSE1 and tubulin detyrosination (PMID:27881713, PMID:36459065) and by proteasomal degradation that limits late-mitotic activity (PMID:18843200). Beyond mitosis, KIF2C functions in directional cell migration through focal-adhesion turnover and microtubule dynamics (PMID:34830827, PMID:33566676), in DNA double-strand break repair by promoting PARP/ATM-dependent DSB mobility (PMID:31951198), in neuronal synaptic plasticity by regulating dendritic microtubule invasion and Rab8-dependent receptor trafficking (PMID:35138249, PMID:37431690), and forms Aurora B/PLK1-dependent phospho-binding condensates that concentrate signaling factors at microtubule ends (PMID:40498077).

Mechanistic history

Synthesis pass · year-by-year structured walk · 17 steps
  1. 2003 High

    Established the core enzymatic identity of MCAK by showing it is not a motile motor but a catalytic depolymerase that actively destabilizes microtubule ends.

    Evidence In vitro ATPase and depolymerization kinetics with single-molecule analysis

    PMID:12620232

    Open questions at the time
    • Did not define how MCAK reaches ends in cells
    • Did not address regulation of activity in vivo
  2. 2003 High

    Defined MCAK's primary cellular role as error correction of kinetochore-microtubule attachments rather than driving chromosome movement, resolving what its depolymerase activity accomplishes in mitosis.

    Evidence Dominant-negative centromere-targeting domain microinjection with high-resolution imaging of attachment defects

    PMID:14699064

    Open questions at the time
    • Did not establish how activity is spatially restricted to centromeres
    • Mechanism of attachment-error sensing unresolved
  3. 2004 High

    Identified Aurora B as the master regulator that phosphorylates MCAK at S196 to inhibit depolymerization and control its centromere targeting, linking a kinase to spatial regulation of microtubule dynamics.

    Evidence In vitro kinase assay with site mapping, phosphomimetic/null mutants, antibody injection in Xenopus extracts and cells, FRAP

    PMID:14960279 PMID:14972678 PMID:15064354

    Open questions at the time
    • Structural basis of inhibition not yet defined
    • Did not address pole-specific regulation
  4. 2006 High

    Revealed the end-targeting strategy: MCAK uses ATP-independent 1D lattice diffusion to find microtubule ends faster than 3D diffusion permits, decoupling search from catalysis.

    Evidence Single-molecule TIRF fluorescence diffusion measurements

    PMID:16672973

    Open questions at the time
    • Did not define molecular determinants of lattice vs end binding
    • In-cell relevance of diffusion not directly tested
  5. 2007 Medium

    Placed MCAK among kinesin-13 paralogs with distinct pathway positions and identified EB1/EB3 and hSgo2 as targeting determinants for plus-end and centromere localization.

    Evidence Double-depletion epistasis, Co-IP, GST domain mapping, siRNA with localization rescue

    PMID:15302853 PMID:17485487 PMID:17538014 PMID:17968321

    Open questions at the time
    • Reciprocal validation across labs limited for some partners
    • Quantitative contribution of each targeting pathway not separated
  6. 2007 High

    Mapped functional domains and demonstrated that centromere-localized MCAK promotes kinetochore microtubule turnover to coordinate sister-kinetochore directional switching.

    Evidence Domain-deletion in vitro depolymerization and egg-extract assays; centromere-targeted chimera rescue with live imaging

    PMID:17093055 PMID:18039936

    Open questions at the time
    • Did not resolve conformational mechanics of domain coordination
    • Force output per molecule not yet measured
  7. 2008 High

    Extended kinase control to spindle poles, showing Aurora A phosphorylates S196 and S719 to regulate MCAK pole activity distinctly from Aurora B centromere control.

    Evidence Xenopus egg extract spindle assembly with site-specific phosphomutants and kinase assays

    PMID:18434591

    Open questions at the time
    • Crosstalk between Aurora A and Aurora B inputs not dissected
    • S719 activation mechanism not structurally defined
  8. 2011 High

    Quantified MCAK's force output and a 'side-sliding, end-catching' mechanism, and identified Kif18b as a partner required for astral microtubule depolymerization.

    Evidence Optical-trap single-molecule force measurement; reciprocal Co-IP, kinase assay, siRNA with microtubule phenotype

    PMID:21602793 PMID:21820309

    Open questions at the time
    • Did not show how force is harnessed at kinetochores in vivo
    • Stoichiometry of Kif18b-MCAK complex unresolved
  9. 2013 High

    Provided the conformational mechanism of inhibition: S196 phosphorylation switches MCAK from a closed to an open state, decreasing microtubule affinity and graded depolymerase activity.

    Evidence FRET/FLIM conformational biosensor, TIRF imaging, phosphomimetic mutagenesis, in vitro depolymerization

    PMID:24291095

    Open questions at the time
    • Atomic-resolution closed-state structure not yet determined here
    • Did not establish in-cell conformational distribution
  10. 2015 High

    Determined the structural basis of autoinhibition (C-terminus bound to two motor domains) and the catalytic role of the KVD motif, defining how tubulin binding rather than ATP hydrolysis triggers release.

    Evidence X-ray crystallography with crosslinking and binding assays; mutagenesis with ATPase/depolymerization assays and structural modeling

    PMID:25915621 PMID:26055718

    Open questions at the time
    • Full-length structure in different nucleotide states not solved
    • Transition pathway between states inferred, not directly observed
  11. 2015 Medium

    Added activating phosphorylation by an Aurora B–PLK1 axis at S715, complementing inhibitory inputs and showing bidirectional kinase control of depolymerase activity.

    Evidence FRET PLK1 activity reporter, kinase assay, phosphomutant functional analysis

    PMID:26206521

    Open questions at the time
    • Single lab without independent replication
    • Temporal ordering of activating vs inhibitory marks not fully resolved
  12. 2017 Medium

    Identified Cdk1 phosphorylation at T537 as a motor-domain switch that abolishes microtubule-end recognition without affecting lattice binding, integrating cell-cycle timing into depolymerase control.

    Evidence Phosphomimetic mutagenesis with single-molecule end/lattice residence kinetics and ATPase assay

    PMID:29230353

    Open questions at the time
    • Endogenous phosphorylation timing not directly tracked
    • Single lab
  13. 2019 High

    Refined the conformational model showing compact-to-extended transitions on end binding and graded, dose-dependent Aurora B inhibition decoupling the N-terminus from the motor.

    Evidence Crosslinking mass spectrometry, electron microscopy, phosphomutant depolymerization assays

    PMID:30578316

    Open questions at the time
    • High-resolution structures of intermediate states absent
    • Quantitative link between phosphorylation level and in-cell output not established
  14. 2022 High

    Demonstrated that Kif18b, MCAK, and EB3 function as an integrated multivalent network for potent cooperative plus-end depolymerization at low concentrations.

    Evidence In vitro reconstitution with single-molecule TIRF and quantitative depolymerization

    PMID:35502670

    Open questions at the time
    • In-cell stoichiometry and regulation of the network not defined
    • How phosphorylation modulates the network not tested here
  15. 2022 Medium

    Extended KIF2C function beyond mitosis into neuronal synaptic plasticity, showing it regulates dendritic microtubule invasion, receptor trafficking, transmission and behavior.

    Evidence Conditional knockout, live microtubule imaging in neurons, electrophysiology, behavioral tests; Rab8 Co-IP in Purkinje cells

    PMID:35138249 PMID:37431690

    Open questions at the time
    • Whether depolymerase activity per se drives trafficking not isolated
    • Single lab per neuronal system
  16. 2020 Medium

    Established a non-mitotic role in DNA double-strand break repair by promoting DSB mobility and foci dynamics in a PARP/ATM-dependent manner.

    Evidence DSB-template pulldown in Xenopus extracts, CRISPR KO/siRNA, foci analysis, NHEJ/HR reporters, live DSB tracking

    PMID:31951198

    Open questions at the time
    • Mechanism linking microtubule depolymerase activity to nuclear DSB mobility not fully defined
    • Single lab
  17. 2025 Medium

    Revealed a phospho-binding N-terminal Tudor/PWWP/MBT fold that drives Aurora B/PLK1-dependent KIF2C condensates concentrating signaling components at microtubule ends, and substrate preference for modified tubulin exploitable for chemoresistance.

    Evidence Structural determination, optogenetic condensate platform, FLIM-FRET, Co-IP; in vitro polyglutamylated-tubulin depolymerization with inhibitor and tumor models

    PMID:40157365 PMID:40498077

    Open questions at the time
    • Condensate findings not yet independently replicated
    • Physiological role of condensates vs canonical depolymerization unresolved

Open questions

Synthesis pass · forward-looking unresolved questions
  • How the multiple kinase inputs, conformational states, partner networks, and condensate behavior are integrated in real time to achieve spatially precise depolymerization at distinct cellular sites remains unresolved.
  • No unified in-cell model coupling phosphorylation state to local activity
  • Relative contribution of canonical depolymerization vs condensate/scaffolding functions unknown
  • Structures of full-length regulated states absent

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0008092 cytoskeletal protein binding 3 GO:0140096 catalytic activity, acting on a protein 3 GO:0140657 ATP-dependent activity 3 GO:0016787 hydrolase activity 2
Localization
GO:0005694 chromosome 3 GO:0005856 cytoskeleton 3 GO:0005815 microtubule organizing center 2 GO:0005634 nucleus 1
Pathway
R-HSA-1640170 Cell Cycle 3 R-HSA-112316 Neuronal System 2 R-HSA-73894 DNA Repair 1
Partners
AURKAAURKBEB1EB3KIF18BPLK1SGO2TIP150

Evidence

Reading pass · 51 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
2003 MCAK is an ATPase that catalytically depolymerizes microtubules by accelerating, ~100-fold, the rate of tubulin dissociation from microtubule ends. It has one high-affinity binding site per protofilament end, and up to 14 MCAK dimers can assemble at the end of a microtubule to form an ATP-hydrolyzing complex that processively depolymerizes the microtubule, removing ~20 tubulin dimers at a rate of 1 s⁻¹. In vitro ATPase assay, microtubule depolymerization kinetics, single-molecule analysis Molecular cell High 12620232
2004 Aurora B phosphorylates MCAK at serine 196 (neck region) and additional sites in the centromere-targeting domain, inhibiting its microtubule depolymerization activity in vitro and in vivo. Aurora B activity is required to localize MCAK to centromeres but not spindle poles. Phospho-S196 MCAK was detected at centromeres and anaphase spindle midzones in vivo. Injection of anti-pS196 antibodies into Xenopus egg extracts or cells caused chromosome positioning/segregation defects. In vitro kinase assay, mass spectrometry phosphorylation site mapping, antibody injection into Xenopus egg extracts and live cells, immunofluorescence Current biology : CB High 14960279 14972678
2004 Aurora B inhibits MCAK microtubule depolymerizing activity in vitro. Phosphomimetic MCAK (S/E) mutants inhibit depolymerization in vivo and localize preferentially to the inner centromere, while phospho-null (S/A) mutants concentrate at kinetochores. Both mutants increase syntelic attachments and mono-oriented chromosomes. FRAP analysis identifies two distinct MCAK binding sites at centromeres. Aurora B kinase-dead mutant or RNAi prevents centromeric targeting of MCAK. In vitro depolymerization assay, phosphomimetic/phosphonull mutagenesis, live-cell fluorescence imaging, FRAP, RNAi Developmental cell High 14960279
2004 In Xenopus egg extracts, recombinant Aurora B–INCENP inhibits MCAK microtubule depolymerase activity in a phosphorylation-dependent manner. An Aurora B-resistant alanine mutant (XMCAK-4A) produces mono-astral and monopolar structures instead of bipolar spindles when substituted for endogenous MCAK, and its ability to localize to inner centromeres is abolished. This demonstrates that Aurora B-dependent phosphorylation differentiates cytoplasmic from spindle-associated MCAK activity. In vitro kinase assay, Xenopus egg extract spindle assembly, phospho-resistant mutagenesis, immunofluorescence localization Molecular biology of the cell High 15064354
2003 Depletion of centromeric MCAK by injection of a dominant-negative centromere-targeting domain into prophase cells leads to reduced centromere stretch, delayed chromosome congression, alignment defects, severe chromosome missegregation, and multiple kinetochore-microtubule attachment defects (merotelic, syntelic, combined). Rates of chromosome movement are unchanged, indicating MCAK's primary role is not chromosome translocation but error correction of kinetochore-microtubule attachments. Dominant-negative protein microinjection, high-resolution immunofluorescence, live-cell imaging Molecular biology of the cell High 14699064
2006 MCAK moves along the microtubule lattice via one-dimensional (1D) random walk (diffusion coefficient 0.38 μm² s⁻¹, average duration 0.83 s). This lattice diffusion is ATP-independent, whereas catalytic depolymerization requires ATP hydrolysis. The 1D diffusion enables MCAK to target microtubule ends at rates exceeding 3D diffusion limits ('reduction in dimensionality' search strategy). Single-molecule fluorescence microscopy, TIRF-based in vitro assay Nature High 16672973
2007 Among the three human kinesin-13 paralogs, MCAK (Kif2c) specifically functions at kinetochores to regulate microtubule dynamics for chromosome alignment; its loss creates a permissive background that restores bipolar spindle assembly in Kif2a-depleted or Kif2b-depleted cells, demonstrating distinct pathway positions. MCAK and Kif2a activities must be balanced at kinetochores vs. poles for spindle bipolarity. siRNA knockdown, epistasis by double depletion, live-cell imaging, spindle assembly assays Molecular biology of the cell High 15302853 17538014
2005 MCAK tracks (treadmills) with the tips of polymerizing microtubules in living cells. This tip-tracking behavior requires the extreme C-terminal tail of MCAK and is inhibited by phosphorylation. Tip tracking is not essential for MCAK's microtubule-depolymerizing activity, suggesting it serves as a localization mechanism to regions of active plus-end regulation. Live-cell fluorescence imaging, C-terminal deletion mutants, phospho-mutant analysis The Journal of cell biology High 15883193
2006 Aurora B is specifically enriched at merotelic attachment sites. Aurora B activity (but not its localization) is required to enrich MCAK at merotelic attachments and phosphorylates MCAK on residues that regulate its microtubule depolymerase activity at these sites. Immunofluorescence, Aurora B inhibition, MCAK localization analysis at merotelic sites Current biology : CB Medium 16950107
2007 hSgo2 is required for MCAK to localize to the centromere. Delocalization of MCAK in hSgo2-depleted cells accounts for uncorrected kinetochore attachment defects. hSgo2 is associated with PP2A and contributes to spatial regulation of MCAK activity within the inner centromere/kinetochore region. siRNA depletion, immunofluorescence colocalization, Co-immunoprecipitation The Journal of cell biology Medium 17485487
2010 Aurora B phosphorylates hSgo2 at its N-terminal coiled-coil and middle regions; these phosphorylations separately promote binding of hSgo2 to PP2A and MCAK, respectively. Aurora B-phosphorylated hSgo2 is essential for recruiting both PP2A and MCAK to centromeres. In vitro kinase assay, phospho-mutant analysis, Co-immunoprecipitation, immunofluorescence Genes & development High 20889715
2009 TIP150 is a plus-end tracking protein (+TIP) that binds EB1 and co-localizes with it at microtubule plus ends. TIP150 also directly binds MCAK; suppression of TIP150 diminishes MCAK plus-end localization. Aurora B-mediated phosphorylation disrupts the TIP150–MCAK interaction in vitro, linking Aurora B regulation to MCAK plus-end targeting. Co-immunoprecipitation, in vitro binding assay, siRNA knockdown, immunofluorescence, in vitro phosphorylation assay EMBO reports Medium 19543227
2007 MCAK associates with the C-terminus of EB1 and EB3 through an interaction involving the N-terminal localization and regulatory domain of MCAK (not the motor domain). EB1 knockdown impairs GFP-MCAK tip localization in cells. The EB1–MCAK interaction is competitive with other EB1 ligands and does not require microtubules. Co-immunoprecipitation, GST pulldown domain mapping, siRNA knockdown, live-cell imaging Oncogene Medium 17968321
2010 In vitro reconstitution shows that EB3 targets MCAK to growing microtubule ends by increasing MCAK's association rate with microtubule tips via direct EB3–MCAK interaction. While MCAK alone blocks microtubule assembly, addition of EB3 restores robust growth. The MCAK–EB3 combination enhances catastrophe frequency, promoting rapid switching between growth and shortening, without affecting growth or shortening velocity. In vitro reconstitution of dynamic microtubule assay, TIRF microscopy, domain mutants, quantitative kinetics Current biology : CB High 20850319
2011 Kif18b binds directly to MCAK, and this interaction is required for robust microtubule depolymerization of astral microtubules. Aurora kinases negatively regulate the Kif18b–MCAK interaction through phosphorylation of MCAK, demonstrating that Aurora kinases regulate spindle microtubule plus-end stability through control of Kif18b–MCAK complex formation. Co-immunoprecipitation, siRNA knockdown, in vitro kinase assay, live-cell imaging, microtubule dynamics assays Current biology : CB High 21820309
2008 Aurora A phosphorylates MCAK at S196 (shared with Aurora B) to regulate MCAK localization and activity at aster centers during Ran-induced spindle assembly, and at S719 to positively enhance bipolar spindle formation. This defines a distinct role for MCAK at spindle poles regulated by Aurora A, separate from Aurora B regulation at centromeres. Xenopus egg extract spindle assembly, in vitro kinase assay, phosphosite mutagenesis, immunofluorescence Molecular biology of the cell High 18434591
2006 The N-terminal domain of MCAK is essential for regulating microtubule dynamics and kinetochore targeting; the C-terminal domain is essential for tight microtubule lattice binding and robust in vitro depolymerization activity. The neck is essential for microtubule end binding. Both C-terminal domain and neck are required for robust in vitro depolymerization activity. Purified GFP-domain deletion mutants, in vitro depolymerization assay, Xenopus egg extract spindle assay Molecular biology of the cell High 17093055
2007 Depletion of centromere-associated MCAK using chimeric constructs decreases directional coordination between sister kinetochores, reduces movement speed, and increases tension. Sister centromeres cannot detach efficiently from kinetochore microtubules during directional switching. Anchoring ectopic MCAK to the centromere reverses these effects. This demonstrates that centromere-MCAK promotes kinetochore microtubule turnover to coordinate directional switching. MCAK chimera/dominant-negative constructs, live-cell imaging, sister centromere distance and dynamics measurements The Journal of cell biology High 18039936
2011 MCAK depolymerizes microtubules from both plus and minus ends and generates significant tension (~1 pN per motor). An MCAK-decorated bead slides along microtubule sides under weak loads and captures/disassembles both microtubule ends. This 'side-sliding, end-catching' mechanism allows MCAK to generate driving force for chromosome movement at both kinetochores and spindle poles. Optical trap, bead-MCAK decoration assay, single-molecule microtubule depolymerization force measurements Nature cell biology High 21602793
2013 Aurora B phosphorylation at S196 in the neck region opens MCAK from a closed (inhibited) conformation (detected by FRET/FLIM biosensor) to an open conformation, diminishing the interaction between the C-terminal domain and neck. This conformational opening decreases MCAK affinity for the microtubule, reducing its depolymerization activity. MCAK bound to microtubule ends is in a closed conformation relative to lattice-bound MCAK. FRET biosensor, FLIM, TIRF imaging, phosphomimetic mutagenesis, in vitro depolymerization assay Current biology : CB High 24291095
2015 The C-terminus of MCAK binds to two motor domains in solution (crystal structure determined), acting as an autoinhibitory interaction that is displaced allosterically upon microtubule binding. This allows robust MCAK accumulation at microtubule ends. The C-terminus–motor interaction represents a structural intermediate in the MCAK catalytic cycle involving long-range conformational changes. X-ray crystallography (structure of motor domain bound to C-terminus), crosslinking, biochemical binding assays eLife High 25915621
2015 The KVD motif at the tip of kinesin-13-specific loop 2 of Kif2C is required for microtubule-stimulated ATPase activity and depolymerization. Upon microtubule binding, Kif2C undergoes a conformational change governed in part by KVD interaction with the tubulin interdimer interface. A switch-2 glutamate mutant (E to A) that blocks ATP hydrolysis in motile kinesins still depolymerizes microtubules and yields Kif2C–two-tubulin complexes, demonstrating that the conformational change upon tubulin binding is sufficient for tubulin release and ATP hydrolysis is not required for this step. In vitro ATPase assay, microtubule depolymerization assay, mutagenesis, structural modeling, biochemical complex analysis The Journal of biological chemistry High 26055718
2016 The α4-helix residues K524, E525, and R528 of the MCAK motor domain are critical for microtubule end recognition. Mutations at these conserved kinesin-13-specific positions specifically disrupt the ability of MCAK to recognize microtubule ends (reducing end residence time and end-specific ADP dissociation stimulation) without affecting lattice binding, impairing depolymerization. Mutagenesis, in vitro microtubule end-binding assay, single-molecule fluorescence imaging, ATPase assay Open biology High 27733589
2019 MCAK has a compact conformation in solution (confirmed by crosslinking and electron microscopy). When bound to microtubule ends, MCAK adopts an extended conformation in which the N-terminus and neck interact with the microtubule. The level of Aurora B phosphorylation of the N-terminus results in a graded (not binary) inhibition of MCAK depolymerase activity through allosteric regulation decoupling the N-terminus from the motor domain. Chemical crosslinking mass spectrometry, electron microscopy, in vitro kinase assay, phosphomimetic mutants, microtubule depolymerization assay Journal of cell science High 30578316
2016 GTSE1 inhibits MCAK microtubule depolymerase activity. Cells lacking GTSE1 show defects in chromosome alignment and spindle positioning due to MT instability caused by excess MCAK activity. Artificially elevated GTSE1 hyperstabilizes kinetochore microtubules and increases chromosome missegregation/CIN. siRNA depletion, overexpression, co-immunoprecipitation, in vitro depolymerization assay, live-cell imaging The Journal of cell biology Medium 27881713
2016 NuSAP is a novel binding partner of MCAK and modulates MCAK depolymerization activity. Aurora B kinase phosphorylation of MCAK significantly enhances the NuSAP–MCAK interaction, and NuSAP modulates MCAK depolymerization in an Aurora B-dependent manner to regulate kinetochore microtubule dynamics. Co-immunoprecipitation, in vitro depolymerization assay, siRNA knockdown, phospho-mutant analysis Scientific reports Medium 26733216
2015 Aurora B–PLK1 signaling axis regulates MCAK in mitosis: Aurora B phosphorylates PLK1 at Thr210 to activate PLK1 at kinetochores; active PLK1 in turn phosphorylates MCAK at Ser715 to promote its microtubule depolymerase activity. Non-phosphorylatable MCAK S715A prevents correct kinetochore–microtubule attachment, resulting in chromosome bridges in anaphase. FRET-based PLK1 activity reporter, phosphorylation site mutagenesis, in vitro kinase assay, immunofluorescence, live-cell imaging Scientific reports Medium 26206521
2014 A Rac1–Aurora A–MCAK signaling pathway mediates endothelial cell polarization and directional migration. Aurora A kinase activity (regionally enhanced by Rac1 signaling) locally inhibits MCAK microtubule depolymerizing activity at the trailing edge of polarized wound-edge endothelial cells, promoting regional differences in MT dynamics. siRNA knockdown, dominant-negative/constitutively active Rac1, inhibitor treatment, high-resolution fluorescence microscopy with MT plus-end tracking, quantitative image analysis The Journal of cell biology Medium 25002679
2012 MCAK tip-tracking (EB-dependent binding to growing microtubule ends via the SKIP motif N-terminal to the neck) negatively regulates microtubule length within the assembling bipolar spindle. This function requires MCAK's ability to bind EB proteins. Abolishing tip tracking (EB-binding mutant) leads to over-long non-kinetochore microtubules, antagonizes centrosome separation, but ultimately impairs robust kinetochore attachment. EB-binding SKIP motif mutants, siRNA rescue, live-cell imaging, spindle microtubule length measurements The Journal of cell biology Medium 22492725
2013 Lateral-to-end-on conversion of chromosome-microtubule attachment requires MCAK to release laterally attached microtubules after partial end-on attachment is formed, acting sequentially after CENP-E-mediated lateral tethering. High-resolution live imaging assay, siRNA knockdown of MCAK and CENP-E, classification of attachment intermediates Current biology : CB Medium 23891108
2014 TIP150–MCAK interaction governs entosis via Aurora A-mediated phosphorylation of MCAK. MCAK forms an intramolecular association required for TIP150 binding; Aurora A phosphorylation of MCAK modulates this intramolecular association, disrupting the MCAK–TIP150 interaction in vitro and inhibiting entosis in vivo. MCAK cooperates with TIP150 to modulate cell mechanical rigidity during entosis. Co-immunoprecipitation, in vitro kinase/binding assay, optical trap (cell rigidity), live-cell imaging, siRNA knockdown Journal of molecular cell biology Medium 24847103
2016 The far C-terminal residues E715/E716 of MCAK regulate MCAK conformation and spindle pole focusing. Point mutation E715A/E716A increases MCAK targeting to poles and reduces MT lifetimes, inducing unfocused spindle poles—a phenotype phenocopied by Aurora A phosphomimetic S719E. The kinesin-14 XCTK2 rescues unfocused-pole phenotype, placing MCAK and XCTK2 in opposing activities at poles. Xenopus egg extract spindle assembly, point mutagenesis, immunofluorescence, FRET conformation assay Molecular biology of the cell Medium 26941326
2020 KIF2C (MCAK) is recruited to DNA double-strand break (DSB) sites in a PARP- and ATM-dependent manner. KIF2C knockdown/knockout leads to accumulation of endogenous DNA damage, DNA damage hypersensitivity, and reduced DSB repair via both NHEJ and HR. KIF2C depletion or inhibition of its microtubule depolymerase activity reduces DSB mobility, impairs DNA damage foci formation, and decreases foci fusion/resolution. DSB-mimicking DNA template pulldown in Xenopus extracts, CRISPR knockout, siRNA knockdown, γH2AX foci analysis, live-cell DSB tracking, NHEJ/HR reporter assays eLife Medium 31951198
2020 KIF2C interacts with TBC1D7, and this interaction disrupts formation of the TSC complex, resulting in enhanced mTORC1 signal transduction. KIF2C is a direct transcriptional target of the Wnt/β-catenin pathway and mediates crosstalk between Wnt/β-catenin and mTORC1 signaling in hepatocellular carcinoma. Co-immunoprecipitation, gain/loss-of-function assays, luciferase reporter assay, Western blot, in vivo xenograft Protein & cell Medium 32748349
2022 KIF2C regulates microtubule dynamics in neuronal dendrites and activity-dependent microtubule invasion into dendritic spines. KIF2C knockdown or conditional knockout impairs spine morphology, synaptic AMPA receptor expression, excitatory transmission, long-term potentiation, and cognitive behavior in mice. RNAi knockdown, conditional knockout (Cre-lox), live microtubule imaging in neurons, electrophysiology, behavioral tests eLife Medium 35138249
2023 KIF2C regulates transport of mGlu1 receptors in cerebellar Purkinje cells by binding to Rab8. KIF2C deficiency in Purkinje cells reduces mGlu1 and GluA2 synaptic expression, alters excitatory but not inhibitory transmission, and causes motor incoordination in male mice. Conditional knockout (Purkinje cell-specific), Co-immunoprecipitation with Rab8, immunofluorescence, electrophysiology, behavioral motor tests The Journal of physiology Medium 37431690
2021 Both overexpression and downregulation of MCAK/KIF2C reduce cell motility and migration. Specifically, altered MCAK levels impair focal adhesion protein composition and phosphorylation, assembly/disassembly rate of focal adhesions, cell adhesion, and plus-tip microtubule dynamics. This demonstrates MCAK acts as a regulator of cell motility through actin-MT cytoskeleton dynamics and focal adhesion turnover. CRISPR/dCas9 overexpression and knockdown cell lines, live-cell imaging, focal adhesion lifetime assays, MT plus-tip tracking, Western blot Cancers Medium 34830827
2021 MCAK's spatial distribution of activity (higher at trailing edge than leading edge) is required for cell polarity, centrosome positioning, focal adhesion disassembly, and directional migration. Rac1 overexpression has a dominant effect over MCAK activity, placing Rac1 downstream of or parallel to MCAK in the migration pathway. siRNA knockdown, Rac1 overexpression epistasis, live-cell imaging, FA lifetime measurements, MT dynamics analysis Molecular biology of the cell Medium 33566676
1999 MCAK contains multiple nuclear localization sequences (NLS) and a nuclear exclusion sequence (NES) in the amino-terminal region that balance its nucleocytoplasmic distribution. Amino acid substitutions in the ATP-binding domain of the MCAK motor affect nuclear localization, in turn influencing the degree of centromere binding. GFP-MCAK deletion constructs, ATP-binding domain mutagenesis, fluorescence microscopy localization Cell biology international Medium 10600236
2008 MCAK accumulates during the cell cycle, reaches maximum at G2/M, and is rapidly degraded by the proteasome during mitosis. A phosphorylated form of MCAK appears during mitosis and is preferentially degraded. This degradation limits MCAK activity during late mitosis, arguing against a role in anaphase chromosome movement. Cell cycle fractionation, immunofluorescence, proteasome inhibitor treatment, Western blot Cell cycle (Georgetown, Tex.) Medium 18843200
2012 A phosphorylation site on MCAK controls its proteasomal degradation; phosphorylation-resistant mutation prolongs MCAK stability beyond the metaphase-to-anaphase transition and prevents MCAK removal from centromeres, causing MCAK retention throughout the cell cycle and mitotic defects. A phosphomimetic mutation accelerates degradation. Phosphosite mutagenesis, proteomic phosphorylation site identification, immunofluorescence, cell division assays Cytoskeleton (Hoboken, N.J.) Medium 22422706
2017 Cdk1 phosphorylates MCAK at T537 within the motor domain. A phosphomimetic T537E mutant significantly impairs microtubule depolymerization by reducing the ability of MCAK to recognize microtubule ends specifically: microtubule-end residence time is reduced, lattice residence time is unaffected, and end-specific ADP dissociation stimulation is abolished. Phosphomimetic mutagenesis, single-molecule TIRF imaging (end/lattice residence times), ATPase assay, cell transfection phenotype PeerJ Medium 29230353
2022 In vitro reconstitution shows that Kif18b, MCAK, and EB3 act as an integrated network to potently promote microtubule depolymerization at very low concentrations. Kif18b transports EB3 and MCAK to microtubule plus ends through multivalent weak interactions, enabling cooperative plus-end shortening. In vitro reconstitution, single-molecule TIRF imaging, quantitative microtubule depolymerization assay Journal of cell science High 35502670
2011 DDA3 localizes to kinetochores and interacts with MCAK. Depletion of DDA3 causes chromosome congression defects associated with loss of MCAK function at kinetochores, and results in CENP-E accumulation at unaligned kinetochores, without affecting Aurora B/CPC activity. Co-immunoprecipitation, siRNA knockdown, immunofluorescence Biochemical and biophysical research communications Low 21426902
2005 CaMKIIgamma depletion leads to disorganized multipolar spindles by failing to suppress MCAK depolymerase activity. Two distinct but overlapping mechanisms for negative regulation of the cytosolic/centrosomal pool of MCAK exist: one involving CaMKIIgamma and another involving TOGp. Both are essential for spindle bipolarity; their effects are abolished in MCAK-depleted cells, placing both upstream of MCAK in spindle assembly. siRNA RNAi depletion, inducible overexpression, epistasis by double depletion, immunofluorescence The EMBO journal Medium 15775983
2022 α-Tubulin detyrosination suppresses MCAK activity; experimental increase of detyrosinated α-tubulin and MCAK depletion produce non-cumulative enhancement of taxol cytotoxicity and cell death in mitosis/interphase, identifying a mechanistic link between α-tubulin detyrosination and MCAK activity suppression. siRNA knockdown, detyrosination manipulation, flow cytometry cell death assay, clonogenic assay, combinatorial treatment epistasis The Journal of cell biology Medium 36459065
2025 KIF2C preferentially depolymerizes polyglutamylated tubulin even in the presence of paclitaxel. A chemical inhibitor 7S9 prohibits dissociation of KIF2C from microtubules, counteracting KIF2C-mediated paclitaxel resistance. Combination of 7S9 and paclitaxel significantly reduces tumorigenesis in chemoresistant TNBC mouse models. In vitro depolymerization assay with polyglutamylated tubulin, KIF2C inhibitor development, in vivo mouse tumor model Developmental cell Medium 40157365
2021 KIF2C directly binds PKM2 (confirmed by Co-IP), and this interaction prevents PKM2 ubiquitination, increasing PKM2 stability. Domain 2 of KIF2C mediates the PKM2 binding. Elevated KIF2C promotes autophagy and glycolysis in doxorubicin-resistant breast cancer cells via PKM2 stabilization. Co-immunoprecipitation, Western blot (ubiquitination assay), domain deletion mapping, functional metabolic assays Cancer cell international Low 34663310
2025 The N-terminal domain of KIF2C adopts a Tudor/PWWP/MBT fold that binds phosphorylated motifs, including phosphorylated BRCA2-pT207. KIF2C forms membrane-less organelles (condensates) in an Aurora B- and PLK1-dependent manner via this phospho-binding domain. KIF2C condensation concentrates PLK1 and BRCA2-pT207 at microtubule ends/extremities; condensates exclude tubulin. KIF2C depolymerase activity promotes condensate formation. Aurora B is required for condensate formation. Structural determination (NTD fold), Co-immunoprecipitation, optogenetic condensate platform, FLIM-FRET, immunofluorescence, mutagenesis Nucleic acids research Medium 40498077
2024 Nek2A interacts with KIF2C (identified by TurboID proximity labeling and confirmed by Co-immunoprecipitation and colocalization). KIF2C silencing diminishes Nek2A's ability to prevent centrosome clustering, placing KIF2C downstream of Nek2A in the centrosome clustering/anti-clustering pathway. TurboID proximity labeling, Co-immunoprecipitation, siRNA knockdown epistasis, immunofluorescence colocalization Cell death & disease Low 38493150
2024 CCDC69 microtubule depolymerization activity is dependent on KIF2C, as demonstrated by the finding that a fraction of CCDC69 localizes to centromeres and KIF2C mediates CCDC69's depolymerization effects. CCDC69 also regulates stability of the chromosomal passenger complex (CPC) by protecting its members from degradation. Overexpression, siRNA epistasis, immunofluorescence colocalization, microtubule depolymerization assays Scientific reports Low 39638803

Source papers

Stage 0 corpus · 100 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2004 Aurora B regulates MCAK at the mitotic centromere. Developmental cell 444 14960279
2004 Aurora B phosphorylates centromeric MCAK and regulates its localization and microtubule depolymerization activity. Current biology : CB 396 14972678
2006 The depolymerizing kinesin MCAK uses lattice diffusion to rapidly target microtubule ends. Nature 358 16672973
2003 The kinesin-related protein MCAK is a microtubule depolymerase that forms an ATP-hydrolyzing complex at microtubule ends. Molecular cell 302 12620232
2003 Depletion of centromeric MCAK leads to chromosome congression and segregation defects due to improper kinetochore attachments. Molecular biology of the cell 233 14699064
2006 Aurora B is enriched at merotelic attachment sites, where it regulates MCAK. Current biology : CB 208 16950107
2007 The kinesin-13 proteins Kif2a, Kif2b, and Kif2c/MCAK have distinct roles during mitosis in human cells. Molecular biology of the cell 201 17538014
2004 The KinI kinesin Kif2a is required for bipolar spindle assembly through a functional relationship with MCAK. The Journal of cell biology 195 15302853
2004 Differentiation of cytoplasmic and meiotic spindle assembly MCAK functions by Aurora B-dependent phosphorylation. Molecular biology of the cell 194 15064354
2005 MCAK associates with the tips of polymerizing microtubules. The Journal of cell biology 126 15883193
2010 In vitro reconstitution of the functional interplay between MCAK and EB3 at microtubule plus ends. Current biology : CB 122 20850319
2007 Tripin/hSgo2 recruits MCAK to the inner centromere to correct defective kinetochore attachments. The Journal of cell biology 115 17485487
2011 A complex of Kif18b and MCAK promotes microtubule depolymerization and is negatively regulated by Aurora kinases. Current biology : CB 114 21820309
2010 Phosphorylation of mammalian Sgo2 by Aurora B recruits PP2A and MCAK to centromeres. Genes & development 112 20889715
2013 Lateral to end-on conversion of chromosome-microtubule attachment requires kinesins CENP-E and MCAK. Current biology : CB 110 23891108
2007 MCAK facilitates chromosome movement by promoting kinetochore microtubule turnover. The Journal of cell biology 107 18039936
2008 Aurora A phosphorylates MCAK to control ran-dependent spindle bipolarity. Molecular biology of the cell 102 18434591
2020 KIF2C: a novel link between Wnt/β-catenin and mTORC1 signaling in the pathogenesis of hepatocellular carcinoma. Protein & cell 99 32748349
2004 Differential functional interplay of TOGp/XMAP215 and the KinI kinesin MCAK during interphase and mitosis. The EMBO journal 79 14749730
2009 TIP150 interacts with and targets MCAK at the microtubule plus ends. EMBO reports 76 19543227
2007 MCAK associates with EB1. Oncogene 60 17968321
2012 MCAK activity at microtubule tips regulates spindle microtubule length to promote robust kinetochore attachment. The Journal of cell biology 58 22492725
2011 Mitotic centromere-associated kinesin (MCAK): a potential cancer drug target. Oncotarget 56 22249213
2019 KIF2C exerts an oncogenic role in nonsmall cell lung cancer and is negatively regulated by miR-325-3p. Cell biochemistry and function 54 31328811
2013 Evidence of colorectal cancer-associated mutation in MCAK: a computational report. Cell biochemistry and biophysics 54 23564489
2013 Aurora B inhibits MCAK activity through a phosphoconformational switch that reduces microtubule association. Current biology : CB 54 24291095
2010 NY-CO-58/KIF2C is overexpressed in a variety of solid tumors and induces frequent T cell responses in patients with colorectal cancer. International journal of cancer 54 19937794
2015 Spatiotemporal dynamics of Aurora B-PLK1-MCAK signaling axis orchestrates kinetochore bi-orientation and faithful chromosome segregation. Scientific reports 51 26206521
2014 Rac1 and Aurora A regulate MCAK to polarize microtubule growth in migrating endothelial cells. The Journal of cell biology 47 25002679
2011 The bidirectional depolymerizer MCAK generates force by disassembling both microtubule ends. Nature cell biology 47 21602793
2008 MCAK-independent functions of ch-Tog/XMAP215 in microtubule plus-end dynamics. Molecular and cellular biology 47 18809577
2016 Molecular insight into the regulation and function of MCAK. Critical reviews in biochemistry and molecular biology 46 27146484
2016 GTSE1 tunes microtubule stability for chromosome alignment and segregation by inhibiting the microtubule depolymerase MCAK. The Journal of cell biology 45 27881713
2021 TBX15/miR-152/KIF2C pathway regulates breast cancer doxorubicin resistance via promoting PKM2 ubiquitination. Cancer cell international 44 34663310
2020 Kinesin Kif2C in regulation of DNA double strand break dynamics and repair. eLife 43 31951198
2014 Aurora A orchestrates entosis by regulating a dynamic MCAK-TIP150 interaction. Journal of molecular cell biology 43 24847103
2010 MCAK regulates chromosome alignment but is not necessary for preventing aneuploidy in mouse oocyte meiosis I. Development (Cambridge, England) 41 20504960
2005 Mammalian mitotic centromere-associated kinesin (MCAK): a new molecular target of sulfoquinovosylacylglycerols novel antitumor and immunosuppressive agents. The FEBS journal 41 15853798
2006 The interplay of the N- and C-terminal domains of MCAK control microtubule depolymerization activity and spindle assembly. Molecular biology of the cell 40 17093055
2004 MCAK, a Kin I kinesin, increases the catastrophe frequency of steady-state HeLa cell microtubules in an ATP-dependent manner in vitro. FEBS letters 40 15304328
2020 Circular RNA circRGNEF promotes bladder cancer progression via miR-548/KIF2C axis regulation. Aging 39 32305958
2005 CaMKIIgamma-mediated inactivation of the Kin I kinesin MCAK is essential for bipolar spindle formation. The EMBO journal 38 15775983
2004 Mitosis: MCAK under the aura of Aurora B. Current biology : CB 38 15120087
1999 Mutations in the ATP-binding domain affect the subcellular distribution of mitotic centromere-associated kinesin (MCAK). Cell biology international 37 10600236
2021 Mitotic Centromere-Associated Kinesin (MCAK/KIF2C) Regulates Cell Migration and Invasion by Modulating Microtubule Dynamics and Focal Adhesion Turnover. Cancers 34 34830827
2016 NuSAP modulates the dynamics of kinetochore microtubules by attenuating MCAK depolymerisation activity. Scientific reports 34 26733216
2011 Mitotic centromere-associated kinesin (MCAK) mediates paclitaxel resistance. The Journal of biological chemistry 33 21903575
2016 Aurora A, MCAK, and Kif18b promote Eg5-independent spindle formation. Chromosoma 32 27354041
2022 Down regulated oncogene KIF2C inhibits growth, invasion, and metastasis of hepatocellular carcinoma through the Ras/MAPK signaling pathway and epithelial-to-mesenchymal transition. Annals of translational medicine 29 35284538
2019 The depolymerase activity of MCAK shows a graded response to Aurora B kinase phosphorylation through allosteric regulation. Journal of cell science 29 30578316
2015 The C-terminal region of the motor protein MCAK controls its structure and activity through a conformational switch. eLife 29 25915621
2010 MCAK is present at centromeres, midspindle and chiasmata and involved in silencing of the spindle assembly checkpoint in mammalian oocytes. Molecular human reproduction 29 20406800
2006 A perikinetochoric ring defined by MCAK and Aurora-B as a novel centromere domain. PLoS genetics 29 16741559
2022 KIF2C regulates synaptic plasticity and cognition in mice through dynamic microtubule depolymerization. eLife 27 35138249
2008 Effects of anti-microtubule agents on microtubule organization in cells lacking the kinesin-13 MCAK. Cell cycle (Georgetown, Tex.) 27 18635958
2015 New Insights into the Coupling between Microtubule Depolymerization and ATP Hydrolysis by Kinesin-13 Protein Kif2C. The Journal of biological chemistry 25 26055718
2012 Mitotic centromere-associated kinase (MCAK/Kif2C) regulates cellular senescence in human primary cells through a p53-dependent pathway. FEBS letters 23 23098759
2010 Chromosomal and cytoplasmic context determines predisposition to maternal age-related aneuploidy: brief overview and update on MCAK in mammalian oocytes. Biochemical Society transactions 23 21118147
2023 KIF2C accelerates the development of non-small cell lung cancer and is suppressed by miR-186-3p via the AKT-GSK3β-β-catenin pathway. Scientific reports 22 37142638
2022 α-Tubulin detyrosination links the suppression of MCAK activity with taxol cytotoxicity. The Journal of cell biology 18 36459065
2008 Cell cycle dependent degradation of MCAK: evidence against a role in anaphase chromosome movement. Cell cycle (Georgetown, Tex.) 18 18843200
2021 Downregulation of KIF2C and TEKT2 is associated with male infertility and testicular carcinoma. Aging 17 34591790
2006 Global and local control of microtubule destabilization promoted by a catastrophe kinesin MCAK/XKCM1. Journal of muscle research and cell motility 16 16450057
2021 KIF2C promotes the proliferation of hepatocellular carcinoma cells in vitro and in vivo. Experimental and therapeutic medicine 15 34504548
2021 Cell cycle dysregulation with overexpression of KIF2C/MCAK is a critical event in nasopharyngeal carcinoma. Genes & diseases 15 37013060
2019 Functional characterization of MCAK/Kif2C cancer mutations using high-throughput microscopic analysis. Molecular biology of the cell 15 31746663
2023 KIF2C promotes clear cell renal cell carcinoma progression via activating JAK2/STAT3 signaling pathway. Molecular and cellular probes 14 37863123
2022 Potent microtubule-depolymerizing activity of a mitotic Kif18b-MCAK-EB network. Journal of cell science 14 35502670
2023 KIF2C Facilitates Tumor Growth and Metastasis in Pancreatic Ductal Adenocarcinoma. Cancers 13 36900292
2021 Spatial regulation of MCAK promotes cell polarization and focal adhesion turnover to drive robust cell migration. Molecular biology of the cell 13 33566676
2020 Collective effects of XMAP215, EB1, CLASP2, and MCAK lead to robust microtubule treadmilling. Proceedings of the National Academy of Sciences of the United States of America 13 32457163
2016 The family-specific α4-helix of the kinesin-13, MCAK, is critical to microtubule end recognition. Open biology 13 27733589
2011 DDA3 associates with MCAK and controls chromosome congression. Biochemical and biophysical research communications 13 21426902
2017 MCAK-mediated regulation of endothelial cell microtubule dynamics is mechanosensitive to myosin-II contractility. Molecular biology of the cell 12 28298485
2010 Identification of HLA-A*0201/-A*2402-restricted CTL epitope-peptides derived from a novel cancer/testis antigen, MCAK, and induction of a specific antitumor immune response. Oncology reports 12 21165574
2016 The far C-terminus of MCAK regulates its conformation and spindle pole focusing. Molecular biology of the cell 11 26941326
2022 KIF2C affects sperm cell differentiation in patients with Klinefelter syndrome, as revealed by RNA-Seq and scRNA-Seq data. FEBS open bio 10 35622500
2008 Regulation of the human mitotic centromere-associated kinesin (MCAK) promoter by the transcription factors Sp1 and E2F1. Biochimica et biophysica acta 10 18440323
2023 EGFR-mediated hyperacetylation of tubulin induced docetaxel resistance by downregulation of HDAC6 and upregulation of MCAK and PLK1 in prostate cancer cells. The Kaohsiung journal of medical sciences 9 37916740
2023 Silencing of KIF2C enhances the sensitivity of hepatocellular carcinoma cells to cisplatin through regulating the PI3K/AKT/MAPK signaling pathway. Anti-cancer drugs 9 38170762
2020 Role of kif2c, A Gene Related to ALL Relapse, in Embryonic Hematopoiesis in Zebrafish. International journal of molecular sciences 9 32354205
2023 MCAK Inhibitors Induce Aneuploidy in Triple-Negative Breast Cancer Models. Cancers 8 37444419
2022 Identification of aberrantly methylated differentially expressed genes and pro-tumorigenic role of KIF2C in melanoma. Frontiers in genetics 8 35991567
2021 Activation of the TGF-β1/Smad signaling by KIF2C contributes to the malignant phenotype of thyroid carcinoma cells. Tissue & cell 8 34624565
2025 KIF2C promotes paclitaxel resistance by depolymerizing polyglutamylated microtubules. Developmental cell 7 40157365
2021 Modeling processive motion of kinesin-13 MCAK and kinesin-14 Cik1-Kar3 molecular motors. Protein science : a publication of the Protein Society 7 34382258
2024 Nek2A prevents centrosome clustering and induces cell death in cancer cells via KIF2C interaction. Cell death & disease 5 38493150
2024 Modeling study of kinesin-13 MCAK microtubule depolymerase. European biophysics journal : EBJ 5 39093405
2023 Sulforaphane Targets the TBX15/KIF2C Pathway to Repress Glycolysis and Cell Proliferation in Gastric Carcinoma Cells. Nutrition and cancer 5 37139873
2017 A Cdk1 phosphomimic mutant of MCAK impairs microtubule end recognition. PeerJ 4 29230353
2013 Intracellular targets for a phosphotyrosine peptidomimetic include the mitotic kinesin, MCAK. Biochemical pharmacology 4 23830822
2011 Multi-talented MCAK: Microtubule depolymerizer with a strong grip. Nature cell biology 4 21725286
2025 Overexpression of KIF2C amplifies tamoxifen resistance and lung metastasis of breast cancer through PLK1/C-Myc pathway. Naunyn-Schmiedeberg's archives of pharmacology 3 40100379
2024 MEF2C contributes to axonal branching by regulating Kif2c transcription. The European journal of neuroscience 3 38663879
2024 CCDC69 maintains genome integrity by regulating KIF2C/MCAK depolymerase activity and the stability of the chromosomal passenger complex. Scientific reports 3 39638803
2023 Ablation of KIF2C in Purkinje cells impairs metabotropic glutamate receptor trafficking and motor coordination in male mice. The Journal of physiology 3 37431690
2023 Lumican silencing ameliorates β-glycerophosphate-mediated vascular smooth muscle cell calcification by attenuating the inhibition of APOB on KIF2C activity. Open medicine (Warsaw, Poland) 3 37711155
2024 KIF2C as a potential therapeutic target: insights from lung adenocarcinoma subtype classification and functional experiments. Molecular omics 2 38940931
2012 Control of MCAK degradation and removal from centromeres. Cytoskeleton (Hoboken, N.J.) 2 22422706
2025 KIF2C condensation concentrates PLK1 and phosphorylated BRCA2 on kinetochore microtubules in mitosis. Nucleic acids research 1 40498077

Missed literature

Know a paper Affinage missed for KIF2C? Flag it for the maintainers and the community.

No submissions yet.