Affinage

CLASP2

CLIP-associating protein 2 · UniProt O75122

Length
1294 aa
Mass
141.1 kDa
Annotated
2026-06-09
42 papers in source corpus 30 papers cited in narrative 30 extracted findings
Cross-family judge vs UniProt: Affinage preferred faithfulness: 8/8 claims corpus-supported (100%)

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

CLASP2 is a microtubule plus-end tracking protein that stabilizes microtubules by suppressing catastrophe and promoting rescue, and that cross-links the actin and microtubule cytoskeletons to organize polarized cell behaviors (PMID:29540526, PMID:36598814). Purified CLASP2 intrinsically suppresses catastrophe and promotes rescue without altering growth or shrinkage rates, and its activity is targeted and amplified by direct binding to EB1, which delivers CLASP2 to and prolongs its dwell at growing plus-ends (PMID:29540526); together with EB1, XMAP215, and MCAK it reconstitutes plus-end-leading microtubule treadmilling in vitro (PMID:32457163). Mechanistically, its tandem TOG domains adopt distinct curved tubulin-binding conformations that discriminate states of dynamic instability, and the TOG2 domain forms a load-bearing, nucleotide-state-sensitive bond with terminal non-GTP tubulins at curved protofilament tips, releasing upon conversion to GTP-tubulin to enable persistent assembly at load-bearing ends (PMID:26003921, PMID:36598991). CLASP2 cross-links F-actin to the microtubule lattice through a minimal TOG2 plus serine-arginine-rich module (PMID:36598814). This activity is gated by multisite phosphorylation: GSK3β phosphorylation near the SXIP EB1-binding motifs disrupts the salt-bridge interactions required for EB1 binding and abolishes plus-end tracking, with CDK priming required beforehand (PMID:22467876, PMID:19638411), while Cdk1 priming and Plk1 act during mitosis to stabilize kinetochore-microtubule attachments (PMID:23045552). At kinetochores, centrosomes, and the spindle, CLASP2 is required for chromosome segregation and spindle integrity, with kinetochore localization, EB-protein binding, and TOG-mediated recognition of curved protofilaments each independently necessary for normal kinetochore-MT dynamics (PMID:16914514, PMID:31757788). At the cell cortex, CLASP2 captures and tethers microtubule plus-ends through partners including LL5β and protein 4.1R to direct focal vesicle delivery and AChR insertion at the neuromuscular junction and insulin-stimulated GLUT4 delivery, and it drives persistent directional migration via cortical localization controlled by ACF7 (PMID:25589673, PMID:23943871, PMID:22992739, PMID:17113391). CLASP2 additionally functions as a cytoskeletal effector in Reelin/Dab1 signaling during neocortical neuron migration and regulates neuronal polarity and synapse formation (PMID:28285824, PMID:23035100).

Mechanistic history

Synthesis pass · year-by-year structured walk · 15 steps
  1. 2005 High

    Established how CLASP2 stabilizes microtubules: by directly binding EB1 and tethering microtubules to the cell cortex, confining dynamics to the cell periphery.

    Evidence RNAi, direct binding assays, domain deletion, and live imaging in HeLa cells

    PMID:15631994

    Open questions at the time
    • Identity of the cortical anchor undefined at this stage
    • No in vitro reconstitution of stabilization activity
  2. 2006 High

    Defined CLASP2's cellular roles in polarized motility and in mitosis, placing ACF7 upstream of its cortical localization and demonstrating segregation/spindle requirements.

    Evidence CLASP2 knockout MEFs in wound-healing and mitotic assays, FRAP, ACF7 RNAi

    PMID:16914514 PMID:17113391

    Open questions at the time
    • Molecular link between ACF7 and CLASP2 cortical capture unresolved
    • Kinetochore recruitment mechanism unknown
  3. 2007 Medium

    Showed CLASP2 is an actin/microtubule crosslinker, mapping actin-binding to its MT-binding and N-terminal TOG domains.

    Evidence Co-IP, deletion mapping, and FRET in Xenopus fibroblasts/neurons

    PMID:17342765

    Open questions at the time
    • Crosslinking not reconstituted with purified proteins
    • Functional consequence of actin binding not established
  4. 2009 High

    Identified GSK3β as a direct regulator that switches off CLASP2 by phosphorylating Ser533/Ser537 to dissociate it from EB1, IQGAP1, and microtubules, establishing phospho-gating of plus-end tracking.

    Evidence In vitro phosphorylation, mutagenesis, co-IP, imaging in migrating fibroblasts

    PMID:19638411

    Open questions at the time
    • Phosphatase that reverses the mark unidentified
    • Spatial control of GSK3β activity not defined
  5. 2012 High

    Resolved the structural logic of phospho-control and extended it to mitosis: GSK3 multisite phosphorylation disrupts SXIP salt-bridge contacts (with CDK priming) and Cdk1/Plk1 cascades stabilize kinetochore-MT attachments.

    Evidence In vitro binding, 31P NMR, MD simulations, phospho-site mutagenesis, kinase assays, live imaging

    PMID:22467876 PMID:23045552

    Open questions at the time
    • How local dephosphorylation is achieved at specific sites unclear
    • Integration of multiple kinase inputs in vivo not fully mapped
  6. 2012 High

    Connected CLASP2 to physiological cortical capture: agrin/PI3K/GSK3β signaling licenses CLASP2 to capture plus-ends at AChR clusters, and CLASP2 controls neuronal polarity and synapse formation.

    Evidence RNAi/overexpression in myotubes and neurons, pharmacological pathway manipulation, electrophysiology, imaging

    PMID:22851317 PMID:23035100

    Open questions at the time
    • Cortical receptor linking CLASP2 to AChR clusters not yet identified here
    • Mechanism coupling capture to subsynaptic gene expression unknown
  7. 2012 Medium

    Linked CLASP2 to metabolic vesicle delivery, showing insulin-stimulated phosphorylation and a requirement for insulin-stimulated GLUT4 delivery and glucose transport.

    Evidence Mass spectrometry, phosphoantibody IP, siRNA, glucose transport assay in myotubes/adipocytes

    PMID:22992739

    Open questions at the time
    • Insulin-responsive kinase site not defined
    • Direct role at GLUT4 vesicle docking versus indirect not separated
  8. 2013 Medium

    Identified cortical/junctional partners (p120-catenin, protein 4.1R) that recruit CLASP2 and locally tune GSK3 to govern microtubule tethering at the cell edge and adherens junctions.

    Evidence Co-IP, siRNA, live MT dynamics imaging, GSK3 activity assays

    PMID:23943871 PMID:24368809

    Open questions at the time
    • Whether 4.1R/p120 interactions are direct or scaffolded not fully resolved
    • Mechanism of local GSK3 regulation by 4.1R unclear
  9. 2014 High

    Expanded the kinase repertoire and structural basis: Abl phosphorylates CLASP2 within actin/MT-binding domains to modulate growth-cone cytoskeleton, aPKC/PAR3 control Golgi organization via GCC185, and TOG crystal structures reveal distinct tubulin-binding curvatures.

    Evidence In vitro kinase assays, MS phosphosite mapping, co-IP, X-ray crystallography, mutagenesis

    PMID:24520051 PMID:25231989 PMID:25518939 PMID:26003921

    Open questions at the time
    • How distinct TOG conformations map to specific dynamic-instability states not directly demonstrated in cells
    • Crosstalk among Abl/aPKC/GSK3 inputs unresolved
  10. 2015 Medium

    Established LL5β as the cortical partner required for CLASP2-mediated MT capture and focal vesicle delivery at the NMJ.

    Evidence LL5β RNAi, dominant-negative CLASP2 fragment, live vesicle imaging, in vivo NMJ analysis

    PMID:25589673

    Open questions at the time
    • Whether CLASP2-LL5β binding is direct not established here
    • Cargo specificity of focal delivery undefined
  11. 2017 Medium

    Demonstrated CLASP2 acts as a cytoskeletal effector in Reelin signaling via phospho-regulated Dab1 association, and refined the kinetochore phospho-model where only kinetochore-bound CLASP2 is locally dephosphorylated.

    Evidence Co-IP, phospho-site mutagenesis, in utero electroporation, migration assays, kinetochore tension measurements

    PMID:28232523 PMID:28285824

    Open questions at the time
    • Phosphatase mediating local kinetochore dephosphorylation unidentified
    • Direct Dab1-CLASP2 contact interface not mapped
  12. 2018 High

    Reconstituted CLASP2's intrinsic activity, proving it suppresses catastrophe and promotes rescue and that EB1 targets it to and prolongs its dwell at MT tips through direct interaction.

    Evidence In vitro reconstitution with purified proteins, TIRF microscopy, EB1 truncation controls

    PMID:29540526

    Open questions at the time
    • Stoichiometry of the CLASP2-EB1-MT complex not defined
    • Which TOG domain mediates rescue not resolved here
  13. 2020 High

    Dissected CLASP2's molecular determinants in mitosis (independent requirements for kinetochore localization, EB binding, and TOG2/TOG3 protofilament recognition), defined treadmilling reconstitution, and uncovered roles in HIV-1 infection.

    Evidence Domain-mutant rescue, biophysics, FRAP; multi-MAP in vitro reconstitution; HIV-1 binding and infection assays

    PMID:31757788 PMID:32376623 PMID:32457163

    Open questions at the time
    • How the three activities are coordinated temporally at kinetochores unclear
    • Functional consequence of C-terminal self-association unknown
  14. 2023 High

    Defined the biophysical mechanism of stabilization: TOG2 forms a load-bearing, nucleotide-state-sensitive bond with terminal non-GTP tubulins at curved protofilaments, and reconstituted actin-MT crosslinking via a minimal TOG2/SR module.

    Evidence DNA origami reconstitution with force measurement, nucleotide exchange, in vitro crosslinking, VSMC depletion

    PMID:36598814 PMID:36598991

    Open questions at the time
    • How load-bearing tip binding is integrated with EB1-mediated tip tracking unresolved
    • In vivo contribution of crosslinking to specific tissues limited
  15. 2025 Medium

    Extended CLASP2 regulation to RNA-level control and disease, showing TNF-α/METTL3 m6A stabilization of CLASP2 mRNA driving CLASP2-IQGAP1-dependent actin remodeling and metastasis.

    Evidence Co-IP, MeRIP, siRNA, xenograft model in bladder cancer cells

    PMID:40118293

    Open questions at the time
    • Direct versus scaffolded CLASP2-IQGAP1 interaction in this context not separated
    • Causal contribution of m6A site to phenotype not isolated

Open questions

Synthesis pass · forward-looking unresolved questions
  • How CLASP2's distinct activities — intrinsic tip stabilization, EB-mediated tracking, actin crosslinking, and cortical capture — are integrated and switched by competing phospho-inputs in a single cell remains unresolved.
  • No unified model coupling kinase inputs to spatial activity states
  • Phosphatases reversing GSK3/Cdk1/Plk1 marks largely unidentified
  • Quantitative hierarchy of cortical partners in different tissues undefined

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0008092 cytoskeletal protein binding 5 GO:0060090 molecular adaptor activity 4
Localization
GO:0005856 cytoskeleton 3 GO:0005886 plasma membrane 3 GO:0005815 microtubule organizing center 2 GO:0005794 Golgi apparatus 1
Pathway
R-HSA-1640170 Cell Cycle 4 R-HSA-162582 Signal Transduction 3 R-HSA-1266738 Developmental Biology 2 R-HSA-9609507 Protein localization 2
Partners
CLIP1DAB1EB1EPB41IQGAP1LL5BMARK2PARD3
Complex memberships
kinetochore

Evidence

Reading pass · 30 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
2005 CLASP1 and CLASP2 bind directly to EB1 via their middle domain, and CLASP2 associates with the cell cortex through its C-terminal domain in an MT-independent manner. Both EB1-binding and cortex-binding domains are required for MT stabilization. CLASPs stabilize MTs by promoting pauses and restricting growth/shortening episodes to the cell periphery. RNA interference in HeLa cells, direct binding assays, live-cell fluorescence imaging, domain deletion analysis The Journal of cell biology High 15631994
2006 CLASP2 is required for formation of a stable, polarized microtubule array at the leading edge of migrating fibroblasts and for persistent directional motility. ACF7 acts upstream of CLASP2 by regulating its cortical localization. CLASP2 is immobilized in a bimodal manner near cell edges to stabilize MTs. Mouse embryonic fibroblast (MEF) wound-healing assay with CLASP2 knockout, GFP-CLASP2 fluorescence imaging (FRAP), RNAi knockdown of ACF7 in HeLa cells Current biology : CB High 17113391
2006 CLASP2 localizes to kinetochores, centrosomes, and the spindle throughout mitosis with fast microtubule-independent turnover. Loss of CLASP2 in primary fibroblasts causes spindle and chromosome segregation defects, slower chromosome movement during anaphase A and B, and severe chromosomal instability, which can be partially rescued by ectopic CLASP1 or CLASP2 expression. Clasp2 knockout mouse fibroblasts, ectopic rescue expression, live-cell imaging, FRAP Molecular biology of the cell High 16914514
2007 CLASP2α co-localizes with stress fibers and co-immunoprecipitates with actin. Both the microtubule-binding domain and the N-terminal TOG domain of CLASP2α possess actin-binding activity. FRET experiments confirm proximity between YFP-CLASP2α and CFP-actin, establishing CLASPs as actin/microtubule crosslinkers. Co-immunoprecipitation, deletion mapping, FRET (YFP/CFP), retrograde flow imaging in Xenopus fibroblasts and neurons Cell motility and the cytoskeleton Medium 17342765
2009 GSK-3β directly phosphorylates CLASP2 at Ser533 and Ser537, causing dissociation of CLASP2 from IQGAP1, EB1, and microtubules. IQGAP1 was identified as a novel CLASP2-binding protein. Expression of active GSK-3β abolishes CLASP2 distribution on microtubules at leading edges, but a nonphosphorylatable CLASP2 mutant resists this effect. In vitro phosphorylation assay, co-immunoprecipitation, site-directed mutagenesis, confocal imaging in migrating fibroblasts Journal of cell science High 19638411
2012 During mitosis, CLASP2 is phosphorylated by Cdk1 at S1234, which primes it for Plk1 association and enhances Plk1 recruitment to kinetochores. Plk1 then phosphorylates CLASP2 C-terminal sites, stabilizing kinetochore-MT attachments required for chromosome alignment and spindle bipolarity, and enabling timely SAC satisfaction. Phospho-site mutagenesis, kinase assays, live-cell imaging, dominant-negative and phosphomimetic constructs The Journal of cell biology High 23045552
2012 Multisite GSK3 phosphorylation of CLASP2 near its two SXIP EB1-binding motifs disrupts arginine-glutamate salt bridge (electrostatic 'molecular Velcro') interactions required for EB1 binding. Priming phosphorylation by CDKs is required before GSK3 can act; this multisite phosphorylation completely abolishes CLASP2 microtubule plus-end tracking in mitosis. In vitro binding assays, molecular dynamics simulations, 31P NMR spectroscopy, phosphomimetic mutagenesis, live-cell tracking The Journal of biological chemistry High 22467876
2012 Agrin activates PI3K and inactivates GSK3β locally, leading to CLASP2-mediated capture of dynamic microtubule plus-ends at acetylcholine receptor (AChR) clusters at the neuromuscular junction. Loss of CLASP2 reduces microtubule plus-end density at the synaptic membrane, AChR density, cluster size, and subsynaptic gene expression programs. RNAi knockdown of CLASP2 in myotubes, pharmacological PI3K/GSK3β manipulation, live and fixed imaging The Journal of cell biology High 22851317
2012 CLASP2 knockdown in primary mouse neurons decreases axon and dendritic length, while overexpression causes multiple axon formation, enhanced dendritic branching, Golgi condensation, and increased excitatory synapse number and synaptic transmission, identifying CLASP2 as a regulator of neuronal polarity and synapse formation. shRNA knockdown and overexpression in primary mouse neurons, confocal imaging, electrophysiology (miniature events), immunostaining The Journal of neuroscience High 23035100
2012 CLASP2 undergoes insulin-stimulated phosphorylation and co-localizes with GLUT4 at the plasma membrane in areas of cortical actin remodeling. CLASP2 siRNA knockdown in L6 myotubes impairs insulin-stimulated GLUT4 localization to the plasma membrane, and CLASP2 knockdown in 3T3-L1 adipocytes inhibits insulin-stimulated glucose transport. Mass spectrometry, phosphoantibody immunoprecipitation, confocal imaging, siRNA knockdown, glucose transport assay The Journal of biological chemistry Medium 22992739
2013 CLASP2 directly interacts with p120-catenin and localizes to adherens junctions in primary basal keratinocytes. Reduction in p120 or CLASP2 levels decreases localization of the other protein to cell-cell contacts, alters junction dynamics/stability, and reduces MT density and dynamics at intercellular junctions. Co-immunoprecipitation (direct interaction), siRNA knockdown, confocal imaging, live-cell MT dynamics analysis The Journal of cell biology Medium 24368809
2013 Protein 4.1R interacts and co-localizes with cortical CLASP2 and is required for correct number and dynamics of CLASP2 cortical platforms. 4.1R controls CLASP2 binding to MTs at the cell edge by locally altering GSK3 activity. Loss of 4.1R causes MT plus-ends to continue growing and bending rather than being tethered to the cortex. Co-immunoprecipitation, siRNA knockdown, confocal live imaging, GSK3 activity assays Journal of cell science Medium 23943871
2014 Abl tyrosine kinase binds to CLASP2 and phosphorylates it (Km ~1.89 µM) in response to serum or PDGF stimulation. Abl-phosphorylated tyrosine residues map within F-actin and MT plus-end interaction domains. Abl phosphorylation of CLASP2 modulates its direct binding to MTs and actin, and alters its localization and F-actin distribution in spinal cord growth cones. In vitro kinase assay with purified proteins, mass spectrometry phosphosite identification, co-immunoprecipitation, pulldown with purified proteins, confocal imaging Cytoskeleton (Hoboken, N.J.) High 24520051
2014 PAR3 directly interacts with CLASP2 and aPKC phosphorylates CLASP2. This phosphorylation inhibits the interaction between CLASP2 and GCC185 (a TGN protein). Loss of PAR3 or aPKC causes aberrant accumulation of CLASP2 at the TGN and disrupts Golgi ribbon organization. A CLASP2 mutant blocking PAR3 interaction disrupts Golgi organization. Co-immunoprecipitation, in vitro phosphorylation, dominant-negative mutants, siRNA knockdown, confocal imaging of Golgi Molecular biology of the cell Medium 25518939
2015 Crystal structures of the two TOG domains of CLASP2 reveal paddle-like tubulin-binding conformations with six HEAT repeats each, but with distinct degrees and directions of curvature. Biochemical and cell biological analyses show each TOG domain associates differently with αβ-tubulin, suggesting they discriminate between different states of MT dynamic instability. X-ray crystallography, biochemical binding assays, molecular modeling, cell biology analysis Journal of molecular biology High 26003921
2015 CLASP2-mediated microtubule capture at NMJ AChR clusters requires the CLASP2-binding partner LL5β. Forced expression of a CLASP2 fragment blocking CLASP2/LL5β interaction inhibits MT capture and impairs focal vesicle delivery to clusters. LL5β knockdown at the NMJ in vivo reduces AChR density and insertion. MT and actin depolymerization also inhibit MT capture and focal vesicle delivery. RNAi knockdown of LL5β, dominant-negative CLASP2 fragment expression, live imaging of vesicle delivery, in vivo NMJ analysis Molecular biology of the cell Medium 25589673
2017 GSK3-mediated global phosphorylation of CLASP2α largely abolishes its microtubule association in metaphase but does not directly control its kinetochore localization. Phosphorylation-site mutants reveal that CLASP2α phosphorylation weakens kinetochore-MT interactions (reduced sister kinetochore tension) and increases chromosome segregation defects. A model is proposed where only kinetochore-bound CLASP2α is locally dephosphorylated to engage microtubule binding. Dominant phosphorylation-site variants (phosphomimetic and phospho-resistant), live-cell imaging, sister kinetochore tension measurements Journal of cell science Medium 28232523
2017 CLASP2 is a cytoskeletal effector in the Reelin signaling pathway. Reelin regulates phosphorylation of GSK3β consensus sites within the CLASP2 serine/arginine-rich region. CLASP2 phosphorylation status regulates its interaction with the Reelin adaptor Dab1, and this association is required for CLASP2 effects on neurite extension and motility during neocortical neuron migration. Co-immunoprecipitation, phosphorylation site mutagenesis, in utero electroporation knockdown, confocal imaging, neuron migration assays Neuron High 28285824
2017 CLASP2 co-immunoprecipitates with SOGA1, MARK2, and G2L1 in 3T3-L1 adipocytes. Reciprocal co-IP confirmed CLASP2-MARK2 and CLASP2-SOGA1 interactions. SOGA1 co-localizes with CLASP2 and tubulin, identifying SOGA1 as a new microtubule-associated protein. Affinity purification-mass spectrometry (AP-MS), reciprocal co-immunoprecipitation, confocal co-localization Molecular & cellular proteomics : MCP Medium 28550165
2018 Purified human CLASP2 suppresses microtubule catastrophe and promotes rescue in vitro without affecting growth or shrinkage rates. Combined with EB1, CLASP2 effects are strongly enhanced in a manner dependent on direct CLASP2-EB1 interaction. EB1 targets CLASP2 to microtubules and increases its dwell time at microtubule tips. In vitro reconstitution with purified proteins, TIRF microscopy, truncated EB1 lacking CLASP2-binding domain as control Molecular biology of the cell High 29540526
2020 Human CLASP2 exists predominantly as a monomer in solution but can self-associate through its C-terminal kinetochore-binding domain. Kinetochore localization is independent of self-association. CLASP2 kinetochore localization, EB-protein interaction (for growing plus-end recognition), and association with curved microtubule protofilaments via TOG2 and TOG3 domains are each independently required for normal kinetochore-MT dynamics, spindle length, SAC satisfaction, and chromosome segregation. In vitro biophysical assays, domain mutant rescue experiments, kinetochore-MT half-life measurements, poleward flux measurements, FRAP The Journal of cell biology High 31757788
2020 CLASP2 is required for HIV-1 to induce microtubule stabilization and promote early infection in human microglia cells. CLASP2 binds to intact HIV-1 cores and in vitro-assembled capsid-nucleocapsid (CA-NC) complexes. The C-terminal domain of CLASP2 (which mediates host effector interactions) is specifically required for MT stabilization and early HIV-1 infection, but not for binding to HIV-1 cores. RNAi knockdown, fixed and live-cell imaging of HIV-1 particle trafficking, in vitro binding to assembled CA-NC complexes, C-terminal domain deletion mutant Journal of virology Medium 32376623
2020 The combination of CLASP2 with EB1, XMAP215, and MCAK reconstitutes robust plus-end-leading microtubule treadmilling in vitro. CLASP2's catastrophe suppression and rescue promotion contribute to the dynamic balance enabling treadmilling. In vitro reconstitution with purified proteins (multi-MAP assay), TIRF microscopy, computational simulations Proceedings of the National Academy of Sciences High 32457163
2021 SOCS3 interacts with CLASP2 and CLIP-170 via its N-terminal domain, forming a complex. This SOCS3-CLIP-170/CLASP2 complex is essential for maximal SOCS3 anti-inflammatory effects in lung endothelial cells. IL-6 and HKSA disrupt SOCS3 interaction with CLASP2/CLIP-170. CLASP2 knockdown impairs SOCS3-JAK2 interaction and abolishes anti-inflammatory effects of SOCS3. Co-immunoprecipitation, RNAi knockdown, MT fractionation, endothelial barrier assays, EC-specific SOCS3 KO mice The Journal of biological chemistry Medium 33372035
2021 LRAP35a promotes CLASP2/EB1 interaction for MT stabilization. Sequential phosphorylation of LRAP35a by PKA then GSK3β initiates LRAP35a-CLASP2 association. Subsequent CK1δ phosphorylation of CLASP2 (on GSK3β sites that block EB1 SxIP binding) is directly countered by LRAP35a interaction competing for CK1δ activity, thus regulating MT dynamics during cell migration. Co-immunoprecipitation, phospho-site mutagenesis, kinase inhibition, live-cell MT dynamics imaging Cell reports Medium 34525355
2023 CLASP2α directly cross-links F-actin to the microtubule lattice in vitro. A minimal construct L-TOG2-S (containing TOG2 domain and serine-arginine-rich region) retains this cross-linking ability. CLASP2α promotes accumulation of multiple actin filaments along a single microtubule, and depletion of CLASPs in vascular smooth muscle cells causes disorganized actin fibers and reduced co-alignment with microtubules. In vitro reconstitution with purified proteins, TIRF microscopy, CLASP2 depletion in VSMCs, confocal imaging Molecular biology of the cell High 36598814
2023 CLASP2 forms a load-bearing bond with terminal non-GTP tubulins at stabilized microtubule tips using its TOG2 domain. TOG2 releases its high-affinity bond upon conversion of non-GTP dimers to polymerization-competent GTP-tubulins. This nucleotide-state-sensitive recognition of curved protofilaments suppresses catastrophe and promotes persistent tubulin assembly at load-bearing (e.g., kinetochore) ends. DNA origami-based reconstruction assays, in vitro biochemical assays, nucleotide exchange experiments, force measurement Science advances High 36598991
2009 FEZ1 and CLASP2 interact through coiled-coil regions in vitro, co-localize with NEK1 in a perinuclear/centrosomal region, and all three interact with endogenous gamma-tubulin. CLASP2 is phosphorylated by and interacts with active PKC isoforms; PMA treatment inhibits FEZ1/CLASP2 co-localization. Co-immunoprecipitation, in vitro coiled-coil interaction assay, immunofluorescence co-localization, PMA treatment Molecular and cellular biochemistry Low 19924516
2014 GSK3β phosphorylation of CLASP2 regulates AChR cluster size at the NMJ: a nonphosphorylatable CLASP2 mutant (9XS/9XA) promotes MT capture and increases AChR cluster size, while a phosphomimetic mutant (8XS/D) reduces MT capture and AChR cluster size despite enrichment at clusters. Expression of phosphomimetic and phospho-resistant CLASP2 mutants in myotubes on agrin patches, live MT imaging, quantitative AChR cluster analysis The Journal of biological chemistry Medium 25231989
2025 CLASP2 directly interacts with IQGAP1 to regulate F-actin cytoskeleton remodeling in bladder cancer cells. TNF-α promotes METTL3-mediated m6A modification of CLASP2 mRNA, enhancing its stability and increasing CLASP2 protein levels, which drives CLASP2-IQGAP1-dependent F-actin reorganization and metastasis. Co-immunoprecipitation (Co-IP), MeRIP for m6A detection, immunofluorescence, siRNA knockdown, xenograft mouse model Biochimica et biophysica acta. Molecular basis of disease Medium 40118293

Source papers

Stage 0 corpus · 42 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2005 CLASP1 and CLASP2 bind to EB1 and regulate microtubule plus-end dynamics at the cell cortex. The Journal of cell biology 336 15631994
2006 Role of CLASP2 in microtubule stabilization and the regulation of persistent motility. Current biology : CB 132 17113391
2009 Phosphorylation of CLASP2 by GSK-3beta regulates its interaction with IQGAP1, EB1 and microtubules. Journal of cell science 110 19638411
2006 Mammalian CLASP1 and CLASP2 cooperate to ensure mitotic fidelity by regulating spindle and kinetochore function. Molecular biology of the cell 101 16914514
2012 Cdk1 and Plk1 mediate a CLASP2 phospho-switch that stabilizes kinetochore-microtubule attachments. The Journal of cell biology 79 23045552
2007 Microtubule-binding proteins CLASP1 and CLASP2 interact with actin filaments. Cell motility and the cytoskeleton 76 17342765
2014 Neuronal deletion of GSK3β increases microtubule speed in the growth cone and enhances axon regeneration via CRMP-2 and independently of MAP1B and CLASP2. BMC biology 73 24923837
2012 Multisite phosphorylation disrupts arginine-glutamate salt bridge networks required for binding of cytoplasmic linker-associated protein 2 (CLASP2) to end-binding protein 1 (EB1). The Journal of biological chemistry 67 22467876
2018 Human CLASP2 specifically regulates microtubule catastrophe and rescue. Molecular biology of the cell 60 29540526
2017 Characterization of the CLASP2 Protein Interaction Network Identifies SOGA1 as a Microtubule-Associated Protein. Molecular & cellular proteomics : MCP 50 28550165
2012 Agrin regulates CLASP2-mediated capture of microtubules at the neuromuscular junction synaptic membrane. The Journal of cell biology 50 22851317
2012 Microtubule plus-end tracking protein CLASP2 regulates neuronal polarity and synaptic function. The Journal of neuroscience : the official journal of the Society for Neuroscience 42 23035100
2017 CLASP2 Links Reelin to the Cytoskeleton during Neocortical Development. Neuron 34 28285824
2017 GSK3-mediated CLASP2 phosphorylation modulates kinetochore dynamics. Journal of cell science 30 28232523
2015 CLASP2-dependent microtubule capture at the neuromuscular junction membrane requires LL5β and actin for focal delivery of acetylcholine receptor vesicles. Molecular biology of the cell 30 25589673
2015 CLASP2 Has Two Distinct TOG Domains That Contribute Differently to Microtubule Dynamics. Journal of molecular biology 29 26003921
2013 CLASP2 interacts with p120-catenin and governs microtubule dynamics at adherens junctions. The Journal of cell biology 27 24368809
2020 CLASP2 binding to curved microtubule tips promotes flux and stabilizes kinetochore attachments. The Journal of cell biology 25 31757788
2014 Abelson phosphorylation of CLASP2 modulates its association with microtubules and actin. Cytoskeleton (Hoboken, N.J.) 25 24520051
2020 HIV-1 Exploits CLASP2 To Induce Microtubule Stabilization and Facilitate Virus Trafficking to the Nucleus. Journal of virology 21 32376623
2017 CLASP2 is involved in the EMT and early progression after transurethral resection of the bladder tumor. BMC cancer 18 28166762
2012 Identification of a role for CLASP2 in insulin action. The Journal of biological chemistry 18 22992739
2014 Acetylcholine receptor (AChR) clustering is regulated both by glycogen synthase kinase 3β (GSK3β)-dependent phosphorylation and the level of CLIP-associated protein 2 (CLASP2) mediating the capture of microtubule plus-ends. The Journal of biological chemistry 17 25231989
2014 PAR3 and aPKC regulate Golgi organization through CLASP2 phosphorylation to generate cell polarity. Molecular biology of the cell 17 25518939
2021 SOCS3-microtubule interaction via CLIP-170 and CLASP2 is critical for modulation of endothelial inflammation and lung injury. The Journal of biological chemistry 16 33372035
2013 Protein 4.1R binds to CLASP2 and regulates dynamics, organization and attachment of microtubules to the cell cortex. Journal of cell science 16 23943871
2012 The microtubule plus-end tracking protein CLASP2 is required for hematopoiesis and hematopoietic stem cell maintenance. Cell reports 16 23084744
2009 FEZ1 interacts with CLASP2 and NEK1 through coiled-coil regions and their cellular colocalization suggests centrosomal functions and regulation by PKC. Molecular and cellular biochemistry 15 19924516
2023 CLASP2 facilitates dynamic actin filament organization along the microtubule lattice. Molecular biology of the cell 13 36598814
2023 CLASP2 recognizes tubulins exposed at the microtubule plus-end in a nucleotide state-sensitive manner. Science advances 13 36598991
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
2021 Circ_CLASP2 Regulates High Glucose-Induced Dysfunction of Human Endothelial Cells Through Targeting miR-140-5p/FBXW7 Axis. Frontiers in pharmacology 11 33776760
2013 Interstitial deletion of 3p22.3p22.2 encompassing ARPP21 and CLASP2 is a potential pathogenic factor for a syndromic form of intellectual disability: a co-morbidity model with additional copy number variations in a large family. American journal of medical genetics. Part A 11 24127197
2005 PAR-1 and the microtubule-associated proteins CLASP2 and dynactin-p50 have specific localisation on mouse meiotic and first mitotic spindles. Reproduction (Cambridge, England) 9 16123238
2022 CLASP2 safeguards hematopoietic stem cell properties during mouse and fish development. Cell reports 8 35705037
2014 A lack of association between polymorphisms of three positional candidate genes (CLASP2 , UBP1, and FBXL2) and canine disorder of sexual development (78,XX; SRY -negative). Sexual development : genetics, molecular biology, evolution, endocrinology, embryology, and pathology of sex determination and differentiation 7 24994500
2025 TNF-α drives bladder cancer metastasis via METTL3-mediated m6A modification to promote CLASP2/IQGAP1-dependent cytoskeleton remodeling. Biochimica et biophysica acta. Molecular basis of disease 6 40118293
2019 Exogenous CLASP2 protein treatment enhances wound healing in vitro and in vivo. Wound repair and regeneration : official publication of the Wound Healing Society [and] the European Tissue Repair Society 5 30835922
2021 Cyclical phosphorylation of LRAP35a and CLASP2 by GSK3β and CK1δ regulates EB1-dependent MT dynamics in cell migration. Cell reports 2 34525355
2017 Clasp2 ensures mitotic fidelity and prevents differentiation of epidermal keratinocytes. Journal of cell science 2 28069833
2025 KHSRP promotes the malignant behavior and cisplatin resistance of bladder cancer cells through the CLASP2/MAPRE1 axis. The pharmacogenomics journal 1 40382315
2023 Analysis of clasp2 Transcription Pattern in Male Germ Cells during Spermatogenesis: A Comparative Study in Zebrafish (Danio rerio) and Guppy (Poecilia reticulata). Animals : an open access journal from MDPI 0 38066968

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