Affinage

CLASP2

CLIP-associating protein 2 · UniProt O75122

Length
1294 aa
Mass
141.1 kDa
Annotated
2026-04-28
42 papers in source corpus 30 papers cited in narrative 30 extracted findings

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, while also physically cross-linking microtubules to F-actin, thereby coordinating cytoskeletal organization during cell migration, mitosis, neuronal development, and membrane trafficking. Its TOG2 and TOG3 domains bind curved protofilaments and recognize non-GTP terminal tubulins through a nucleotide-state-sensitive mechanism to form load-bearing attachments that resist depolymerization, while SXIP motifs in its central disordered region mediate EB1 interaction for plus-end targeting (PMID:36598991, PMID:29540526, PMID:26003921). Multiple kinases—GSK3β, Cdk1/Plk1, aPKC, Abl, and CK1δ—phosphorylate distinct CLASP2 regions to regulate its association with EB1, microtubules, and cortical/organelle adaptors including IQGAP1, LL5β, p120-catenin, GCC185, and Dab1, thereby controlling MT stabilization at the cell cortex, kinetochore-MT attachment fidelity during mitosis, Golgi organization, and directed vesicle delivery of cargoes such as GLUT4 and AChRs (PMID:19638411, PMID:23045552, PMID:25518939, PMID:22992739, PMID:25589673). CLASP2 is also required for hematopoietic stem cell maintenance through Golgi-dependent c-Kit surface trafficking and for cortical neuron migration downstream of Reelin-Dab1 signaling (PMID:35705037, PMID:28285824).

Mechanistic history

Synthesis pass · year-by-year structured walk · 12 steps
  1. 2005 High

    Establishing that CLASP2 is an EB1-dependent MT plus-end tracker that stabilizes MTs at the cell cortex resolved how peripheral MT dynamics are spatially regulated, revealing that EB1 binding and a separate cortex-targeting domain are both required.

    Evidence Domain deletion analysis, direct binding assays, RNAi, and live-cell imaging in HeLa cells

    PMID:15631994

    Open questions at the time
    • Identity of the cortical receptor for the C-terminal domain was unknown
    • Upstream signals controlling cortical recruitment not yet defined
  2. 2006 High

    Demonstrating that CLASP2-null fibroblasts lose polarized MT arrays and persistent migration, and exhibit mitotic spindle/chromosome segregation defects, established CLASP2 as essential for both interphase MT polarity and faithful chromosome segregation.

    Evidence Clasp2 knockout mouse fibroblasts, wound-healing assays, live-cell imaging, FRAP, rescue experiments

    PMID:16914514 PMID:17113391

    Open questions at the time
    • How CLASP2 is recruited to kinetochores was unknown
    • Relative contributions of CLASP1 versus CLASP2 to mitotic fidelity not fully separated
  3. 2007 High

    Discovery that CLASP2α directly binds F-actin through its TOG and MT-binding domains established CLASPs as actin-MT crosslinkers, expanding their role beyond pure plus-end tracking.

    Evidence Co-immunoprecipitation, FRET, domain deletion mapping in Xenopus fibroblasts and neurons

    PMID:17342765

    Open questions at the time
    • Whether actin binding and MT binding are simultaneous or mutually exclusive was unclear
    • Structural basis for actin interaction unknown
  4. 2009 High

    Identifying GSK3β as a direct kinase for CLASP2 Ser533/Ser537 that dissociates it from EB1, IQGAP1, and MTs provided the first signal-dependent switch controlling CLASP2 cortical MT stabilization during cell migration.

    Evidence In vitro kinase assay, phosphomutant expression, Co-IP in migrating fibroblasts

    PMID:19638411

    Open questions at the time
    • How GSK3β activity is spatially restricted at the leading edge was not resolved
    • Phosphatases counteracting GSK3β at the cortex unidentified
  5. 2012 High

    A convergence of studies in 2012 resolved: (1) how Cdk1/Plk1 sequential phosphorylation stabilizes kinetochore-MT attachments, (2) how GSK3β phosphorylation near SXIP motifs causes intramolecular sequestration that abolishes EB1 binding, and (3) how agrin/PI3K/GSK3β signaling through CLASP2 captures MTs at NMJ AChR clusters—collectively establishing phosphorylation as a multisite, context-dependent regulatory code for CLASP2 function.

    Evidence In vitro reconstitution, NMR, kinase assays, phosphomutant TIRF microscopy, in vivo NMJ analysis, kinetochore tension measurements

    PMID:22467876 PMID:22851317 PMID:23045552

    Open questions at the time
    • Identity of phosphatases reversing mitotic phosphorylation at kinetochores unknown
    • Whether different CLASP2 splice variants are differentially phosphorylated in vivo not tested
  6. 2012 High

    Demonstrating that CLASP2 regulates neuronal polarity, dendritic branching, synapse number, and postsynaptic receptor expression, and separately that CLASP2 is required for insulin-stimulated GLUT4 delivery, broadened CLASP2 function to include directed membrane trafficking of specific cargoes.

    Evidence shRNA/overexpression in primary neurons with electrophysiology; siRNA in adipocytes with GLUT4 trafficking and glucose transport assays

    PMID:22992739 PMID:23035100

    Open questions at the time
    • Whether CLASP2 directly engages GLUT4-containing vesicles or acts via MT track stabilization was unresolved
    • Which CLASP2 domains are required for neuronal cargo delivery not mapped
  7. 2014 High

    Abl tyrosine kinase phosphorylation of CLASP2 within its actin- and MT-binding domains modulates cytoskeletal binding in vitro and growth cone organization, adding a tyrosine kinase layer to the previously known serine/threonine kinase regulation; simultaneously, aPKC phosphorylation of CLASP2 was shown to dissociate it from the TGN adaptor GCC185, establishing how CLASP2 organizes Golgi ribbon structure.

    Evidence In vitro kinase assays with purified proteins, mass spectrometry phosphosite mapping, Co-IP, Golgi morphology analysis in epithelial cells

    PMID:24520051 PMID:25518939

    Open questions at the time
    • How Abl and GSK3β phosphorylation events are coordinated on the same CLASP2 molecule was not addressed
    • Direct structural basis for CLASP2-GCC185 interaction unknown
  8. 2015 High

    Showing that LL5β is the essential cortical anchor for CLASP2-mediated MT capture and focal vesicle delivery at NMJ AChR clusters completed the agrin→PI3K→GSK3β→CLASP2→LL5β→MT capture→AChR delivery pathway.

    Evidence RNAi, dominant-negative fragments, in vivo NMJ analysis, live-cell vesicle imaging

    PMID:25589673

    Open questions at the time
    • Whether LL5β-CLASP2 interaction is direct or mediated by additional adaptors not fully resolved
    • Stoichiometry of the cortical platform complex unknown
  9. 2015 High

    Crystal structures of CLASP2 TOG domains revealed curved HEAT-repeat paddle architectures that discriminate between tubulin conformational states, providing the first structural framework for how CLASPs recognize dynamic MT ends.

    Evidence X-ray crystallography, biochemical tubulin-binding assays, molecular modeling

    PMID:26003921

    Open questions at the time
    • No co-crystal with tubulin to confirm binding mode
    • Whether TOG2 and TOG3 bind simultaneously to adjacent protofilaments was not resolved
  10. 2018 High

    In vitro reconstitution with purified CLASP2 and EB1 demonstrated that CLASP2 intrinsically suppresses catastrophe and promotes rescue, and that EB1 synergistically enhances these activities by increasing CLASP2 dwell time at MT tips, resolving the minimal biochemical mechanism.

    Evidence TIRF microscopy reconstitution with purified human proteins

    PMID:29540526

    Open questions at the time
    • How CLASP2 senses catastrophe-prone versus growing MT tips mechanistically not resolved at single-molecule level
  11. 2020 High

    Demonstrating that CLASP2 TOG2 and TOG3 domains bind curved protofilaments at kinetochore-MT interfaces, combined with evidence that CLASP2 operates as a monomer whose EB interaction and protofilament binding are functionally separable, established a multi-input model for kinetochore-MT stabilization; separately, CLASP2/EB1/XMAP215/MCAK were shown to reconstitute MT treadmilling.

    Evidence Domain-specific mutants with kinetochore-MT half-life and poleward flux measurements; multi-MAP TIRF reconstitution with computational simulations

    PMID:31757788 PMID:32457163

    Open questions at the time
    • How CLASP2 is targeted to outer kinetochore components (e.g., through what receptor) is incompletely defined
    • Force-dependent behavior at kinetochores not measured
  12. 2023 High

    Single-molecule force measurements revealed that CLASP2-TOG2 forms a load-bearing bond with non-GTP terminal tubulins that releases upon GTP-tubulin conversion, providing the nucleotide-state-sensitive mechanism for catastrophe suppression; separately, reconstitution showed CLASP2α directly cross-links multiple F-actin filaments to the MT lattice through its TOG2-S region, definitively confirming the actin-MT crosslinker function.

    Evidence DNA origami-based optical trap reconstitution with domain mutants; TIRF reconstitution with purified CLASP2α and domain truncations, validated in vascular smooth muscle cells

    PMID:36598814 PMID:36598991

    Open questions at the time
    • Whether TOG3 also forms force-sensitive bonds with non-GTP tubulins is untested
    • How actin crosslinking and MT plus-end tracking are spatiotemporally coordinated in cells is unresolved

Open questions

Synthesis pass · forward-looking unresolved questions
  • Key unresolved questions include: the structural basis for CLASP2's simultaneous engagement of actin and tubulin, how multiple kinase inputs are integrated on individual CLASP2 molecules in space and time, which phosphatases oppose GSK3β/Cdk1/aPKC to reactivate CLASP2, and whether CLASP2 splice variants serve distinct tissue-specific functions.
  • No co-structure of CLASP2 bound simultaneously to tubulin and actin
  • Phosphatase identity for CLASP2 dephosphorylation unknown
  • Functional specialization of CLASP2 splice variants not systematically tested

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0008092 cytoskeletal protein binding 8 GO:0060090 molecular adaptor activity 3
Localization
GO:0005856 cytoskeleton 7 GO:0005886 plasma membrane 5 GO:0005694 chromosome 4 GO:0005794 Golgi apparatus 2 GO:0005829 cytosol 2
Pathway
R-HSA-162582 Signal Transduction 5 R-HSA-1640170 Cell Cycle 4 R-HSA-5653656 Vesicle-mediated transport 3 R-HSA-112316 Neuronal System 2 R-HSA-1266738 Developmental Biology 2 R-HSA-1852241 Organelle biogenesis and maintenance 2
Partners
DAB1EB1GCC185IQGAP1LL5BMARK2P120-CATENINSOGA1

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 through their middle domain and to MTs, and the association of CLASP2 with the cell cortex is MT-independent and relies on its C-terminal domain; both EB1- and cortex-binding domains are required to promote MT stability by promoting pauses and restricting MT growth/shortening to the cell periphery. RNA interference in HeLa cells, direct binding assays, domain deletion analysis, live-cell imaging The Journal of cell biology High 15631994
2006 CLASP2 is required for formation of a stable, polarized MT array at the leading edge of migrating fibroblasts and for persistent directional motility; ACF7 acts upstream of CLASP2 to regulate its cortical localization; GFP-CLASP2 is immobilized in a bimodal manner near cell edges. CLASP2 knockout mouse embryonic fibroblasts, wound-healing assay, fluorescence microscopy (FRAP), RNAi in HeLa cells Current biology : CB High 17113391
2006 CLASP2 localizes to kinetochores, centrosomes, and spindle during mitosis with fast MT-independent turnover; CLASP2-deficient primary fibroblasts exhibit spindle and chromosome segregation defects, slower chromosome movement during anaphase A and B, and chromosomal instability, demonstrating a role in regulating kinetochore and spindle MT dynamics. Clasp2 knockout mouse fibroblasts, live-cell imaging, FRAP, rescue by ectopic CLASP1/CLASP2 expression Molecular biology of the cell High 16914514
2007 CLASP2α co-localizes with stress fibers and co-immunoprecipitates with actin; both the MT-binding domain and the N-terminal TOG domain of CLASP2α possess actin-binding activity; FRET experiments confirm close proximity of YFP-CLASP2α and CFP-actin, indicating CLASPs function as actin/MT crosslinkers. Co-immunoprecipitation, deletion mapping, FRET, live-cell imaging in Xenopus fibroblasts and neurons Cell motility and the cytoskeleton High 17342765
2009 GSK3β directly phosphorylates CLASP2 at Ser533 and Ser537, causing dissociation of CLASP2 from IQGAP1, EB1, and microtubules; IQGAP1 (an actin-binding protein) was identified as a novel CLASP2-binding partner; active GSK3β abolishes MT-end distribution of CLASP2 but not of a nonphosphorylatable CLASP2 mutant. In vitro kinase assay, Co-IP, phosphomutant expression, immunofluorescence in migrating fibroblasts Journal of cell science High 19638411
2012 During mitosis, Cdk1 phosphorylates CLASP2 at S1234, priming it for Plk1 association; Plk1 is recruited to kinetochores enhanced by this phosphorylation; Plk1-dependent C-terminal phosphorylation of CLASP2 stabilizes KT-MT attachments required for chromosome alignment and timely spindle-assembly checkpoint satisfaction. Phosphosite mutagenesis, kinase assays, live-cell imaging, kinetochore tension measurements The Journal of cell biology High 23045552
2012 The central intrinsically disordered region of CLASP2 contains two SXIP EB1-binding motifs required for plus-end tracking in vitro; conserved arginine residues in CLASP2 form electrostatic hydrogen-bond networks with the acidic C-terminal tail of EB1; multisite GSK3 phosphorylation of serines near SXIP motifs causes intramolecular sequestration of these arginines, disrupting EB1 binding and abolishing MT plus-end tracking during mitosis. In vitro reconstitution, molecular dynamics simulation, 31P NMR spectroscopy, phosphomutant TIRF microscopy The Journal of biological chemistry High 22467876
2012 CLASP2 knockdown in primary mouse neurons decreased axon and dendritic length; overexpression caused multiple axon formation, enhanced dendritic branching, Golgi condensation, increased excitatory miniature event frequency, increased presynaptic terminal size and synapse number, and increased GluA1 postsynaptic surface expression, establishing CLASP2 as a regulator of neuronal polarity and synaptic function. shRNA knockdown, overexpression, live-cell imaging, electrophysiology in primary mouse neurons The Journal of neuroscience High 23035100
2012 Agrin locally activates PI3K and inactivates GSK3β to enable CLASP2-mediated capture of MT plus ends at AChR clusters; in the absence of CLASP2, MT plus-end density at the subsynaptic membrane, AChR density, AChR cluster size, and subsynaptic nuclei number are reduced. RNAi knockdown in myotubes and in vivo NMJ, pharmacological inhibition of PI3K/GSK3β, live-cell imaging The Journal of cell biology High 22851317
2012 CLASP2 undergoes insulin-stimulated phosphorylation in L6 myotubes; CLASP2 co-localizes with GLUT4 at the plasma membrane in areas of cortical actin remodeling; siRNA knockdown of CLASP2 impairs insulin-stimulated GLUT4 plasma membrane localization and glucose transport in adipocytes. Mass spectrometry phosphoproteomics, phosphoantibody Co-IP, confocal imaging, siRNA knockdown, glucose transport assay The Journal of biological chemistry High 22992739
2013 CLASP2 directly interacts with p120-catenin and localizes to adherens junctions in primary keratinocytes; reductions in p120 or CLASP2 decrease localization of the other protein to cell-cell contacts and alter MT density and dynamics at junctions. Co-IP, immunofluorescence, RNAi knockdown in primary keratinocytes The Journal of cell biology Medium 24368809
2013 Protein 4.1R interacts and co-localizes with cortical CLASP2, is required for correct number and dynamics of CLASP2 cortical platforms, and locally controls GSK3 activity to regulate CLASP2-MT binding at the cell edge; 4.1R knockdown causes MT plus ends to grow past cell edges rather than being tethered to the cortex. Co-IP, RNAi knockdown, immunofluorescence, live-cell MT dynamics imaging Journal of cell science Medium 23943871
2014 Abl tyrosine kinase binds to CLASP2 and phosphorylates it in response to serum or PDGF stimulation (Km ~1.89 µM); Abl-phosphorylated tyrosines lie within F-actin and MT plus-end interaction domains; Abl phosphorylation of CLASP2 modulates its direct binding to MTs and actin in vitro, and alters its localization and F-actin distribution in spinal cord growth cones. In vitro kinase assay, purified protein binding assay, mass spectrometry, immunofluorescence in vertebrate cells Cytoskeleton (Hoboken, N.J.) High 24520051
2014 GSK3β phosphorylation of CLASP2 regulates AChR cluster size at the NMJ; a phosphorylation-resistant CLASP2 (9XS/9XA) promotes MT capture and increases AChR cluster size, while phosphomimetic CLASP2 (8XS/D) reduces MT capture and cluster size despite being enriched at clusters. Phosphomutant expression in myotubes cultured on agrin patches, live-cell MT imaging, AChR cluster size measurement The Journal of biological chemistry High 25231989
2014 PAR3 directly interacts with CLASP2 and aPKC phosphorylates CLASP2, inhibiting CLASP2 interaction with the TGN protein GCC185; knockdown of PAR3 or aPKC causes aberrant CLASP2 accumulation at the TGN and disruption of Golgi ribbon organization; non-phosphorylatable CLASP2 enhances colocalization with GCC185 and perturbs Golgi organization. Co-IP, in vitro phosphorylation assay, RNAi knockdown, immunofluorescence in epithelial cells Molecular biology of the cell High 25518939
2015 CLASP2-mediated MT capture at NMJ AChR clusters requires the CLASP2-interaction partner LL5β; forced expression of a CLASP2 fragment blocking CLASP2/LL5β interaction inhibits MT capture and focal vesicle delivery to clusters; LL5β knockdown at the NMJ in vivo reduces AChR density and insertion into the postsynaptic membrane. RNAi knockdown, dominant-negative fragment expression, in vivo NMJ analysis, live-cell vesicle imaging Molecular biology of the cell High 25589673
2015 Crystal structures of the two TOG domains of CLASP2 reveal six-HEAT-repeat paddle-like structures with distinct arched conformations and different degrees of curvature; biochemical and molecular modeling show each TOG domain associates differently with αβ-tubulin, suggesting they discriminate between different states of MT dynamic instability. X-ray crystallography, biochemical tubulin-binding assays, molecular modeling, cell biology Journal of molecular biology High 26003921
2017 GSK3-mediated phosphorylation of CLASP2α largely abolishes its MT association in metaphase but does not directly control its kinetochore localization; phosphorylation-site mutants alter kinetochore-MT tension and increase chromosome segregation defects; only kinetochore-bound CLASP2α is proposed to be locally dephosphorylated to engage MT-binding activity. Phosphomutant expression, sister kinetochore tension measurements, chromosome segregation analysis in mammalian cells Journal of cell science High 28232523
2017 Reelin signaling regulates phosphorylation of GSK3β consensus sites within the serine/arginine-rich region of CLASP2; CLASP2 phosphorylation regulates its interaction with the Reelin adaptor Dab1; CLASP2-Dab1 association is required for CLASP2 effects on neurite extension and motility during neocortical development. Co-IP, phosphomutant analysis, in utero electroporation knockdown, cortical neuron migration assays Neuron High 28285824
2017 AP-MS interactome of CLASP2 in 3T3-L1 adipocytes identifies SOGA1, MARK2, G2L1, AGAP1, and AGAP3 as interacting proteins; reciprocal Co-IP confirms CLASP2-MARK2 and CLASP2-SOGA1 interactions; SOGA1 co-localizes with CLASP2 and tubulin, establishing SOGA1 as a microtubule-associated protein. Affinity purification-mass spectrometry (AP-MS), SAINT analysis, reciprocal Co-IP, immunofluorescence co-localization Molecular & cellular proteomics : MCP Medium 28550165
2018 Purified human CLASP2 suppresses MT catastrophe and promotes MT rescue without affecting growth or shrinkage rates; when combined with EB1, these effects are strongly enhanced in a direct-interaction-dependent manner; EB1 increases CLASP2 dwell time at MT tips and targets it to microtubules. TIRF microscopy in vitro reconstitution with purified proteins, truncated EB1 controls Molecular biology of the cell High 29540526
2020 Human CLASP2 exists predominantly as a monomer but can self-associate through its C-terminal kinetochore-binding domain; kinetochore localization is independent of self-association; CLASP2 regulates kinetochore-MT dynamics by (1) EB-protein interaction recognizing growing MT plus ends, (2) TOG2 and TOG3 domain association with curved MT protofilaments, and (3) binding curved protofilaments at MT plus ends to suppress depolymerization and detachment. Size exclusion chromatography, monomeric CLASP2 targeting constructs, kinetochore-MT half-life measurements, poleward flux assays, domain-specific mutants The Journal of cell biology High 31757788
2020 CLASP2 is required for HIV-1-induced MT stabilization and early infection; CLASP2 binds to intact HIV-1 cores and in vitro-assembled CA-NC complexes; the C-terminal domain of CLASP2 is required for MT stabilization and promotion of early HIV-1 infection but not for binding to viral cores. Fixed- and live-cell imaging, CLASP2 knockdown, C-terminal deletion mutant, in vitro CA-NC binding assay Journal of virology Medium 32376623
2020 CLASP2 combined with EB1, XMAP215, and MCAK reconstitutes robust plus-end-leading microtubule treadmilling in vitro, demonstrating that CLASP2 is one of the collective contributors to MT treadmilling. In vitro reconstitution with purified proteins, TIRF microscopy, computational simulations Proceedings of the National Academy of Sciences of the United States of America High 32457163
2021 SOCS3 interacts with MT plus-end binding proteins CLIP-170 and CLASP2 via its N-terminal domain; the SOCS3-CLIP-170/CLASP2 complex is required for maximal SOCS3 anti-inflammatory effects; knockdown of CLASP2 impairs SOCS3-JAK2 interaction and abolishes protective SOCS3 effects in lung endothelium. Co-IP, MT fractionation, RNAi knockdown in human lung ECs and EC-specific KO mice, lung injury model The Journal of biological chemistry Medium 33372035
2021 LRAP35a promotes CLASP2/EB1 interaction to potentiate MT stabilization; sequential phosphorylation of LRAP35a by PKA then GSK3β initiates LRAP35a-CLASP2 association, while subsequent CK1δ phosphorylation induces their dissociation; CK1δ directly phosphorylates CLASP2 to regulate GSK3β phosphorylation of SxIP motifs that block EB1 binding, countered by LRAP35a binding. Co-IP, phosphomutant analysis, kinase assays, MT dynamics imaging in migrating cells Cell reports Medium 34525355
2022 In CLASP2-deficient hematopoietic stem cells, c-Kit cell surface expression is reduced due to increased lysosomal degradation and reduced trafficking to the plasma membrane, attributed to a dysfunctional Golgi apparatus; this leads to impaired c-Kit signaling and failure to maintain HSC stemness. Clasp2 KO mouse and zebrafish models, flow cytometry, lysosomal degradation assays, trafficking assays Cell reports Medium 35705037
2023 CLASP2α directly cross-links F-actin to the microtubule lattice in vitro; a minimal construct containing the TOG2 domain and serine-arginine-rich region (L-TOG2-S) retains cross-linking ability; CLASP2α promotes accumulation of multiple actin filaments along a single MT region; CLASP depletion in vascular smooth muscle cells disorganizes actin fibers and reduces their co-alignment with MTs. In vitro TIRF reconstitution with purified proteins, domain truncation constructs, RNAi knockdown with immunofluorescence Molecular biology of the cell High 36598814
2023 Clusters of human CLASP2 form a load-bearing bond with terminal non-GTP tubulins at the stabilized MT tip via the unconventional TOG2 domain; CLASP2-TOG2 releases its high-affinity bond upon conversion of non-GTP dimers to GTP-tubulins; this nucleotide-state-sensitive recognition stabilizes the catastrophe-promoting non-GTP tubulins to suppress catastrophe and promote persistent assembly at load-bearing ends. DNA origami-based single-molecule reconstitution, optical trap force measurements, domain mutants Science advances High 36598991
2009 FEZ1 and CLASP2 interact through coiled-coil regions in vitro and colocalize with NEK1 and γ-tubulin in a perinuclear centrosomal region; CLASP2 is phosphorylated by and interacts with active PKC isoforms; FEZ1/CLASP2 colocalization is inhibited by PMA treatment (PKC activation). In vitro coiled-coil interaction assay, co-immunoprecipitation, co-localization by immunofluorescence, pharmacological PKC activation Molecular and cellular biochemistry Low 19924516

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 78 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
2012 Agrin regulates CLASP2-mediated capture of microtubules at the neuromuscular junction synaptic membrane. The Journal of cell biology 50 22851317
2017 Characterization of the CLASP2 Protein Interaction Network Identifies SOGA1 as a Microtubule-Associated Protein. Molecular & cellular proteomics : MCP 49 28550165
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
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
2012 Identification of a role for CLASP2 in insulin action. The Journal of biological chemistry 17 22992739
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
2014 PAR3 and aPKC regulate Golgi organization through CLASP2 phosphorylation to generate cell polarity. Molecular biology of the cell 16 25518939
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
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
2023 CLASP2 recognizes tubulins exposed at the microtubule plus-end in a nucleotide state-sensitive manner. Science advances 12 36598991
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
2021 Circ_CLASP2 Regulates High Glucose-Induced Dysfunction of Human Endothelial Cells Through Targeting miR-140-5p/FBXW7 Axis. Frontiers in pharmacology 10 33776760
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
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
2022 CLASP2 safeguards hematopoietic stem cell properties during mouse and fish development. Cell reports 6 35705037
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 5 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 0 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