Affinage

KNSTRN

Small kinetochore-associated protein · UniProt Q9Y448

Length
316 aa
Mass
35.4 kDa
Annotated
2026-06-10
39 papers in source corpus 21 papers cited in narrative 21 extracted findings
Cross-family judge vs UniProt: Affinage preferred faithfulness: 7/7 claims corpus-supported (100%)

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

KNSTRN (SKAP/kinastrin) is a microtubule plus-end tracking protein and kinetochore component that, as the major astrin partner, governs the stability and force-responsiveness of kinetochore-microtubule attachments during mitosis (PMID:21402792, PMID:20937697). It assembles into a reconstituted four-subunit Astrin-SKAP complex containing DYNLL1/LC8 and MYCBP, and this complex binds microtubules synergistically with the Ndc80 complex through a microtubule-binding domain that is distinct and separable from its EB1-dependent SXIP plus-tip-tracking module (PMID:28841134, PMID:27095104, PMID:20937697). The complex localizes preferentially to bioriented, tension-bearing kinetochores, a restriction imposed by Aurora B, and is recruited there through interaction with MIS13 of the KMN network and cooperation with CENP-E (PMID:20937697, PMID:23035123, PMID:22110139). Rather than acting as a static clamp, Astrin-SKAP reduces friction at the kinetochore-microtubule interface, acting as a lubricant that coordinates sister-kinetochore movement, dissipates force, and prevents detachment under load; this depends directly on SKAP's microtubule binding (PMID:35580605, PMID:40154475). KNSTRN function is tuned by post-translational modification: GSK3β phosphorylation directs SKAP binding to the Kif2b depolymerase, while Src-family phosphorylation of Tyr-87 impairs microtubule binding (PMID:27982129, PMID:33510346). Beyond mitosis, KNSTRN supports EGF-directed and T-cell migration via IQGAP1 and MAP4, modulates UV-induced apoptosis through Prp19, and in cancer activates AKT signaling by competing with PTEN at the plasma membrane (PMID:26242911, PMID:29180244, PMID:24718257, PMID:33452459). Cancer-associated mutation (p.Ser24Phe) disrupts sister chromatid cohesion and promotes aneuploidy, and loss-of-expression underlies the cellular defects of Roifman-Chitayat syndrome (PMID:25194279, PMID:29180244).

Mechanistic history

Synthesis pass · year-by-year structured walk · 13 steps
  1. 2009 Medium

    Established that KNSTRN is a mitotic spindle and kinetochore protein whose loss compromises segregation fidelity without triggering the spindle assembly checkpoint, distinguishing it from core checkpoint machinery.

    Evidence RNAi depletion with live imaging and separase activity assays

    PMID:19667759

    Open questions at the time
    • Molecular partners at the kinetochore not yet defined
    • Mechanism of segregation delay unresolved
  2. 2010 High

    Defined KNSTRN as part of an Astrin-SKAP-LC8 complex restricted to bioriented kinetochores by Aurora B, linking it to tension-sensing and CLASP recruitment.

    Evidence Co-IP, RNAi, live imaging, in vitro microtubule binding

    PMID:20937697

    Open questions at the time
    • Full subunit composition incomplete (MYCBP not yet identified)
    • Direct vs indirect microtubule contacts unresolved
  3. 2011 High

    Showed KNSTRN/kinastrin is the principal astrin-targeting factor and a CENP-E-cooperating microtubule binder, establishing both its complex hierarchy and contribution to inter-kinetochore tension.

    Evidence Reciprocal Co-IP, in vitro binding, immunoelectron microscopy, RNAi

    PMID:21402792 PMID:22110139

    Open questions at the time
    • Kinetochore receptor for SKAP not identified
    • Quantitative contribution to attachment strength unmeasured
  4. 2012 High

    Identified MIS13/KMN as the kinetochore receptor specifying SKAP localization and demonstrated EB1-dependent plus-end tracking in vitro, connecting recruitment to plus-end dynamics.

    Evidence Co-IP, siRNA, in vitro TIRF reconstitution, live imaging

    PMID:23035123

    Open questions at the time
    • Separation of kinetochore vs plus-tip functions not yet achieved
    • Mechanism of dynamics regulation unclear
  5. 2014 Medium

    Linked KNSTRN to chromatid cohesion and tumorigenesis, showing the recurrent p.Ser24Phe mutation disrupts cohesion and drives aneuploidy, and tied SKAP to UV-induced apoptosis via Prp19.

    Evidence Cancer mutant expression with cohesion assay, tumorigenesis model, tumor sequencing; Co-IP and rescue for Prp19

    PMID:24718257 PMID:25194279

    Open questions at the time
    • Molecular basis of cohesion defect not mechanistically resolved
    • Prp19 regulatory mechanism partly defined
  6. 2015 Medium

    Extended KNSTRN function beyond mitosis by mapping an IQGAP1 interaction (C-terminus) distinct from its N-terminal EB1 binding, required for directed cell migration.

    Evidence Co-IP, domain mapping, peptide perturbation, migration assay

    PMID:26242911

    Open questions at the time
    • Interplay between mitotic and migratory roles unclear
    • Structural basis of dual-terminus binding not solved
  7. 2016 High

    Resolved isoform-specific function and architecture: a short mitotic isoform mediates plus-end tracking via a dedicated microtubule-binding domain separable from the SXIP/EB module, with mutations giving separation-of-function phenotypes.

    Evidence Isoform rescue, in vitro microtubule binding, cross-linking MS, mutagenesis, live imaging

    PMID:27095104 PMID:27138257

    Open questions at the time
    • Atomic structure of the microtubule-binding domain undetermined
    • Testis isoform mitotic relevance excluded but its own role unclear
  8. 2016 Medium

    Placed KNSTRN under kinase control, showing GSK3β phosphorylation couples SKAP to the Kif2b depolymerase to regulate plus-end dynamics.

    Evidence In vitro kinase assay, phosphosite mapping, Co-IP, phosphomimetic rescue, live imaging

    PMID:27982129

    Open questions at the time
    • In vivo phosphorylation stoichiometry unknown
    • Single lab; reciprocal Kif2b regulation not fully mapped
  9. 2017 High

    Completed the complex by reconstituting a four-subunit Astrin-SKAP complex with MYCBP and demonstrated synergistic microtubule binding with the Ndc80 complex, defining an integrated attachment interface; also tied SKAP loss to Roifman-Chitayat syndrome immune-cell defects via MAP4.

    Evidence Complex reconstitution, cross-linking MS, in vitro microtubule binding; patient genetics with MAP4 Co-IP and T-cell assays

    PMID:28841134 PMID:29180244

    Open questions at the time
    • Stoichiometry and structure of the Ndc80-Astrin/SKAP interface not solved
    • MAP4 functional axis single study
  10. 2021 Medium

    Added further regulatory and signaling layers: Src phosphorylation at Tyr-87 displaces SKAP from microtubules, Plk1 acts via astrin within the complex to stabilize attachments, and KNSTRN activates AKT by outcompeting PTEN at the membrane in cancer.

    Evidence MS phosphosite mapping with phosphomimetics; Co-IP and phosphomutant analysis; Co-IP, PIP3 pulldown and AKT inhibitor rescue in tumor models

    PMID:33288550 PMID:33452459 PMID:33510346

    Open questions at the time
    • Physiological trigger for Src/Plk1 modification unclear
    • AKT axis mechanistic detail from single lab
  11. 2022 High

    Reframed the mechanical role of Astrin-SKAP as a friction-reducing 'lubricant' that coordinates sister kinetochores and dissipates force, and linked a SKAP-Aurora B phase-separation behavior to lateral-to-end-on attachment conversion.

    Evidence Live imaging, laser ablation force measurements, RNAi; in vitro phase separation and Co-IP

    PMID:34554241 PMID:35580605

    Open questions at the time
    • Physiological relevance of in vitro coacervates uncertain
    • Molecular origin of reduced friction not structurally defined
  12. 2025 High

    Confirmed that SKAP's direct microtubule binding is the basis of force dissipation, attachment force-responsiveness, and prevention of detachment under applied force.

    Evidence Microtubule-binding mutants, live imaging, laser ablation, microneedle force application

    PMID:40154475

    Open questions at the time
    • Quantitative model of grip/slip behavior incomplete
    • Interplay with Ndc80 under force not directly tested
  13. 2026 Medium

    Implicated KNSTRN in cancer cell survival through autophagy, where its loss causes ROS accumulation and lysosomal dysfunction that block autophagic flux.

    Evidence siRNA, ROS and lysosomal assays, autophagic flux measurement, pharmacological rescue, in vivo

    PMID:41704764

    Open questions at the time
    • Direct molecular link between KNSTRN and lysosome/ROS biology unidentified
    • Relationship to its mitotic function unclear

Open questions

Synthesis pass · forward-looking unresolved questions
  • How KNSTRN's mechanical role at the kinetochore is coordinated with its diverse non-mitotic functions (migration, AKT signaling, autophagy) through a single shared biochemistry remains unresolved.
  • No high-resolution structure of the microtubule- or Ndc80-binding interfaces
  • Unclear whether mitotic and non-mitotic roles use overlapping domains
  • Mechanism linking KNSTRN to lysosomal/ROS homeostasis undefined

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0008092 cytoskeletal protein binding 5 GO:0060090 molecular adaptor activity 3
Localization
GO:0005694 chromosome 4 GO:0005856 cytoskeleton 4 GO:0005886 plasma membrane 1
Pathway
R-HSA-1640170 Cell Cycle 7 R-HSA-162582 Signal Transduction 1 R-HSA-9612973 Autophagy 1
Partners
CENP-EDYNLL1EB1IQGAP1MAP4MIS13MYCBPSPAG5
Complex memberships
Astrin-SKAP complex (Astrin/SPAG5-KNSTRN-DYNLL1-MYCBP)kinetochore corona

Evidence

Reading pass · 21 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
2010 KNSTRN (SKAP) forms a complex with Astrin and dynein light chain LC8 at kinetochores. Localization of this complex to bioriented kinetochores is antagonized by Aurora B kinase, restricting it to tension-bearing (bioriented) kinetochores. Astrin and SKAP bind directly to microtubules and are required for CLASP localization to kinetochores. Co-immunoprecipitation, RNAi depletion, live-cell imaging, in vitro microtubule binding assays The Journal of cell biology High 20937697
2011 KNSTRN (kinastrin/SKAP) is the major astrin-interacting protein in mitotic cells and is required for astrin targeting to microtubule plus ends proximal to the plus-tip tracking protein EB1. Depletion or overexpression of kinastrin mislocalizes astrin and disrupts spindle architecture and chromosome alignment. Co-immunoprecipitation, RNAi depletion, fluorescence live-cell imaging, overexpression studies The Journal of cell biology High 21402792
2009 KNSTRN (SKAP) localizes to spindle microtubules and kinetochores in mitosis. Depletion of SKAP does not activate the spindle assembly checkpoint but increases duration of metaphase, delays separase activation, and decreases fidelity of chromosome segregation. RNAi depletion, live-cell imaging, immunofluorescence, separase activity assay Cell cycle (Georgetown, Tex.) Medium 19667759
2011 KNSTRN (SKAP) physically interacts with the C-terminal tail of CENP-E in vitro and cooperates with CENP-E to regulate kinetochore-microtubule interactions. SKAP is a constituent of kinetochore corona fibers. SKAP binds microtubules in vitro, and this interaction is synergized by CENP-E. Depletion of SKAP reduces inter-kinetochore tension and causes chromosome mis-segregation. In vitro binding/pulldown, immunoelectron microscopy, RNAi, in vitro microtubule binding assay The Journal of biological chemistry High 22110139
2012 KNSTRN (SKAP) physically interacts with MIS13 (a component of the MIS12/KMN complex), which specifies kinetochore localization of SKAP. SKAP exhibits EB1-dependent microtubule plus-end loading and tracking in vitro (TIRF assay) and is essential for kinetochore oscillations and microtubule plus-end dynamics during mitosis. Co-immunoprecipitation, siRNA, TIRF microscopy in vitro, live-cell imaging The Journal of biological chemistry High 23035123
2014 Cancer-associated KNSTRN mutations, most notably p.Ser24Phe, disrupt sister chromatid cohesion in normal cells and correlate with increased aneuploidy in primary tumors, implicating KNSTRN in maintenance of chromatid cohesion. Mutant expression in normal cells (cohesion assay), in vivo tumorigenesis model, sequencing of primary tumors Nature genetics Medium 25194279
2016 SKAP is expressed as two distinct isoforms in mammals: a shorter mitotic isoform and a longer testis-specific isoform. Only the short mitotic isoform rescues SKAP depletion in mitosis and displays robust microtubule plus-end tracking including localization to astral microtubules. SKAP microtubule binding mutants that abolish plus-end tracking cause spindle positioning defects and reduce Clasp1 localization at microtubule plus ends, leading to increased lateral microtubule contacts with the cell cortex. Isoform expression, rescue assays, live-cell imaging, mutant analysis, immunofluorescence The Journal of cell biology High 27138257
2016 KNSTRN (SKAP) contains a microtubule-binding domain distinct from the SXIP motif that mediates EB protein binding and plus-end tracking. This microtubule-binding domain stimulates the growth rate of microtubules possibly through direct interaction with tubulin. Mutations targeting this domain impair plus-end tracking but not kinetochore targeting and recapitulate SKAP depletion phenotypes. In vitro microtubule binding assay, mutagenesis, cross-linking mass spectrometry, biochemical reconstitution Nature communications High 27095104
2017 Biochemical reconstitution of the 4-subunit Astrin-SKAP complex reveals it contains a novel MYCBP subunit. The complex has separable kinetochore localization and microtubule binding domains. Cross-linking analysis and biochemical reconstitution show the Astrin-SKAP complex binds synergistically to microtubules together with the Ndc80 complex to form an integrated interface. Complex reconstitution, cross-linking mass spectrometry, in vitro microtubule binding, biochemical domain mapping eLife High 28841134
2016 GSK3β phosphorylates KNSTRN (SKAP) in vitro; phosphorylation sites mapped by mass spectrometry. GSK3β-mediated phosphorylation of SKAP promotes SKAP binding to the Kif2b microtubule depolymerase, thereby competing with Kif2b for microtubule plus-end binding and regulating Kif2b depolymerase activity. Phosphomimetic SKAP rescues chromosome mis-segregation phenotype. In vitro kinase assay, mass spectrometry phosphosite mapping, Co-IP, rescue with phosphomimetic mutant, live-cell imaging Scientific reports Medium 27982129
2021 Src-family kinases phosphorylate KNSTRN (kinastrin) at Tyr-87 on the mitotic spindle. Phosphomimetic kinastrin at Tyr-87 impairs its ability to bind microtubules, suggesting that SFK-mediated phosphorylation promotes kinastrin delocalization from microtubules during mitosis. Mass spectrometry of mitotic spindle preparations, phosphomimetic mutant analysis, microtubule binding assay Scientific reports Medium 33510346
2022 KNSTRN (SKAP) physically interacts with Aurora B and spontaneously phase-separates in vitro via weak multivalent interactions into droplets. SKAP and Aurora B form heterogeneous coacervates in vitro that recapitulate in vivo SKAP comet dynamics. This SKAP-Aurora B interaction via phase separation is required for accurate chromosome segregation and the lateral-to-end-on conversion of kinetochore-microtubule attachments. In vitro phase separation assay, Co-IP, live-cell imaging, functional mutant analysis Journal of molecular cell biology Medium 34554241
2022 The Astrin-SKAP complex reduces friction at the kinetochore-microtubule interface. SKAP depletion dampens movement and decreases coordination of metaphase sister kinetochores, increases inter-kinetochore tension, and slows kinetochore movement on both polymerizing and depolymerizing microtubules. More force is needed to rescue microtubules to polymerize without SKAP, indicating Astrin-SKAP acts as a 'lubricant' reducing grip on bioriented attachments. Live imaging, laser ablation, SKAP RNAi depletion, kinetochore force measurements Current biology : CB High 35580605
2021 Plk1 directly interacts with Astrin in the Astrin-SKAP complex, and Plk1 phosphorylates astrin at four sites. This Plk1-mediated regulation is dispensable for bipolar spindle formation and bulk chromosome congression but promotes stable microtubule-kinetochore attachments and metaphase plate maintenance. Co-IP (direct astrin-Plk1 interaction), phosphosite mapping, separation-of-function mutants, live-cell imaging Journal of cell science Medium 33288550
2025 SKAP's direct microtubule binding is essential for sister kinetochore coordination, force dissipation at the kinetochore-microtubule interface, attachment responsiveness to force changes, and prevention of chromosome detachment under spindle forces and microneedle-generated forces. SKAP microtubule-binding mutants, live imaging, laser ablation, microneedle force application Current biology : CB High 40154475
2021 KNSTRN physically interacts with AKT at the cell membrane via AKT's PH domain, competing with PTEN. KNSTRN promotes AKT movement to PIP3 and alleviates PTEN suppression of AKT, thereby activating AKT phosphorylation at Thr308 and Ser473, which promotes bladder cancer metastasis and gemcitabine resistance. Co-IP, PIP3 pulldown assay, AKT phosphorylation assays, AKT inhibitor rescue, in vitro and in vivo tumorigenesis Oncogene Medium 33452459
2017 Loss of KNSTRN (SKAP) expression in patients with Roifman-Chitayat syndrome leads to aberrant T-cell spreading, cell-cell interaction, and migration. A novel SKAP-binding partner, microtubule-associated protein 4 (MAP4), was identified; MAP4 undergoes relocalization in patient T cells with associated areas of microtubule hyperstabilization. Patient genetic analysis, protein expression studies, Co-IP/pulldown (MAP4 interaction), cellular functional assays in patient T cells The Journal of allergy and clinical immunology Medium 29180244
2014 KNSTRN (SKAP) interacts with Pre-mRNA processing Factor 19 (Prp19) and negatively regulates Prp19 protein levels. Overexpression or knockdown of SKAP both sensitize cells to UV-induced apoptosis, and this pro-apoptotic effect of SKAP is executed through Prp19. Co-IP, knockdown, overexpression, rescue experiments, UV-induced apoptosis assay PloS one Medium 24718257
2015 KNSTRN (SKAP) interacts with IQGAP1; binding interfaces map to the WWIQ motif of IQGAP1 and the C-terminus of SKAP. The N-terminus of SKAP binds EB1 while the C-terminus binds IQGAP1. Disruption of the IQGAP1-SKAP interaction inhibits EGF-directed cell migration. Co-IP, domain mapping, TAT-WWIQ peptide perturbation, directional migration assay The Journal of biological chemistry Medium 26242911
2016 KNSTRN (SKAP/kinastrin) exists in two isoforms in human and mouse: ubiquitously expressed SKAP16 and testis/sperm-specific SKAP1. The testis-specific isoform SKAP1 interacts with Pontin, and SKAP1 and Pontin co-localize in the flagellar region of human sperm, suggesting a role in sperm motility. RT-PCR, Western blotting, immunocytochemistry, Co-IP (Pontin interaction), co-localization Human molecular genetics Low 27170314
2026 KNSTRN knockdown causes intracellular ROS accumulation and lysosomal dysfunction, impairing autophagosome-lysosome fusion and blocking autophagic flux in bladder cancer cells. Restoring lysosomal function (clioquinol) or scavenging ROS (NAC) rescues autophagy flux; autophagy activator rapamycin counteracts KNSTRN knockdown-induced cell death. siRNA knockdown, ROS assays, lysosomal pH measurement, autophagic flux assays, pharmacological rescue (clioquinol, NAC, rapamycin), in vitro and in vivo iScience Medium 41704764

Source papers

Stage 0 corpus · 39 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2014 Recurrent point mutations in the kinetochore gene KNSTRN in cutaneous squamous cell carcinoma. Nature genetics 124 25194279
2010 Aurora B kinase controls the targeting of the Astrin-SKAP complex to bioriented kinetochores. The Journal of cell biology 107 20937697
2011 The astrin-kinastrin/SKAP complex localizes to microtubule plus ends and facilitates chromosome alignment. The Journal of cell biology 96 21402792
2007 RIAM links the ADAP/SKAP-55 signaling module to Rap1, facilitating T-cell-receptor-mediated integrin activation. Molecular and cellular biology 96 17403904
2003 SKAP-55 regulates integrin adhesion and formation of T cell-APC conjugates. Nature immunology 94 12652296
2008 SKAP-55, SKAP-55-related and ADAP adaptors modulate integrin-mediated immune-cell adhesion. Trends in cell biology 81 18760924
1998 SKAP-HOM, a novel adaptor protein homologous to the FYN-associated protein SKAP55. FEBS letters 74 9755858
2005 Regulation of in vitro and in vivo immune functions by the cytosolic adaptor protein SKAP-HOM. Molecular and cellular biology 70 16135797
2009 SKAP associates with kinetochores and promotes the metaphase-to-anaphase transition. Cell cycle (Georgetown, Tex.) 58 19667759
2005 An essential role for SKAP-55 in LFA-1 clustering on T cells that cannot be substituted by SKAP-55R. The Journal of experimental medicine 48 15939789
2007 Functional defects of SKAP-55-deficient T cells identify a regulatory role for the adaptor in LFA-1 adhesion. Molecular and cellular biology 47 17646386
2021 KNSTRN promotes tumorigenesis and gemcitabine resistance by activating AKT in bladder cancer. Oncogene 45 33452459
2011 CENP-E kinesin interacts with SKAP protein to orchestrate accurate chromosome segregation in mitosis. The Journal of biological chemistry 42 22110139
2012 Mitotic regulator SKAP forms a link between kinetochore core complex KMN and dynamic spindle microtubules. The Journal of biological chemistry 41 23035123
2008 The Skap-hom dimerization and PH domains comprise a 3'-phosphoinositide-gated molecular switch. Molecular cell 40 19026786
2017 Astrin-SKAP complex reconstitution reveals its kinetochore interaction with microtubule-bound Ndc80. eLife 39 28841134
2016 A mitotic SKAP isoform regulates spindle positioning at astral microtubule plus ends. The Journal of cell biology 33 27138257
2016 Molecular requirements for the inter-subunit interaction and kinetochore recruitment of SKAP and Astrin. Nature communications 32 27095104
2011 Substrate specificity of lymphoid-specific tyrosine phosphatase (Lyp) and identification of Src kinase-associated protein of 55 kDa homolog (SKAP-HOM) as a Lyp substrate. The Journal of biological chemistry 28 21719704
2017 Dual loss of p110δ PI3-kinase and SKAP (KNSTRN) expression leads to combined immunodeficiency and multisystem syndromic features. The Journal of allergy and clinical immunology 27 29180244
2006 Regulation and function of SKAP-55 non-canonical motif binding to the SH3c domain of adhesion and degranulation-promoting adaptor protein. The Journal of biological chemistry 26 16461356
2015 Signaling Scaffold Protein IQGAP1 Interacts with Microtubule Plus-end Tracking Protein SKAP and Links Dynamic Microtubule Plus-end to Steer Cell Migration. The Journal of biological chemistry 24 26242911
2009 Expression of SKAP-HOM in DCs is required for an optimal immune response in vivo. Journal of leukocyte biology 23 19369640
2010 HPK1 associates with SKAP-HOM to negatively regulate Rap1-mediated B-lymphocyte adhesion. PloS one 19 20824186
2019 Somatic mutations in kinetochore gene KNSTRN are associated with basal proliferating actinic keratoses and cutaneous squamous cell carcinoma. Journal of the European Academy of Dermatology and Venereology : JEADV 15 30972880
2008 Adaptor SKAP-55 binds p21 activating exchange factor RasGRP1 and negatively regulates the p21-ERK pathway in T-cells. PloS one 15 18320039
2022 The Astrin-SKAP complex reduces friction at the kinetochore-microtubule interface. Current biology : CB 12 35580605
2022 SKAP interacts with Aurora B to guide end-on capture of spindle microtubules via phase separation. Journal of molecular cell biology 11 34554241
2021 The association of Plk1 with the astrin-kinastrin complex promotes formation and maintenance of a metaphase plate. Journal of cell science 10 33288550
2018 Immune adaptor protein SKAP1 (SKAP-55) forms homodimers as mediated by the N-terminal region. BMC research notes 8 30522503
2015 SKAP, an outer kinetochore protein, is required for mouse germ cell development. Reproduction (Cambridge, England) 7 26667018
2016 Phosphorylation of SKAP by GSK3β ensures chromosome segregation by a temporal inhibition of Kif2b activity. Scientific reports 6 27982129
2014 Small kinetochore associated protein (SKAP) promotes UV-induced cell apoptosis through negatively regulating pre-mRNA processing factor 19 (Prp19). PloS one 6 24718257
2025 SKAP binding to microtubules reduces friction at the kinetochore-microtubule interface and increases attachment stability under force. Current biology : CB 5 40154475
2016 Characterization of SKAP/kinastrin isoforms: the N-terminus defines tissue specificity and Pontin binding. Human molecular genetics 2 27170314
2014 Hippocampus-dependent learning in SKAP-HOM deficient mice. Behavioural brain research 2 24815314
2024 SKAP binding to microtubules reduces friction at the kinetochore-microtubule interface and increases attachment stability under force. bioRxiv : the preprint server for biology 1 39149232
2021 Src-mediated tyrosine phosphorylation of PRC1 and kinastrin/SKAP on the mitotic spindle. Scientific reports 1 33510346
2026 KNSTRN knockdown impairs autophagy flux to inhibit bladder cancer progression. iScience 0 41704764

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