Affinage

CAMSAP3

Calmodulin-regulated spectrin-associated protein 3 · UniProt Q9P1Y5

Length
1249 aa
Mass
134.8 kDa
Annotated
2026-04-28
24 papers in source corpus 23 papers cited in narrative 23 extracted findings

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

CAMSAP3 is a microtubule minus-end binding protein that stabilizes noncentrosomal microtubule arrays and orients apico-basal polarity in diverse epithelial tissues, neurons, and ciliated cells. It dimerizes through a C-terminal α-helix that enhances CKK domain minus-end binding affinity, and its MBD and CKK domains cooperate to decorate and dynamically regulate minus ends; its CC1 domain directs apical cortical localization, where the spectraplakin ACF7/MACF1 anchors CAMSAP3-decorated minus ends to actin, and paracingulin/CGNL1 recruits CAMSAP3 to tight junctions (PMID:39479887, PMID:27802168, PMID:27693509, PMID:37013686). In motile cilia and kinocilia, CAMSAP3 concentrates at the axonemal basal plate and is required for central microtubule pair formation; its loss produces primary ciliary dyskinesia-like phenotypes with disorganized ciliary beating (PMID:32482850, PMID:34319756, PMID:35783105). CAMSAP3 suppresses αTAT1-dependent tubulin acetylation to maintain neuronal polarity and epithelial identity, and its loss deregulates Akt, ERK/cyclin D1, and mTORC1 signaling, disrupts endosomal-lysosomal trafficking, activates mechanosensors YAP/PIEZO1, and promotes epithelial-mesenchymal transition (PMID:30190432, PMID:30282632, PMID:33462112, PMID:33712686, PMID:41381443).

Mechanistic history

Synthesis pass · year-by-year structured walk · 18 steps
  1. 2012 High

    Establishing that CAMSAP3 and CAMSAP2 specifically recognize and stabilize noncentrosomal microtubule minus ends answered the fundamental question of how epithelial cells maintain acentrosomal microtubule networks and organize endomembranes.

    Evidence siRNA depletion with immunofluorescence and live imaging in epithelial cells

    PMID:23169647

    Open questions at the time
    • Mechanism of minus-end recognition not defined at the molecular level
    • Relative contributions of CAMSAP2 vs CAMSAP3 not separated
    • How microtubule stabilization suppresses centrosomal organization unclear
  2. 2015 High

    Demonstrating that CAMSAP3 accumulates at apical cortices via its CC1 domain and tethers minus ends there established the molecular basis of apico-basal microtubule orientation in intestinal epithelia.

    Evidence Domain mutagenesis and forced mislocalization in mouse intestinal cells and Caco-2 cells

    PMID:26715742

    Open questions at the time
    • Identity of the apical receptor for the CC1 domain unknown
    • Whether CC1-mediated localization is conserved across all polarized epithelia not tested
  3. 2016 High

    Identification of ACF7/MACF1 as a direct CAMSAP3 partner that anchors minus-end-decorated microtubules to actin filaments resolved how the noncentrosomal microtubule network is physically connected to the cortical cytoskeleton and influences focal adhesion dynamics and migration.

    Evidence Reciprocal Co-IP, pulldown, KO cell lines, live imaging, focal adhesion and migration assays in Caco-2 cells and 3D cysts

    PMID:27693509 PMID:27802168

    Open questions at the time
    • Structural basis of CAMSAP3–ACF7 interaction not mapped to specific domains
    • Contribution of other spectraplakins not excluded
  4. 2016 High

    Discovery that CDH23-C directly binds the CKK domain via a conserved CBM motif and inhibits CAMSAP3-induced microtubule bundling linked CAMSAP3 to stereocilia/inner ear biology and the Usher Syndrome 1D mutation R3175H.

    Evidence Co-IP, in vitro pulldown, mutagenesis, in vivo mouse models

    PMID:27349180

    Open questions at the time
    • Physiological consequence of CDH23–CAMSAP3 disruption on hearing not directly shown
    • Whether other CKK-binding partners compete with CDH23 unknown
  5. 2016 Medium

    Identification of CAMSAP3 interaction with CG-NAP and its role in Golgi vesicle translocation provided the first link between CAMSAP3-organized microtubules and Golgi ribbon integrity.

    Evidence Co-IP, siRNA depletion, Golgi morphology assays in epithelial cells

    PMID:28089391

    Open questions at the time
    • Direct binding interface between CAMSAP3 and CG-NAP not mapped
    • Golgi phenotype not validated in vivo
    • Whether CAMSAP2 compensates at the Golgi not tested
  6. 2017 Medium

    Showing that CAMSAP3 cooperates with dynein and katanin at the pericentrosomal area to release microtubules from centrosomes answered how noncentrosomal microtubules are generated from centrosomal precursors.

    Evidence siRNA depletion, live imaging, Co-IP with dynein and katanin

    PMID:28386021

    Open questions at the time
    • Order of recruitment (CAMSAP3 vs dynein vs katanin) not resolved
    • Reconstitution of microtubule release in vitro not achieved
    • Single lab finding
  7. 2018 High

    Genetic epistasis placing CAMSAP3 upstream of αTAT1-dependent tubulin acetylation in maintaining single-axon polarity established a new regulatory axis: CAMSAP3 suppresses tubulin acetylation to restrict axon number.

    Evidence Double knockdown epistasis, mouse Camsap3 mutants, nocodazole resistance assays in hippocampal neurons

    PMID:30190432

    Open questions at the time
    • Molecular mechanism by which CAMSAP3 inhibits αTAT1 access not defined
    • Whether this axis operates in other neuronal subtypes not tested
  8. 2018 Medium

    Linking CAMSAP3 loss to increased tubulin acetylation, Akt activation, and EMT in lung carcinoma extended the tubulin acetylation axis to signaling and cancer biology, showing CAMSAP3 protects epithelial identity.

    Evidence CAMSAP3 deletion cell lines, Akt activity assays, EMT marker analysis

    PMID:30282632

    Open questions at the time
    • Direct mechanism connecting tubulin acetylation to Akt activation not delineated
    • In vivo tumor progression data lacking at this point
  9. 2020 High

    Demonstrating that CAMSAP3 localizes to axonemal bases and is required for central microtubule pair formation in motile cilia revealed an unexpected structural role, explaining PCD-like phenotypes upon CAMSAP3 loss.

    Evidence Hypomorphic knockdown mouse, Xenopus morpholino, electron microscopy, ciliary beat analysis

    PMID:32482850

    Open questions at the time
    • How CAMSAP3 nucleates or stabilizes the central pair specifically is unknown
    • Whether CAMSAP3 acts alone or requires cofactors at the basal plate not resolved
  10. 2021 High

    Refining CAMSAP3 localization to the basal plate (transition zone) and demonstrating that its loss distorts basal plate ultrastructure and disrupts basal body coordination in multiciliated airways and oviduct cells consolidated the ciliary role and separated it mechanistically from planar cell polarity signaling via CELSR1.

    Evidence Mouse mutants, super-resolution microscopy, electron microscopy, basal body orientation quantification in tracheal and oviduct cells

    PMID:33468623 PMID:34319756

    Open questions at the time
    • Basal plate binding partners of CAMSAP3 not identified
    • Whether CAMSAP3 functions at primary (non-motile) cilia not tested
  11. 2021 Medium

    Connecting CAMSAP3-organized microtubules to lysosomal positioning, mTORC1 signaling, and ependymal cell apical domain expansion broadened the downstream effector repertoire beyond acetylation-Akt, and showed tissue-level consequences (ventricle narrowing) of CAMSAP3 loss.

    Evidence Camsap3 mutant mice, mTORC1 activity assays, lysosome immunofluorescence, ventricle morphometry

    PMID:33462112

    Open questions at the time
    • Whether mTORC1 downregulation is a direct consequence of lysosome mispositioning or an indirect effect not resolved
    • Single lab finding
  12. 2021 Medium

    Revealing that CAMSAP3 mutation activates mechanosensors YAP and PIEZO1 and causes proximal convoluted tubule cystogenesis established that noncentrosomal microtubule loss alters cell mechanics and mechanotransduction.

    Evidence Camsap3 mutant mice, YAP/PIEZO1 immunostaining, electron microscopy, proliferation assays

    PMID:33712686

    Open questions at the time
    • Whether microtubule-dependent cortical stiffness change directly activates PIEZO1 not shown
    • Cyst progression and reversibility not characterized
  13. 2021 Medium

    Demonstrating that CAMSAP3 KO in lung cancer cells causes senescence-associated phenotypes through ERK/cyclin D1 downregulation, with vimentin scaffolding a CAMSAP3-ERK complex, identified a signaling axis linking microtubule organization to cell cycle control.

    Evidence CRISPR KO, IP/mass spectrometry, immunoblotting, flow cytometry, xenograft model

    PMID:34724356

    Open questions at the time
    • Direct binding between CAMSAP3 and ERK vs vimentin-mediated proximity not resolved
    • Cancer-type specificity not addressed
  14. 2022 Medium

    Extending the central pair phenotype to vestibular hair cell kinocilia confirmed that CAMSAP3-dependent central pair formation is a generalizable mechanism across 9+2 axonemes.

    Evidence Conditional KO mouse, TEM, immunofluorescence, behavioral assays

    PMID:35783105

    Open questions at the time
    • Whether kinocilium shortening is due to central pair loss or independent function not delineated
    • Behavioral phenotype not extensively characterized
  15. 2023 High

    Identification of paracingulin/CGNL1 as the tight junction receptor that recruits CAMSAP3 via coiled-coil interactions through ZO-1 answered how CAMSAP3 is targeted to cell-cell junctions and linked junctional microtubules to epithelial barrier architecture.

    Evidence GST pulldown, KO cell lines, ultrastructure expansion microscopy, in vivo mouse intestinal epithelium

    PMID:37013686

    Open questions at the time
    • Whether CGNL1 is the sole junctional receptor or additional anchors exist not excluded
    • Functional consequence on barrier permeability not quantified
  16. 2024 High

    Biochemical reconstitution showing that CAMSAP3 dimerizes through its C-terminal α-helix to enhance CKK domain minus-end binding provided the first molecular-level explanation for how CAMSAP3 achieves high-affinity minus-end decoration and dynamic regulation.

    Evidence In vitro dimerization assays, microtubule-binding assays, domain mutagenesis, live cell imaging

    PMID:39479887

    Open questions at the time
    • Crystal or cryo-EM structure of the dimer not available
    • Whether dimerization is regulated in vivo (e.g., by phosphorylation) unknown
  17. 2024 Medium

    Showing that CAMSAP3 loss drives centrosomal microtubule clustering, impairs endosomal-lysosomal trafficking of EGFR, and confers osimertinib resistance — reversed by CAMSAP3 re-expression — provided a mechanistic link between noncentrosomal microtubule loss and drug resistance in NSCLC.

    Evidence siRNA/CRISPR depletion and overexpression, EGFR trafficking assays, xenograft model

    PMID:41381443

    Open questions at the time
    • Generalizability to other receptor tyrosine kinases not tested
    • Patient-level validation of CAMSAP3 loss in osimertinib resistance lacking
  18. 2024 Medium

    Demonstrating that CAMSAP3 deficiency in keratinocytes shifts microtubules to centrosomal configuration and impairs both cell cycle progression and adherens/tight junction stability established that CAMSAP3-dependent noncentrosomal arrays are required for proliferation and intercellular adhesion in stratified epithelia.

    Evidence Inducible KO and rescue in HaCaT cells, immunofluorescence, flow cytometry

    PMID:38190868

    Open questions at the time
    • In vivo skin phenotype not characterized
    • Whether other CAMSAP family members compensate in keratinocytes not addressed

Open questions

Synthesis pass · forward-looking unresolved questions
  • Key unresolved questions include the structural basis of CAMSAP3 dimerization and CKK minus-end recognition, the mechanism by which CAMSAP3 nucleates or stabilizes the central microtubule pair at the axonemal basal plate, and how CAMSAP3 minus-end occupancy suppresses αTAT1-dependent acetylation at the molecular level.
  • No high-resolution structure of CAMSAP3 dimer or CKK-microtubule complex
  • Basal plate cofactors required for central pair formation unidentified
  • Molecular mechanism linking minus-end binding to αTAT1 exclusion unknown

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0008092 cytoskeletal protein binding 4 GO:0060090 molecular adaptor activity 2
Localization
GO:0005929 cilium 4 GO:0005856 cytoskeleton 3 GO:0005829 cytosol 2 GO:0005886 plasma membrane 2 GO:0005815 microtubule organizing center 1
Pathway
R-HSA-1852241 Organelle biogenesis and maintenance 4 R-HSA-162582 Signal Transduction 3 R-HSA-5653656 Vesicle-mediated transport 3 R-HSA-1500931 Cell-Cell communication 2
Partners
CDH23CGNL1DYNC1H1HMGB1KATNA1MACF1NCLVIM
Complex memberships
CAMSAP3–ACF7/MACF1 minus-end anchoring complex

Evidence

Reading pass · 23 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
2012 CAMSAP3 (Nezha) and CAMSAP2 co-cluster at the minus ends of noncentrosomal microtubules in epithelial cells, stabilizing them and suppressing centrosomal microtubule organization; depletion of both CAMSAPs caused marked reduction of microtubules with polymerizing plus ends and perturbed early endosome and Golgi distribution. siRNA depletion, immunofluorescence, live imaging in epithelial cells Proceedings of the National Academy of Sciences of the United States of America High 23169647
2015 CAMSAP3 accumulates at apical cortices of polarized intestinal epithelial cells and tethers longitudinal microtubule minus ends there, orienting microtubules along the apical-to-basal axis; its CC1 domain is required for apical localization, and forced mislocalization disrupts epithelial architecture. Camsap3 mutation/depletion in mouse intestinal cells and Caco-2 cells, domain mutagenesis, immunofluorescence, forced mislocalization experiments Proceedings of the National Academy of Sciences of the United States of America High 26715742
2016 ACF7 (MACF1), a spectraplakin family cytoskeletal crosslinking protein, specifically binds CAMSAP3 and is required for apical localization of CAMSAP3-decorated microtubule minus ends in intestinal epithelial cells; CAMSAP3 knockout (but not CAMSAP2) caused microtubule reorganization into a centrosomal radial array and redistribution of Rab11-positive endosomes away from the apical surface. Reciprocal Co-IP, knockout cell lines, immunofluorescence, 3D cyst culture Journal of cell science High 27802168
2016 ACF7 interacts with CAMSAP3 at the minus ends of noncentrosomal microtubules and anchors them to actin filaments; this CAMSAP3-ACF7 complex couples microtubule and actin dynamics to regulate retrograde flow, focal adhesion size, and cell migration in Caco-2 epithelial cells. Co-IP, pulldown, live imaging, siRNA depletion, focal adhesion and migration assays Developmental cell High 27693509
2017 CAMSAP3 accumulates in the pericentrosomal area and cooperates with dynein and katanin to mediate microtubule detachment from the centrosome; depletion of CAMSAP3 prevents microtubule release and causes focusing of microtubules at centrosomes. siRNA depletion, immunofluorescence, live imaging, Co-IP with dynein and katanin Journal of cell science Medium 28386021
2016 CAMSAP3 interacts with CG-NAP and regulates Golgi vesicle translocation in epithelial cells; depletion of either CAMSAP3 or CG-NAP causes Golgi membrane fragmentation, and stathmin-dependent microtubule dynamics graded along the radial axis contributes to perinuclear Golgi assembly. Co-IP, siRNA depletion, immunofluorescence, Golgi morphology assays Journal of genetics and genomics Medium 28089391
2018 CAMSAP3 is enriched in axons of hippocampal neurons and preferentially localizes to less-acetylated microtubules; CAMSAP3 mutation causes supernumerary axons and increased tubulin acetylation; CAMSAP3 depletion promotes αTAT1-dependent tubulin acetylation, and αTAT1 depletion abolishes multi-axon formation caused by CAMSAP3 loss, placing CAMSAP3 upstream of αTAT1 in axonal polarity maintenance. Genetic epistasis (double KD), mouse mutants, immunofluorescence, nocodazole resistance assays Proceedings of the National Academy of Sciences of the United States of America High 30190432
2018 Loss of CAMSAP3 in lung carcinoma cells increases tubulin acetylation, which upregulates Akt activity and promotes EMT at the transcriptional level; CAMSAP3 thus protects epithelial phenotype by suppressing Akt activity via microtubule regulation. CAMSAP3 deletion cell lines, Akt activity assays, tubulin acetylation immunoblot, EMT marker analysis Journal of cell science Medium 30282632
2020 CAMSAP3 localizes to the base of axonemes and at basal bodies in multiciliated cells; its loss results in absence of the central microtubule pair in most cilia and disorganized basal body polarity, causing defective synchronized ciliary beating and PCD-like phenotypes; confirmed in Xenopus by morpholino knockdown. Hypomorphic knockdown mouse model, Xenopus morpholino, electron microscopy, immunofluorescence, ciliary beat analysis Proceedings of the National Academy of Sciences of the United States of America High 32482850
2021 CAMSAP3 concentrates at the axonemal basal plate (transition zone) where the central microtubule pair initiates; CAMSAP3 dysfunction causes loss of the central pair and partial distortion of the basal plate, as well as failure of coordinated multicilia beating in tracheal airway epithelial cells. Mouse mutants, super-resolution immunofluorescence, electron microscopy, ciliary beat analysis Molecular biology of the cell High 34319756
2021 CAMSAP3 localizes to the base of cilia in a polarized manner in oviduct multiciliated cells; its mutation disrupts intracellular coordination of basal body orientation and the assembly of microtubules interconnecting basal bodies, without affecting planar cell polarity factor localization, indicating a distinct mechanism from CELSR1. Mouse mutants, immunofluorescence, super-resolution microscopy, basal body orientation quantification Journal of cell science High 33468623
2021 CAMSAP3 concentrates at apical domains of differentiating ependymal cells and generates apical MT networks that support lysosomal positioning; CAMSAP3 mutation downregulates mTORC1 activity, reduces apical lysosome distribution, and impairs ependymal cell apical domain expansion, leading to abnormal lateral ventricle narrowing. Camsap3 mutant mice, mTORC1 activity assays, lysosome immunofluorescence, ventricle morphometry Development (Cambridge, England) Medium 33462112
2021 CAMSAP3-mediated microtubule networks are required to maintain mechanical properties of proximal convoluted tubule (PCT) cells; CAMSAP3 mutation activates mechanosensors YAP and PIEZO1, induces cell flattening and proliferation, and causes PCT cyst formation. Camsap3 mutant mice, YAP/PIEZO1 immunostaining, electron microscopy, proliferation assays Scientific reports Medium 33712686
2021 CAMSAP3 knockout promotes lung cancer cell senescence-associated phenotypes and G1 arrest via downregulation of phospho-ERK and cyclin D1; vimentin acts as a scaffold for the CAMSAP3-ERK signaling complex, identified by immunoprecipitation/mass spectrometry. CRISPR-Cas9 KO, IP/mass spectrometry, immunoblotting, flow cytometry, xenograft model Cancer medicine Medium 34724356
2016 The C isoform of CDH23 directly binds the CKK domain of CAMSAP3 via a conserved N-terminal CKK-binding motif (CBM) and inhibits CAMSAP3-induced microtubule bundle formation; the Usher Syndrome 1D mutation CDH23 R3175H (mouse R55H) reduces this interaction both in vitro and in vivo. Co-IP, pulldown, in vitro binding assays, mutagenesis, in vivo mouse models Scientific reports High 27349180
2023 Paracingulin (CGNL1), but not PLEKHA7, interacts with CAMSAP3 via their coiled-coil regions (GST pulldown) and recruits CAMSAP3 to tight junctions via the ZO-1-associated pool; CGNL1 knockout causes loss of junctional CAMSAP3, disorganized cytoplasmic microtubules, and disrupted epithelial architecture. GST pulldown, KO cell lines, ultrastructure expansion microscopy, in vivo mouse intestinal epithelium Journal of cell science High 37013686
2023 CAMSAP3 interacts with nucleolin (NCL) to regulate HIF-1α mRNA stabilization; CAMSAP3 knockout increases HIF-1α expression and downstream VEGFA and MMP2/9, promoting invasion and angiogenesis; identified by proteomic analysis and RNA immunoprecipitation. CRISPR-Cas9 KO, IP/mass spectrometry, RNA immunoprecipitation, in vitro invasion/angiogenesis assays, in vivo xenograft Life sciences Medium 37019300
2024 CAMSAP3 forms dimers through its C-terminal α-helix domain; dimerization enhances the microtubule-binding affinity of the CKK domain and enables the CKK domain to regulate minus-end dynamics; the combined action of the microtubule-binding domain (MBD) and C-terminal α-helix mediates minus-end decoration and dynamic regulation. Biochemical dimerization assays, in vitro microtubule-binding assays, domain mutagenesis, live cell imaging Journal of cell science High 39479887
2024 CAMSAP3 interacts with acetylated HMGB1 in the cytoplasm; TSA-induced HMGB1 acetylation drives HMGB1 cytoplasmic translocation and secretion promoting autophagic cell death, a process that requires CAMSAP3; CAMSAP3 knockout abolishes this TSA-mediated autophagic cell death. CRISPR-Cas9 KO, proteomic analysis, immunoprecipitation, immunofluorescence, autophagic detection assays Biochimica et biophysica acta. General subjects Medium 38598971
2024 CAMSAP3 depletion in NSCLC cells causes centrosomal microtubule clustering, impairs the endosomal-lysosomal system, and drives EGFR translocation to the perinuclear MTOC, blocking plasma membrane recycling and promoting lysosomal EGFR degradation, thereby conferring osimertinib resistance; CAMSAP3 overexpression in resistant cells restores microtubule organization and drug sensitivity. siRNA/CRISPR depletion, CAMSAP3 overexpression, EGFR trafficking assays, xenograft model Cell death & disease Medium 41381443
2024 CAMSAP3 deficiency in keratinocytes shifts microtubules from non-centrosomal to centrosomal configuration, causes cell cycle exit, delayed cytokinesis, and impairs formation and stability of adherens junctions and tight junctions; re-expression of CAMSAP3 rescues these defects. Inducible CAMSAP3 KO and re-expression in HaCaT cells, immunofluorescence, flow cytometry Experimental cell research Medium 38190868
2022 CAMSAP3 is required for formation and/or maintenance of the central microtubule pair in vestibular hair cell kinocilia; conditional knockout of CAMSAP3 results in shorter kinocilia and more frequent absence of the central MT pair, linking CAMSAP3 to axoneme length and stability. Conditional KO mouse model, immunofluorescence, transmission electron microscopy, behavioral assays Frontiers in cellular neuroscience Medium 35783105
2025 CAMSAP3-mediated microtubules are required for maintenance of transzonal projections (TZPs) between granulosa cells and oocytes in ovarian follicles; CAMSAP3 KO mice are infertile with fewer late-stage follicles, reduced TZP number, and disorganized microtubules in TZPs; CAMSAP3 also modulates TZP morphology by organizing both microtubules and F-actin. CAMSAP3 KO mice, super-resolution microscopy, TZP quantification, follicle staging bioRxivpreprint Medium bio_10.1101_2025.09.26.678897

Source papers

Stage 0 corpus · 24 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2012 Nezha/CAMSAP3 and CAMSAP2 cooperate in epithelial-specific organization of noncentrosomal microtubules. Proceedings of the National Academy of Sciences of the United States of America 130 23169647
2015 CAMSAP3 orients the apical-to-basal polarity of microtubule arrays in epithelial cells. Proceedings of the National Academy of Sciences of the United States of America 115 26715742
2016 Control of apico-basal epithelial polarity by the microtubule minus-end-binding protein CAMSAP3 and spectraplakin ACF7. Journal of cell science 70 27802168
2018 CAMSAP3 maintains neuronal polarity through regulation of microtubule stability. Proceedings of the National Academy of Sciences of the United States of America 59 30190432
2016 The CAMSAP3-ACF7 Complex Couples Noncentrosomal Microtubules with Actin Filaments to Coordinate Their Dynamics. Developmental cell 51 27693509
2018 Loss of CAMSAP3 promotes EMT via the modification of microtubule-Akt machinery. Journal of cell science 31 30282632
2020 CAMSAP3 facilitates basal body polarity and the formation of the central pair of microtubules in motile cilia. Proceedings of the National Academy of Sciences of the United States of America 29 32482850
2007 Nezha, a novel active miniature inverted-repeat transposable element in cyanobacteria. Biochemical and biophysical research communications 27 18035045
2021 Intercellular and intracellular cilia orientation is coordinated by CELSR1 and CAMSAP3 in oviduct multi-ciliated cells. Journal of cell science 21 33468623
2017 CAMSAP3 accumulates in the pericentrosomal area and accompanies microtubule release from the centrosome via katanin. Journal of cell science 18 28386021
2023 Paracingulin recruits CAMSAP3 to tight junctions and regulates microtubule and polarized epithelial cell organization. Journal of cell science 16 37013686
2016 Cadherin 23-C Regulates Microtubule Networks by Modifying CAMSAP3's Function. Scientific reports 14 27349180
2023 CAMSAP3 negatively regulates lung cancer cell invasion and angiogenesis through nucleolin/HIF-1α mRNA complex stabilization. Life sciences 13 37019300
2021 Cyst formation in proximal renal tubules caused by dysfunction of the microtubule minus-end regulator CAMSAP3. Scientific reports 13 33712686
2021 CAMSAP3 depletion induces lung cancer cell senescence-associated phenotypes through extracellular signal-regulated kinase inactivation. Cancer medicine 13 34724356
2021 Tracheal motile cilia in mice require CAMSAP3 for the formation of central microtubule pair and coordinated beating. Molecular biology of the cell 12 34319756
2016 CAMSAP3-dependent microtubule dynamics regulates Golgi assembly in epithelial cells. Journal of genetics and genomics = Yi chuan xue bao 12 28089391
2021 CAMSAP3 is required for mTORC1-dependent ependymal cell growth and lateral ventricle shaping in mouse brains. Development (Cambridge, England) 11 33462112
2024 Adaptability and nutritional analysis of a newly isolated Chlorella sp. NeZha in brackish and marine environments with potential bioeconomic impacts. Frontiers in nutrition 5 39206305
2024 CAMSAP3, a microtubule orientation regulator, plays a vital role in manifesting differentiation-dependent characteristics in keratinocytes. Experimental cell research 4 38190868
2024 CAMSAP3-mediated regulation of HMGB1 acetylation and subcellular localization in lung cancer cells: Implications for cell death modulation. Biochimica et biophysica acta. General subjects 3 38598971
2022 Vestibular Hair Cells Require CAMSAP3, a Microtubule Minus-End Regulator, for Formation of Normal Kinocilia. Frontiers in cellular neuroscience 3 35783105
2024 CAMSAP3 forms dimers via its α-helix domain that directly stabilize non-centrosomal microtubule minus ends. Journal of cell science 2 39479887
2025 Cytoskeletal remodeling via CAMSAP3 downregulation drives resistance to osimertinib in NSCLC cells. Cell death & disease 0 41381443