Affinage

CAMSAP3

Calmodulin-regulated spectrin-associated protein 3 · UniProt Q9P1Y5

Length
1249 aa
Mass
134.8 kDa
Annotated
2026-06-09
25 papers in source corpus 21 papers cited in narrative 21 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

CAMSAP3 is a microtubule minus-end binding protein that organizes noncentrosomal microtubule arrays, working together with CAMSAP2 to decorate and stabilize minus ends while suppressing centrosomal microtubule-organizing activity (PMID:23169647). It binds minus ends through its CKK domain, and C-terminal α-helix-mediated dimerization both enhances CKK affinity and enables dynamic regulation of the minus end (PMID:39479887). By accumulating at and coordinating with dynein and katanin, it drives microtubule release from the centrosome to generate the noncentrosomal pool (PMID:28386021). In epithelial cells CAMSAP3 concentrates at apical cortices to tether longitudinal microtubule minus ends and establish apico-basal polarity, a localization that requires its CC1 domain and recruitment to tight junctions via direct coiled-coil interaction with paracingulin (CGNL1) (PMID:26715742, PMID:37013686); apical anchoring and crosstalk with the actin cytoskeleton additionally depend on the spectraplakin ACF7/MACF1 (PMID:27802168, PMID:27693509). Through this microtubule scaffold CAMSAP3 positions organelles including the Golgi (via CG-NAP) and the endosomal-lysosomal system (PMID:28089391, PMID:41381443). In neurons it preferentially decorates less-acetylated axonal microtubules and antagonizes αTAT1-mediated tubulin acetylation to enforce single-axon polarity (PMID:30190432). In multiciliated cells it localizes to the basal body/basal plate region and is required for assembly of the central microtubule pair and synchronized ciliary beating (PMID:32482850, PMID:34319756, PMID:33468623), and it supports transzonal projection architecture and follicle maturation in the ovary (PMID:42199928). CAMSAP3 also constrains tumor-relevant signaling, suppressing acetylation-driven Akt activity and EMT, sustaining ERK signaling via a vimentin scaffold, and modulating HIF-1α, mTORC1, YAP/PIEZO1, and HMGB1-dependent outputs (PMID:30282632, PMID:33462112, PMID:33712686, PMID:34724356, PMID:37019300, PMID:38598971).

Mechanistic history

Synthesis pass · year-by-year structured walk · 11 steps
  1. 2012 High

    Established that CAMSAP3, together with CAMSAP2, defines and stabilizes noncentrosomal microtubules by clustering at their minus ends while suppressing centrosomal microtubule growth, answering how epithelial cells build microtubule arrays not nucleated at the centrosome.

    Evidence siRNA co-depletion with live imaging and immunofluorescence in epithelial cells

    PMID:23169647

    Open questions at the time
    • Did not resolve the molecular basis of minus-end recognition
    • Did not distinguish CAMSAP2- vs CAMSAP3-specific roles
  2. 2015 High

    Showed CAMSAP3 tethers microtubule minus ends to the apical cortex via its CC1 domain to orient arrays along the apico-basal axis, connecting minus-end binding to epithelial architecture and organelle positioning.

    Evidence Mutation/knockdown, domain deletion, and forced mislocalization in mouse intestine and Caco-2 cells

    PMID:26715742

    Open questions at the time
    • Did not identify the apical anchor that captures CAMSAP3
    • Mechanism of CC1-dependent localization unresolved
  3. 2016 High

    Identified ACF7/MACF1 as a CAMSAP3 partner that anchors minus-end-decorated microtubules to the apical cortex and to F-actin, explaining how the noncentrosomal array is physically coupled to the actin cytoskeleton and migration machinery.

    Evidence Co-IP/pulldown, CAMSAP3 vs CAMSAP2 knockout comparison, live imaging, and migration/focal adhesion assays in two labs

    PMID:27693509 PMID:27802168

    Open questions at the time
    • Structural basis of the CAMSAP3-ACF7 interaction not defined
    • How retrograde actin flow is transmitted to minus ends unresolved
  4. 2016 Medium

    Linked CAMSAP3 to Golgi organization and identified the CKK-binding CDH23-C interaction, showing CAMSAP3 microtubule output positions the Golgi and that a disease-associated CDH23 mutation weakens the interaction.

    Evidence Co-IP and knockdown for CG-NAP; in vitro binding, bundling assays and mutagenesis for CDH23-C

    PMID:27349180 PMID:28089391

    Open questions at the time
    • CG-NAP findings from a single lab with two methods
    • Functional consequence of CDH23-C regulation of bundling in vivo not established
  5. 2017 Medium

    Defined the source of noncentrosomal microtubules by showing CAMSAP3 acts with dynein and katanin to release microtubules from the centrosome, establishing its role upstream of minus-end stabilization.

    Evidence siRNA knockdown, co-depletion epistasis with dynein/katanin, and live imaging in epithelial cells

    PMID:28386021

    Open questions at the time
    • Single lab
    • Order of severing vs CAMSAP3 capping at the centrosome not fully resolved
  6. 2018 High

    Revealed a neuronal function in which CAMSAP3 maintains a nonacetylated axonal microtubule pool by antagonizing αTAT1, placing it upstream of tubulin acetylation in single-axon polarity, and connected the same acetylation axis to Akt-driven EMT in cancer.

    Evidence Mouse mutation, knockdown/overexpression with αTAT1 epistasis in neurons; deletion with EMT/Akt readouts in lung carcinoma

    PMID:30190432 PMID:30282632

    Open questions at the time
    • Mechanism by which CAMSAP3 inhibits αTAT1 not defined
    • Cancer Akt/EMT findings from a single lab
  7. 2020 High

    Extended CAMSAP3 function to motile cilia, showing it localizes to basal bodies/basal plate and is required for central microtubule pair assembly and synchronized beating, and to basal body orientation in oviduct MCCs.

    Evidence Mouse hypomorph and Xenopus morpholino knockdown with EM and ciliary beat analysis; mutant mice with super-resolution imaging

    PMID:32482850 PMID:33468623 PMID:34319756

    Open questions at the time
    • How a minus-end protein templates the central pair mechanistically unclear
    • Relationship between CAMSAP3 cilia role and PCP signaling only placed parallel/downstream
  8. 2021 Medium

    Connected CAMSAP3-dependent microtubule organization to downstream signaling in tissue morphogenesis, linking it to mTORC1/lysosome positioning in ependymal cells and to YAP/PIEZO1 mechanosensing in renal tubules.

    Evidence Camsap3 mutant mice with lysosome/mTORC1 readouts and with YAP/PIEZO1 assays and histology

    PMID:33462112 PMID:33712686

    Open questions at the time
    • Each pathway shown by a single lab
    • Direct vs indirect coupling of microtubule arrays to these signaling nodes not dissected
  9. 2023 High

    Identified paracingulin (CGNL1) as the direct tight-junction receptor that recruits CAMSAP3 to junctions, providing the long-sought apical anchor and confirming junction-tethered minus-end capping by super-resolution imaging.

    Evidence GST pulldown, CGNL1/PLEKHA7 knockout, ultrastructure expansion microscopy, 3D cyst and in vivo intestine

    PMID:37013686

    Open questions at the time
    • How CGNL1-ZO-1 pool coordinates with ACF7 anchoring unresolved
    • Structure of the CGNL1-CAMSAP3 coiled-coil interface not defined
  10. 2024 Medium

    Provided the biochemical basis of minus-end engagement by showing C-terminal α-helix dimerization enhances CKK-domain affinity and enables dynamic minus-end regulation, and extended the cancer scaffolding role to vimentin/ERK, nucleolin/HIF-1α, HMGB1, and EGFR trafficking.

    Evidence In vitro dimerization/MT binding assays with mutagenesis; CRISPR KO with IP-MS, RNA-IP, trafficking and drug-resistance assays in NSCLC

    PMID:34724356 PMID:37019300 PMID:38598971 PMID:39479887 PMID:41381443

    Open questions at the time
    • Signaling scaffold findings each from single labs
    • Whether scaffolding is microtubule-dependent or a distinct moonlighting function unresolved
  11. 2025 Medium

    Demonstrated an organismal reproductive requirement, showing CAMSAP3 microtubules support granulosa cell transzonal projections and follicle maturation, with knockout mice infertile.

    Evidence Camsap3 knockout mice with super-resolution microscopy and fertility assays

    PMID:42199928

    Open questions at the time
    • Single lab
    • Mechanism linking minus-end organization to TZP stability not defined

Open questions

Synthesis pass · forward-looking unresolved questions
  • How CAMSAP3's biochemical minus-end activity is integrated across its diverse anchoring partners and signaling scaffolds to produce tissue-specific outcomes remains unresolved.
  • No unified structural model of CAMSAP3 with its anchors
  • Whether signaling scaffold roles require microtubule binding is untested across contexts

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0008092 cytoskeletal protein binding 3
Localization
GO:0005815 microtubule organizing center 3 GO:0005856 cytoskeleton 3 GO:0005886 plasma membrane 3 GO:0005929 cilium 3
Pathway
R-HSA-1266738 Developmental Biology 3 R-HSA-1852241 Organelle biogenesis and maintenance 3
Partners
AKAP9CAMSAP2CDH23CGNL1HMGB1MACF1NCLVIM

Evidence

Reading pass · 21 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. Depletion of both CAMSAPs caused marked reduction of microtubules with polymerizing plus ends and induced centrosomal microtubule growth, demonstrating that CAMSAP2 and CAMSAP3 cooperatively maintain noncentrosomal microtubules and suppress centrosomal microtubule-organizing activity. 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 intestinal and Caco-2 epithelial cells and tethers longitudinal microtubule minus ends to these sites, thereby orienting microtubule arrays along the apico-basal axis with minus ends apical. The CC1 domain of CAMSAP3 is required for apical localization; forced mislocalization of CAMSAP3 disrupts epithelial architecture. Loss of CAMSAP3 causes random microtubule orientation and perturbed Golgi/nucleus positioning. Camsap3 mutation/siRNA knockdown, domain deletion analysis, forced mislocalization, immunofluorescence in mouse intestinal cells and Caco-2 cells Proceedings of the National Academy of Sciences of the United States of America High 26715742
2016 ACF7 (MACF1), a spectraplakin, specifically binds to CAMSAP3 and is required for apical localization of CAMSAP3-decorated microtubule minus ends in intestinal epithelial cells. Knockout of CAMSAP3 (but not CAMSAP2) caused microtubule reorganization into a radial centrosomal array, redistribution of Rab11-positive endosomes from apical surface to pericentrosomal region, and inhibition of actin brush border formation at the apical side. Co-IP/binding assay, CAMSAP3 knockout, CAMSAP2 knockout, 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 in Caco-2 epithelial cells. This CAMSAP3-ACF7 complex enables noncentrosomal microtubules to crosstalk with F-actin via retrograde flow, maintaining microtubule length and perpendicular orientation to the cell edge, and regulating focal adhesion size and cell migration. Co-IP, pulldown, live imaging, siRNA knockdown, focal adhesion/migration assays in Caco-2 cells Developmental cell High 27693509
2016 CAMSAP3 binds CG-NAP (centrosome and Golgi localized PKN-associated protein) and plays a role in translocation and clustering of Golgi vesicles in epithelial cells. Depletion of either CAMSAP3 or CG-NAP causes Golgi membrane fragmentation. Stathmin-dependent microtubule dynamics, highest at the perinuclear region, also contributes to perinuclear Golgi distribution. Co-IP, siRNA knockdown, immunofluorescence in epithelial cells Journal of genetics and genomics Medium 28089391
2016 CDH23-C (C isoform of cadherin-related 23) directly binds the CKK domain of CAMSAP3 via a conserved N-terminal CKK-binding motif (CBM), and this interaction inhibits CAMSAP3-induced microtubule bundle formation. The Usher Syndrome 1D-associated mutation CDH23 R3175H (mouse R55H) reduces CDH23-C interaction with CAMSAP3 both in vivo and in vitro. In vitro binding assay, pulldown, in vitro MT bundling assay, site-directed mutagenesis Scientific reports Medium 27349180
2017 CAMSAP3 accumulates in the pericentrosomal area and accompanies microtubule release from the centrosome. Depletion of CAMSAP3 prevents MT release and causes MT focusing at centrosomes. CAMSAP3 coordinates with dynein and katanin to regulate MT detachment from the centrosome, identifying it as a key molecule for generation of noncentrosomal microtubules. siRNA knockdown, immunofluorescence, live imaging, co-depletion experiments with dynein and katanin in epithelial cells Journal of cell science Medium 28386021
2018 CAMSAP3 is enriched in axons of hippocampal neurons where it localizes preferentially along less-acetylated microtubules. CAMSAP3 mutation causes supernumerary axons and increased nocodazole-resistant/acetylated microtubules. CAMSAP3 depletion promotes tubulin acetylation and overexpression inhibits it, indicating CAMSAP3 retains a nonacetylated microtubule pool by interfering with αTAT1 activity. Depletion of αTAT1 abolished CAMSAP3-loss-dependent multiple-axon formation, placing CAMSAP3 upstream of αTAT1 in neuronal polarity maintenance. Camsap3 mouse mutation, siRNA knockdown, overexpression, αTAT1 depletion epistasis, immunofluorescence, nocodazole resistance assay in hippocampal neurons Proceedings of the National Academy of Sciences of the United States of America High 30190432
2018 CAMSAP3 loss in lung carcinoma cells increases tubulin acetylation, which upregulates Akt (protein kinase B) activity and promotes epithelial-to-mesenchymal transition (EMT) at the transcriptional level. CAMSAP3 therefore functions to suppress Akt activity via microtubule regulation, protecting epithelial phenotype. CAMSAP3 deletion, immunoblotting, EMT marker analysis, Akt activity assay in lung carcinoma cell lines Journal of cell science Medium 30282632
2020 CAMSAP3 localizes to the base of axonemes and at basal bodies in multiciliated cells (MCCs). In Camsap3 knockdown/hypomorph mice and Xenopus morpholino knockdown, the central microtubule pairs are missing from the majority of cilia, basal body polarity is disorganized, and synchronized ciliary beating is defective. This identifies CAMSAP3 as required for central MT pair assembly/stability in motile cilia. Camsap3 hypomorph mouse model, Xenopus morpholino knockdown, immunofluorescence, electron microscopy, ciliary beat analysis Proceedings of the National Academy of Sciences of the United States of America High 32482850
2021 CAMSAP3 concentrates at multiple sites of the cilium-basal body complex including the axonemal basal plate where the central pair of microtubules (CP) initiates. CAMSAP3 dysfunction results in loss of the CP, partial distortion of the basal plate, and failure of multicilia to undergo synchronized beating in tracheal airway epithelial cells. Camsap3 mutant mouse model, immunofluorescence, electron microscopy, high-speed videomicroscopy of ciliary beating Molecular biology of the cell High 34319756
2021 In mouse oviduct MCCs, CAMSAP3 localizes to the base of cilia in a polarized manner and is critical for intracellular basal body (BB) orientation and for assembly of microtubules interconnecting basal bodies. CAMSAP3 mutation disrupts intracellular coordination of BB orientation without affecting planar cell polarity (PCP) factor localization, placing CAMSAP3 function downstream of or parallel to PCP signaling. Camsap3 mutant mice, immunofluorescence, super-resolution microscopy, genetic comparison with CELSR1 mutants Journal of cell science Medium 33468623
2021 In ependymal cells, CAMSAP3 concentrates at apical domains to generate MT networks. Camsap3-mutated mice exhibit narrowed lateral ventricles due to failure of ependymal cells to broaden their apical domain. mTORC1 activity, required for ependymal cell growth, is downregulated in mutant cells, and lysosomes (which activate mTORC1) are reduced at apical regions where MT networks are disorganized, linking CAMSAP3-dependent MT organization to mTORC1 signaling and ventricle shaping. Camsap3 mutant mouse, immunofluorescence, lysosome localization assay, mTORC1 activity measurement, apical domain morphometry Development (Cambridge, England) Medium 33462112
2021 In mouse proximal convoluted tubules, CAMSAP3 mutation perturbs microtubule arrays and activates mechanosensors YAP and PIEZO1, leading to enhanced cell proliferation, cell flattening, and cyst formation. This places CAMSAP3-mediated microtubule networks upstream of mechanosensitive YAP/PIEZO1 signaling in renal tubule morphology maintenance. Camsap3 mutant mice, immunofluorescence, YAP/PIEZO1 activity assays, histology Scientific reports Medium 33712686
2021 CAMSAP3 knockout promotes lung cancer cell senescence-associated phenotypes and G1 cell cycle arrest. Mechanistically, phosphorylated ERK is markedly downregulated in CAMSAP3-deleted cells, suppressing cyclin D1. Proteomic analysis identified vimentin as a scaffold required for CAMSAP3-modulated ERK signaling. Full-length CAMSAP3 abrogates these phenotypes. CAMSAP3 CRISPR knockout, immunoprecipitation/mass spectrometry, Western blotting, xenograft model Cancer medicine Medium 34724356
2023 Paracingulin (CGNL1), but not PLEKHA7, recruits CAMSAP3 to tight junctions. GST pulldown shows CGNL1 interacts directly with CAMSAP3 via their respective coiled-coil regions. Knockout of CGNL1 causes loss of junctional CAMSAP3, disorganized cytoplasmic microtubules, irregular nuclei alignment, altered cyst morphogenesis, and disrupted planar apical microtubules. Ultrastructure expansion microscopy shows CAMSAP3-capped microtubules are tethered to junctions by the ZO-1-associated pool of CGNL1. GST pulldown, CGNL1/PLEKHA7 knockout, ultrastructure expansion microscopy, immunofluorescence, 3D cyst culture, in vivo mouse intestinal epithelium Journal of cell science High 37013686
2023 CAMSAP3 interacts with nucleolin (NCL) to regulate HIF-1α mRNA stabilization. In CAMSAP3-knockout NSCLC cells, HIF-1α expression is upregulated along with VEGFA and MMPs 2 and 9, increasing invasion and angiogenesis. These effects were attenuated by reintroduction of wild-type CAMSAP3. CAMSAP3 CRISPR knockout, immunoprecipitation, mass spectrometry, RNA immunoprecipitation, qRT-PCR, in vivo xenograft Life sciences Medium 37019300
2024 CAMSAP3 forms dimers through its C-terminal α-helix domain. This dimerization enhances the microtubule-binding affinity of the CKK domain and enables the CKK domain to regulate microtubule dynamics. The combined action of the microtubule-binding domain (MBD) and the C-terminal α-helix enables CAMSAP3 to decorate minus ends and achieve dynamic regulation of microtubule minus ends. Biochemical dimerization assays, domain deletion/mutagenesis, in vitro microtubule binding and dynamics assays Journal of cell science High 39479887
2024 CAMSAP3 interacts with HMGB1, particularly with its acetylated form. In the presence of the HDAC inhibitor trichostatin A (TSA), CAMSAP3-HMGB1 complex formation is elevated, facilitating HMGB1 cytoplasmic translocation and secretion, thereby inducing autophagic cell death. CAMSAP3 knockout abolishes TSA-mediated autophagic cell death in lung cancer cells. CRISPR-Cas9 knockout, immunoprecipitation, proteomics, immunofluorescence, autophagic detection assays Biochimica et biophysica acta. General subjects Medium 38598971
2024 CAMSAP3 is essential for proper localization of the microtubule-dependent endosomal-lysosomal system. CAMSAP3 depletion causes EGFR translocation to the perinuclear MTOC, blocking plasma membrane recycling and promoting lysosomal EGFR degradation, thereby reducing EGFR signaling and increasing osimertinib resistance in NSCLC. CAMSAP3 siRNA knockdown and overexpression, immunofluorescence, in vitro and xenograft drug sensitivity assays Cell death & disease Medium 41381443
2025 Camsap3-mediated microtubules are present in transzonal projections (TZPs) of granulosa cells extending to oocytes in ovarian follicles. Camsap3 knockout mice are infertile and lack ovulation; their follicles show reduced TZP numbers, disorganized TZP microtubules, and decreased granulosa cell-oocyte contact, identifying CAMSAP3 as required for TZP architecture and follicle maturation. Camsap3 knockout mice, super-resolution microscopy, follicle counting, fertility assays iScience Medium 42199928

Source papers

Stage 0 corpus · 25 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 131 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 117 26715742
2016 Control of apico-basal epithelial polarity by the microtubule minus-end-binding protein CAMSAP3 and spectraplakin ACF7. Journal of cell science 71 27802168
2018 CAMSAP3 maintains neuronal polarity through regulation of microtubule stability. Proceedings of the National Academy of Sciences of the United States of America 62 30190432
2016 The CAMSAP3-ACF7 Complex Couples Noncentrosomal Microtubules with Actin Filaments to Coordinate Their Dynamics. Developmental cell 51 27693509
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 32 32482850
2018 Loss of CAMSAP3 promotes EMT via the modification of microtubule-Akt machinery. Journal of cell science 32 30282632
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 23 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
2023 CAMSAP3 negatively regulates lung cancer cell invasion and angiogenesis through nucleolin/HIF-1α mRNA complex stabilization. Life sciences 14 37019300
2016 Cadherin 23-C Regulates Microtubule Networks by Modifying CAMSAP3's Function. Scientific reports 14 27349180
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
2022 Vestibular Hair Cells Require CAMSAP3, a Microtubule Minus-End Regulator, for Formation of Normal Kinocilia. Frontiers in cellular neuroscience 4 35783105
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
2024 CAMSAP3 forms dimers via its α-helix domain that directly stabilize non-centrosomal microtubule minus ends. Journal of cell science 2 39479887
2026 Camsap3-mediated microtubules maintain transzonal projections essential for soma-germ communication during ovarian follicle maturation in mice. iScience 0 42199928
2025 Cytoskeletal remodeling via CAMSAP3 downregulation drives resistance to osimertinib in NSCLC cells. Cell death & disease 0 41381443

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