Affinage

CNTN1

Contactin-1 · UniProt Q12860

Round 2 corrected
Length
1018 aa
Mass
113.3 kDa
Annotated
2026-04-28
130 papers in source corpus 33 papers cited in narrative 33 extracted findings

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

CNTN1 (contactin-1/F3) is a GPI-anchored immunoglobulin superfamily cell adhesion molecule with six Ig-like domains and four fibronectin type III repeats that functions as a multivalent signaling hub in neural development, myelination, and synaptic plasticity (PMID:2474555, PMID:7959734). Through its Ig domains it engages extracellular ligands including RPTPβ, tenascin-R/C, Caspr, and Notch receptors, while its FNIII repeats recruit the Src-family kinase Fyn and chaperone Caspr to lipid-raft microdomains for surface delivery and paranodal junction assembly (PMID:7628014, PMID:8907714, PMID:10769038, PMID:7595520). CNTN1 acts as a non-canonical Notch ligand on oligodendrocyte precursors, triggering Deltex1-dependent signaling that promotes oligodendrocyte differentiation and myelination, and it increases neuronal Nav1.2 surface density via the β1 subunit at nodes of Ranvier (PMID:14567914, PMID:11567041). In vivo, CNTN1 is required for cerebellar granule cell axon guidance, cortical neuronal migration through suppression of RhoA, and hippocampal neurogenesis and synaptic plasticity via BDNF–CREB signaling and microglia–astrocyte crosstalk (PMID:10595523, PMID:30515076, PMID:37196127, PMID:35609645).

Mechanistic history

Synthesis pass · year-by-year structured walk · 14 steps
  1. 1989 High

    Establishing that CNTN1 is a GPI-anchored Ig-superfamily member on neuronal surfaces resolved its structural class and membrane attachment mode, foundational for all subsequent interaction studies.

    Evidence cDNA cloning, sequence analysis, immunocytochemistry, and subcellular fractionation of mouse brain

    PMID:2474555

    Open questions at the time
    • No functional role demonstrated
    • No interacting partners identified
  2. 1995 High

    Identifying RPTPβ as an extracellular ligand for CNTN1 and demonstrating that CNTN1 resides in lipid rafts in complex with Fyn and L1 established CNTN1 as a signal-transducing receptor despite lacking a transmembrane domain.

    Evidence Expression cloning, neurite outgrowth assays with antibody blocking (RPTPβ), co-IP from cerebellum with detergent-resistant membrane fractionation (Fyn/L1)

    PMID:7595520 PMID:7628014

    Open questions at the time
    • Downstream signaling cascades beyond Fyn phosphorylation undefined
    • Structural basis of RPTPβ–CNTN1 interaction unknown
  3. 1996 High

    Mapping signal transduction to the FNIII repeats of CNTN1 resolved how a GPI-anchored protein without an intracellular domain can activate tyrosine kinase signaling — through domain-specific association with Fyn kinase.

    Evidence Truncation mutants in CHO cells, metabolic 32P labeling, co-IP with Fyn from cerebellum

    PMID:8907714

    Open questions at the time
    • Identity of downstream substrates of Fyn activated by CNTN1 unknown
    • Whether FNIII–Fyn interaction is direct or via an adaptor not resolved
  4. 1998 High

    Demonstrating that CNTN1 Ig domains interact with tenascin-R to promote neurite defasciculation via PKC signaling, and that TAG-1 modulates CNTN1 effects in lipid rafts, revealed CNTN1 as a context-dependent regulator of axon fasciculation.

    Evidence Cerebellar explant cultures, antibody/antisense perturbation, pharmacological PKC inhibition; CHO co-transfection and co-IP from brain for TAG-1

    PMID:9589384 PMID:9712656

    Open questions at the time
    • PKC isoform specificity not determined
    • Stoichiometry and dynamics of the CNTN1–TAG-1 raft complex undefined
  5. 1999 High

    The contactin-null mouse phenotype — lethal ataxia with granule cell axon guidance defects — proved that CNTN1 is essential for cerebellar circuit formation in vivo, moving beyond cell-culture studies.

    Evidence Gene knockout by homologous recombination, histological analysis of cerebellum, behavioral assessment

    PMID:10595523

    Open questions at the time
    • Molecular pathways disrupted in vivo not identified
    • Contribution of individual CNTN1 interactions to cerebellar phenotype unresolved
  6. 1999 High

    Discovering that CNTN1 chaperones Caspr to the plasma membrane via lipid-raft recruitment through its FNIII repeats explained how the Caspr–CNTN1 complex assembles at paranodal junctions.

    Evidence Co-transfection in CHO/neuroblastoma cells, surface biotinylation, Triton X-100 fractionation, domain-deletion mapping

    PMID:10769038

    Open questions at the time
    • Whether additional factors stabilize the complex at paranodes not tested
    • Mechanism by which GPI anchor plus FNIII domains recruit Caspr to rafts structurally unresolved
  7. 2001 High

    Showing that CNTN1 increases Nav1.2 surface density through specific interaction with the β1 subunit at nodes of Ranvier established a direct role in sodium channel clustering and saltatory conduction.

    Evidence Co-IP from brain, electrophysiology showing 3–4-fold current increase, saxitoxin binding, co-localization at nodes

    PMID:11567041

    Open questions at the time
    • Whether CNTN1 is required for Nav channel clustering in vivo not tested with knockout
    • Interplay between CNTN1–β1 and ankyrin-dependent clustering incompletely dissected
  8. 2003 High

    Identifying CNTN1 as a non-canonical Notch ligand that triggers Deltex1-dependent, RBP-J-independent signaling to promote oligodendrocyte differentiation revealed a novel myelination pathway distinct from canonical Notch signaling.

    Evidence Cell co-culture with NICD translocation assays, MAG induction, dominant-negative Notch/Deltex1/RBP-J constructs, gamma-secretase inhibition

    PMID:14567914

    Open questions at the time
    • In vivo requirement for CNTN1–Notch in myelination not demonstrated by conditional knockout
    • Structural basis for CNTN1–Notch interaction unknown
  9. 2003 High

    Demonstrating that Caspr regulates CNTN1 glycoform processing and gates its ability to bind NF155 revealed bidirectional regulation within the paranodal complex — CNTN1 delivers Caspr to the surface, but Caspr reciprocally controls CNTN1's binding repertoire.

    Evidence Co-IP, EndoH glycosylation analysis, Caspr knockout mouse glycoform shift

    PMID:14676309

    Open questions at the time
    • Functional consequence of altered glycoform for paranodal integrity not fully tested
    • Whether glycoform regulation occurs in all neuronal subtypes unclear
  10. 2016 High

    Placing CNTN1 upstream of PI3K/AKT activation and E-cadherin suppression in prostate cancer extended its role beyond neural contexts and identified it as a driver of invasion and chemoresistance via EMT.

    Evidence shRNA knockdown and overexpression in DU145 cells, xenograft models, western blotting for pAKT and E-cadherin

    PMID:26795349 PMID:33488868

    Open questions at the time
    • Direct biochemical mechanism linking CNTN1 to PI3K activation not identified
    • Whether GPI-anchored CNTN1 signals through the same raft/Fyn mechanism in cancer cells unknown
  11. 2018 High

    Demonstrating that CNTN1 knockdown impairs cortical neuronal migration and upregulates RhoA — rescued by dominant-negative RhoA — established CNTN1 as a negative regulator of RhoA during corticogenesis, adding a migration role beyond axon guidance.

    Evidence In utero electroporation with shRNA, dominant-negative RhoAN19 rescue, immunohistochemistry

    PMID:30515076

    Open questions at the time
    • Mechanism by which GPI-anchored CNTN1 suppresses RhoA activity not identified
    • Whether this pathway operates in adult neuronal migration unknown
  12. 2019 High

    Passive transfer of anti-CNTN1 IgG3 autoantibodies causing complement-dependent paranodal conduction block in rats established CNTN1 as a pathogenic autoantibody target in inflammatory neuropathy.

    Evidence Passive transfer to Lewis rats, nerve conduction studies, paranodal complement immunohistochemistry

    PMID:30953561

    Open questions at the time
    • Whether complement fixation directly disrupts CNTN1–Caspr complex or causes broader paranodal damage unresolved
    • Human in vivo validation of IgG subclass-specific pathogenicity limited
  13. 2022 Medium

    Bidirectional AAV manipulation in the hippocampus showed that CNTN1 modulates depressive-like behavior through the BDNF–CREB signaling cascade and neurogenesis, extending its role to adult affective circuits.

    Evidence AAV-mediated overexpression and knockdown in hippocampus, chronic stress models, western blotting for BDNF/pCREB, behavioral assays

    PMID:35609645

    Open questions at the time
    • Direct molecular link between CNTN1 and BDNF expression not established
    • Cell-type specificity of CNTN1 action in hippocampus not resolved
  14. 2023 High

    Identifying microglia–astrocyte crosstalk as the downstream effector of hippocampal CNTN1 overexpression — with aberrant EAAT1/2 upregulation impairing LTP — revealed a non-cell-autonomous mechanism linking CNTN1 to cognitive dysfunction.

    Evidence AAV overexpression, LTP electrophysiology, minocycline pharmacological rescue, EAAT1/2 western blotting, microglia/astrocyte marker immunohistochemistry

    PMID:37196127

    Open questions at the time
    • Mechanism by which neuronal CNTN1 activates microglia is unknown
    • Whether CNTN1-mediated microglial activation involves direct cell contact or secreted factors not determined

Open questions

Synthesis pass · forward-looking unresolved questions
  • Key unresolved questions include the structural basis of CNTN1's multi-ligand recognition, the mechanism by which a GPI-anchored protein activates intracellular pathways such as PI3K/AKT and RhoA suppression, in vivo conditional knockout validation of the CNTN1–Notch myelination pathway, and the cell-type-specific signaling logic that determines whether CNTN1 promotes or impairs neurogenesis and plasticity.
  • No high-resolution structure of full-length CNTN1 or its complexes
  • No conditional knockout addressing myelination or hippocampal functions
  • Mechanism coupling GPI-anchored CNTN1 to intracellular RhoA or AKT signaling undefined

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0098631 cell adhesion mediator activity 8 GO:0060089 molecular transducer activity 3 GO:0048018 receptor ligand activity 2
Localization
GO:0005886 plasma membrane 5 GO:0005576 extracellular region 2 GO:0031410 cytoplasmic vesicle 2
Pathway
R-HSA-112316 Neuronal System 7 R-HSA-1500931 Cell-Cell communication 5 R-HSA-162582 Signal Transduction 4 R-HSA-1266738 Developmental Biology 3
Partners
CNTNAP1FYNL1CAMNOTCH1NRCAMPTPRZ1SCN1BSCN2A
Complex memberships
CNTN1-L1-Fyn lipid raft complexCNTN1-Nav1.2-β1 nodal complexCaspr-CNTN1-NrCAM paranodal complex

Evidence

Reading pass · 33 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
1989 Mouse F3 (CNTN1) is a GPI-anchored member of the immunoglobulin superfamily with six C2-type Ig-like domains and fibronectin type III repeats, anchored to the membrane via a phosphatidylinositol anchor (no transmembrane domain), and is distributed between buffer-soluble, nonionic detergent-soluble, and detergent-insoluble fractions in brain. It is expressed on the neuronal cell surface, most prominently on neurites, and its gene transcripts are developmentally regulated with highest expression between 1–2 weeks after birth. cDNA cloning, sequence analysis, immunoblotting, immunocytochemistry, subcellular fractionation The Journal of cell biology High 2474555
1993 F3/11 (CNTN1) mediates neuronal repulsion by the extracellular matrix glycoprotein J1-160/180 (tenascin): F3 on the neuronal surface recognizes J1-160/180 substrate, and this interaction induces loss of substrate adhesion and inhibition of neurite outgrowth. Antibody blocking of F3 prevents the avoidance response at J1-160/180 substrate borders, establishing F3 as the receptor mediating repellent signaling. Cell adhesion assays with F3-transfected CHO cells, cerebellar neuron culture on J1-160/180 substrates, antibody blocking experiments Neuron High 7678967
1994 Human contactin (CNTN1) encodes a GPI-anchored protein (confirmed by PI-PLC treatment and [3H]-ethanolamine metabolic labeling) with six C2 Ig-domains and four FNIII repeats, 94% identical to mouse F3 and 78% identical to chick contactin/F11. The CNTN1 gene maps to human chromosome 12q11-q12. cDNA cloning, PI-PLC treatment of transfected cells, metabolic labeling with [3H]-ethanolamine, fluorescence in situ hybridization Genomics High 7959734
1995 CNTN1 (F3) is localized to glycolipid-enriched membrane microdomains (lipid rafts) resistant to Triton X-100 solubilization in adult mouse cerebellum, and is physically associated in a complex with both the L1 transmembrane adhesion molecule and the fyn tyrosine kinase within these microdomains, as shown by co-immunoprecipitation. Detergent-resistant membrane fractionation, lipid composition analysis, co-immunoprecipitation from cerebellum extracts Journal of neurochemistry High 7595520
1995 The carbonic anhydrase (CAH) domain of receptor-type protein tyrosine phosphatase beta (RPTPbeta) binds specifically to contactin (CNTN1), a GPI-anchored neuronal recognition molecule, as identified by expression cloning. This interaction mediates cell adhesion and neurite growth of primary tectal neurons, and these responses are blocked by anti-contactin antibodies, establishing contactin as a functional neuronal receptor for RPTPbeta. Expression cloning in COS7 cells, fusion protein binding assays, neurite outgrowth assays with primary tectal neurons, antibody blocking Cell High 7628014
1996 F3 (CNTN1) transduces signals across the membrane despite being GPI-anchored: F3-mediated cell aggregation induces tyrosine phosphorylation in F3-transfected CHO cells. F3 forms non-covalent complexes with protein tyrosine kinase(s), identified as fyn kinase in postnatal cerebellum. The FNIII repeats of F3 are essential for kinase association and for modulation of tyrosine phosphorylation, as a truncated F3 lacking all FNIII repeats fails to associate with a kinase or modulate phosphorylation. 32P metabolic labeling, immunoprecipitation, antibody-mediated cross-linking, co-IP with fyn from cerebellum, truncation mutant analysis in CHO cells Journal of cell science High 8907714
1997 F3/contactin (CNTN1) is expressed not only by neurons but also by oligodendrocyte-lineage cells, including oligodendrocyte precursors and mature oligodendrocytes, and is present in myelin. Oligodendroglial F3 is GPI-anchored (sensitive to PI-PLC) and the same size mRNA as neuronal F3; F3 is absent from astrocytes. Biosynthetic labeling, 2D gel electrophoresis, microsequencing, Western blotting, immunoprecipitation, double immunofluorescence, Northern blots, PI-PLC cleavage Glia High 9063727
1997 RPTPbeta extracellular regions induce neurite outgrowth via both contactin (CNTN1) and Nr-CAM: the betaCFS fusion protein promotes neurite outgrowth that is inhibited by antibodies against both Nr-CAM and contactin. Contactin and Nr-CAM form a complex that co-immunoprecipitates with betaCFS, indicating a ternary complex. Recombinant Fc fusion proteins as substrates, neurite outgrowth assays with primary neurons, antibody inhibition, co-immunoprecipitation The Journal of cell biology High 9049255
1998 F3 and TAG-1 interact functionally on cerebellar granule cell neurites: F3 transfectants inhibit neurite outgrowth and induce fasciculation of granule cells, whereas co-expression of TAG-1 with F3 blocks this inhibitory effect. F3 co-immunoprecipitates with TAG-1 from Triton X-100-insoluble microdomains from newborn brain, and co-clustering of F3 and TAG-1 occurs in double-transfected CHO cells, indicating they associate in a multimolecular complex in lipid rafts to modulate axonal growth. CHO cell transfection co-culture assay with granule cells, microsphere binding, antibody-mediated cross-linking, co-immunoprecipitation from brain The Journal of neuroscience High 9712656
1998 Tenascin-R (TN-R) and its neuronal receptor F3 (CNTN1) promote neurite defasciculation in cerebellar explant cultures. Perturbation of this interaction by antibodies or antisense oligonucleotides increases fasciculation. The relevant domains are the N-terminal region of TN-R (containing cysteine-rich stretch and EGF-like repeats) and the Ig-like domains of F3. Defasciculation can be blocked by a protein kinase C inhibitor and reversed by a phorbol ester, implicating PKC signaling downstream. Cerebellar explant cultures, antibody and antisense oligonucleotide perturbation, domain mapping with recombinant proteins, pharmacological inhibition of PKC Journal of neuroscience research High 9589384
1998 F3/contactin (CNTN1) is localized in secretory granules in all compartments of oxytocin/vasopressin (HNS) neurons and is co-released by exocytosis at axon terminals in the neurohypophysis upon physiological stimulation (lactation, osmotic challenge). Surface expression is upregulated by stimulation and is restricted to axons; F3 mRNA increases more than threefold upon stimulation, following a regulated secretory pathway. Immunocytochemistry, immunoblot, in situ hybridization, confocal/electron microscopy, sucrose density gradient fractionation The Journal of neuroscience High 9651216
1999 NrCAM is identified as the functional receptor on cerebellar granule cell growth cones that mediates the inhibitory effect of F3 (CNTN1) on axonal elongation: F3Fc-conjugated microspheres bind to growth cones via heterophilic interaction with NrCAM but not L1. Time-lapse video microscopy shows F3Fc beads move retrogradely from the leading edge to the base of the growth cone at ~5.7 µm/min, consistent with coupling to retrograde actin flow; cytochalasin B disrupts this movement. Retrograde mobility requires NrCAM clustering. Microsphere binding assay, time-lapse video microscopy, cytochalasin B pharmacology, cross-linked vs. dimeric F3Fc chimera comparison Journal of cell science High 10462518
1999 F3 (CNTN1) Ig domains interact with Caspr/paranodin (a transmembrane neurexin superfamily protein), and this association is required for surface transport of Caspr. Co-transfection of F3 with Caspr in CHO or neuroblastoma cells results in plasma membrane delivery of Caspr (not achieved by Caspr alone). F3's GPI anchor and FNIII repeats cooperate to recruit Caspr into Triton X-100-insoluble lipid raft microdomains, enabling its plasma membrane targeting; a truncated F3 lacking FNIII repeats fails to recruit Caspr to rafts or the cell surface. Co-transfection in CHO/neuroblastoma cells, confocal microscopy, cell surface biotinylation, co-immunoprecipitation domain mapping, Triton X-100 fractionation The Journal of cell biology High 10769038
1999 F3/contactin (CNTN1) participates in bidirectional neuron-glia signaling: F3 Ig domains bind tenascin-R, tenascin-C, and isoforms of the proteoglycan-type protein tyrosine phosphatase RPTPz/beta expressed by glia. Preclustered F3IgFc specifically modifies distribution and intensity of phosphotyrosine labeling in glial C6 cells. Inhibition of tenascin-R/F3 interaction prevents defasciculation of cerebellar explants. F3IgFc binds strongly to astrocytes and C6 astrocytoma cells. F3IgFc chimera binding to primary cultures and astrocytoma cells, fluorosphere binding, brain extract pull-down, cerebellar explant cultures, phosphotyrosine immunostaining Advances in experimental medicine and biology Medium 10635039
2001 F3/contactin (CNTN1) surface expression in hypothalamic oxytocin neurons is polarized to axons and is mobilized to the axonal surface via the activity-dependent regulated secretory pathway. Re-expression after GPI-PLC removal is accelerated by K+ depolarization or bicuculline (GABA-A blockade) and inhibited by Mn2+ (Ca2+ channel block), tetrodotoxin (Na+ channel block), or glutamate antagonists, demonstrating that externalization depends on Ca2+ entry and electrical activity. GPI-PLC treatment of live organotypic slice cultures, immunocytochemistry of live vs. fixed cells, K+ depolarization, pharmacological inhibition The European journal of neuroscience High 11556889
2001 Contactin (CNTN1) associates with voltage-gated Na+ channel Nav1.2 alpha subunits and the beta1 subunit in brain. Co-transfection of contactin with Nav1.2alpha and beta1 in cells increases peak Na+ currents 3–4 fold and increases Na+ channel surface membrane density (confirmed by saxitoxin binding). Contactin interacts specifically with the beta1 subunit (not beta2) by co-immunoprecipitation from cell lines. In the CNS, contactin and Na+ channels colocalize at nodes of Ranvier during development and in adults. Co-immunoprecipitation from brain homogenates and transfected cells, electrophysiology, saxitoxin binding, immunocytochemistry of developing and adult nodes The Journal of neuroscience High 11567041
2003 F3/contactin (CNTN1) acts as a functional ligand for Notch receptors on oligodendrocyte precursor cells. This trans-extracellular interaction triggers gamma-secretase-dependent nuclear translocation of the Notch intracellular domain (NICD). F3/Notch signaling promotes oligodendrocyte precursor cell differentiation and upregulates MAG in OLN-93 cells. This signaling is blocked by dominant-negative Notch1/Notch2 or Deltex1 mutants lacking RING-H2, but not by dominant-negative RBP-J or Hes1 antisense, establishing a non-canonical Notch/Deltex1 pathway distinct from Jagged/Notch canonical signaling. Cell co-culture, NICD nuclear translocation assays, MAG expression by western blot, dominant-negative constructs, gamma-secretase inhibition Cell High 14567914
2003 Caspr regulates the processing and surface transport of contactin (CNTN1): co-expression of Caspr with contactin produces a low molecular weight (LMw), endoglycosidase H-sensitive isoform of contactin at the cell membrane that remains associated with Caspr but is unable to bind neurofascin-155 (NF155). Conversely, NF155 binds directly to contactin when Caspr is absent. Deletion of Caspr in mice shifts contactin from the LMw to a HMw glycoform, confirming that Caspr regulates contactin's intracellular processing and transport, thereby gating its ability to interact with other CAMs. Co-immunoprecipitation, EndoH glycosylation analysis, transfection in heterologous cells, Caspr knockout mice The Journal of cell biology High 14676309
2004 Sodium channel beta1 subunit-mediated modulation of Nav1.2 and increase in cell surface density requires interaction with both contactin (CNTN1) and ankyrin. A beta1Y181E mutant that cannot interact with ankyrinG fails to modulate Nav1.2 channel function even though it associates with Nav1.2 and contactin. The contactin interaction site was mapped to two regions of the beta1 Ig loop using beta1/beta2 chimeras. beta1/beta2 chimera construction, electrophysiology, co-immunoprecipitation, cell surface expression measurement The Journal of biological chemistry High 14761957
1999 Contactin-null (contactin-/-) mice display severe ataxia and survive only until postnatal day 18. Cerebellar analysis reveals defects in granule cell axon guidance and in dendritic projections from granule and Golgi cells, demonstrating that contactin (CNTN1) controls axonal and dendritic interactions of cerebellar interneurons and is required for cerebellar microorganization in vivo. Gene knockout in mice (homologous recombination), behavioral assessment, histological and morphological analysis of cerebellum Neuron High 10595523
2003 Premature expression of F3/contactin (CNTN1) under TAG-1 regulatory sequences in transgenic mice causes a transient reduction in cerebellar size due to decreased granule cell proliferation (at P3) followed by increased cycling (at P8–P11), and failure of Purkinje cell dendritic elaboration. This demonstrates that precise spatiotemporal regulation of CNTN1 expression is critical for granule cell proliferation, differentiation, and Purkinje cell development. Transgenic mouse generation (TAG/F3), histological analysis, BrdU proliferation assays, cerebellar morphometry Development High 12441289
2005 Cntn1 (F3/contactin) is duplicated in teleost fish (goldfish, zebrafish, fugu), resulting in Cntn1a and Cntn1b paralogs that show subfunctionalization. In adult goldfish, Cntn1b is expressed in oligodendrocytes and is upregulated in retinal ganglion cells after optic nerve transection, suggesting a role in axonal regeneration in addition to development. Gene cloning, phylogenetic analysis, in situ hybridization during development, optic nerve transection model with subsequent expression analysis Molecular and cellular neurosciences Medium 15691716
2006 F3/contactin (CNTN1) interacts with Notch receptors and promotes oligodendrocyte development through a Deltex1-dependent, non-canonical Notch pathway. NB-3, another contactin family member, similarly interacts with Notch via Deltex1. This F3/Notch/Deltex1 signaling cascade promotes generation and maturation of oligodendrocyte precursor cells, distinct from the canonical Jagged1/Notch pathway which inhibits further differentiation. Cell co-culture assays, dominant-negative constructs, animal model analysis Developmental neuroscience Medium 16508301
2016 CNTN1 promotes prostate cancer metastasis: CNTN1 knockdown reduces prostate cancer stem-like cell (PCSC)-mediated tumor initiation, whereas CNTN1 overexpression enhances invasion in vitro and promotes xenograft tumor formation and lung metastasis in vivo. CNTN1 overexpression results in elevated AKT activation and reduced E-cadherin expression in DU145 cells and corresponding xenografts, placing CNTN1 upstream of AKT signaling and EMT. shRNA knockdown, overexpression in DU145 cells, xenograft mouse models, in vitro invasion assays, western blotting for AKT phosphorylation and E-cadherin Cancer research High 26795349
2011 VEGF-C upregulates CNTN1 expression in esophageal cancer cells, and CNTN1 mediates VEGF-C's pro-tumorigenic effects on cell proliferation and migration. Silencing of CNTN1 reverses the increased proliferation and migration induced by VEGF-C overexpression, indicating CNTN1 acts downstream of VEGF-C signaling in esophageal cancer progression. VEGF-C overexpression and shRNA knockdown in TE-1 and Eca-109 cells, CNTN1 siRNA rescue, cell proliferation and migration assays, nude mouse xenografts Cytokine Medium 21482472
2018 Contactin-1/F3 (Cntn1) is required for neuronal migration during cortical development. shRNA-mediated knockdown of Cntn1 in neural stem cells via in utero electroporation delays neuronal migration and causes abnormal leading process morphology with more multipolar cells in deep cortical layers. Cntn1 KD upregulates RhoA, and expression of dominant-negative RhoAN19 partially rescues the migration defects, placing Cntn1 upstream of RhoA as a negative regulator of this GTPase during cortical neuronal migration. In utero electroporation with shRNA, immunohistochemistry, dominant-negative RhoA rescue experiment Frontiers in molecular neuroscience High 30515076
2019 Anti-contactin-1 (CNTN1) IgG3 autoantibodies induce acute conduction block and motor deficits in rats via complement deposition at paranodal regions, without inflammatory infiltrates or dispersion of paranodal proteins. Intraneural injection of IgG3-predominant patient IgG caused conduction blocks in 83% of animals and paranodal complement deposition, whereas chronic-phase IgG4-predominant patient IgG caused less frequent and less severe effects, indicating IgG3 anti-CNTN1 mediates acute paranodopathy via complement. Passive transfer of patient IgG to Lewis rats, nerve conduction studies, immunohistochemistry for complement, motor function testing Journal of neuroinflammation High 30953561
2020 CNTN1 promotes docetaxel resistance and epithelial-to-mesenchymal transition (EMT) in prostate cancer via the PI3K/Akt signaling pathway. Knockdown of CNTN1 in docetaxel-resistant PC3 and DU145 cells attenuates proliferation, migration, invasion, EMT phenotype, and drug resistance, and decreases PI3K/Akt activity both in vitro and in vivo (xenograft model). shRNA knockdown in drug-resistant cell lines, CCK-8 proliferation assay, flow cytometry, wound-healing, transwell invasion, western blotting, xenograft mouse model Archives of medical science Medium 33488868
2013 F3/contactin promotes adult hippocampal neurogenesis, synaptic plasticity, and memory in mice: TAG/F3 transgenic mice overexpressing CNTN1 show increased hippocampal size, enhanced precursor proliferation, increased CA1 long-term potentiation, and improved spatial and object recognition memory. These effects correlate with increased phosphorylated CREB expression, suggesting CNTN1 overexpression activates the CREB signaling pathway to promote neurogenesis and synaptic plasticity. Transgenic mouse model (TAG/F3), BrdU/NeuN proliferation assays, LTP electrophysiology, behavioral memory tests, western blotting for pCREB Hippocampus Medium 23939883
2021 Cntn1 expression is upregulated in the hippocampus (but not medial prefrontal cortex) in response to chronic unpredictable stress (CUS) in rodents. Adeno-associated virus-mediated overexpression of Cntn1 in the hippocampus triggers anxiety- and depression-like phenotypes, activates microglia, upregulates pro-inflammatory cytokines (IL1α, IL6, Ccl2), downregulates anti-inflammatory cytokines (IL4, CD206), and impairs hippocampal immature neurons (decreased doublecortin+ cells). Chronic unpredictable stress model, AAV stereotactic injection for Cntn1 overexpression, real-time qPCR for cytokines, immunohistochemistry for doublecortin Brain, behavior, and immunity Medium 33737174
2022 Hippocampal F3/Contactin (CNTN1) is implicated in depression: chronic restraint stress and chronic social defeat stress decrease hippocampal CNTN1 expression. AAV-mediated overexpression of hippocampal CNTN1 prevents stress-induced depressive-like behaviors and reverses dysfunction of the hippocampal BDNF-CREB signaling cascade and neurogenesis impairment. Conversely, AAV-mediated knockdown of hippocampal CNTN1 abolishes the antidepressant effects of vortioxetine. Chronic stress mouse models, AAV-mediated overexpression and knockdown, western blotting, immunofluorescence for neurogenesis markers, behavioral tests Biochemical pharmacology Medium 35609645
2023 Hippocampal CNTN1 overexpression triggers cognitive deficits by boosting crosstalk between microglia and astrocytes. CNTN1 overexpression activates microglia, which triggers astrocyte activation with aberrant upregulation of excitatory amino acid transporters EAAT1/EAAT2, leading to LTP impairment. Minocycline (microglial activation inhibitor) reverses LTP impairment caused by CNTN1 overexpression, establishing that CNTN1-driven microglial activation is mechanistically upstream of astrocyte dysfunction and LTP deficits. AAV stereotactic injection for CNTN1 overexpression, LTP electrophysiology, immunohistochemistry for microglia/astrocyte markers, EAAT1/2 western blotting, minocycline pharmacological rescue, behavioral cognitive tests Aging and disease High 37196127
2024 Clemastine preferentially promotes F3/Contactin-1 (CNTN1)-mediated non-canonical Notch-1/Deltex-1 signaling over canonical Jagged-1/Notch-1 signaling during remyelination. In the EAE rat model, CLM restores CNTN1 levels, elevates Deltex-1 gene expression, and reduces HES1/5 (canonical Notch targets), correlating with enhanced oligodendrocyte differentiation and myelination markers (MBP, CNPase, PLP, ASPA). F3/CNTN1-mediated non-canonical Notch signaling is proposed as the mechanism underlying clemastine's remyelinating effect. EAE rat model, pharmacological clemastine treatment, behavioral tests (rotarod, open-field, grip), Luxol fast blue histology, immunohistochemistry, gene expression analysis International immunopharmacology Medium 38232534

Source papers

Stage 0 corpus · 130 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2002 Generation and initial analysis of more than 15,000 full-length human and mouse cDNA sequences. Proceedings of the National Academy of Sciences of the United States of America 1479 12477932
2015 The BioPlex Network: A Systematic Exploration of the Human Interactome. Cell 1118 26186194
2017 Architecture of the human interactome defines protein communities and disease networks. Nature 1085 28514442
2021 Dual proteome-scale networks reveal cell-specific remodeling of the human interactome. Cell 705 33961781
2011 Phylogenetic-based propagation of functional annotations within the Gene Ontology consortium. Briefings in bioinformatics 656 21873635
2004 The status, quality, and expansion of the NIH full-length cDNA project: the Mammalian Gene Collection (MGC). Genome research 438 15489334
2005 Diversification of transcriptional modulation: large-scale identification and characterization of putative alternative promoters of human genes. Genome research 409 16344560
1996 Normalization and subtraction: two approaches to facilitate gene discovery. Genome research 401 8889548
2008 A genome-wide association study identifies protein quantitative trait loci (pQTLs). PLoS genetics 390 18464913
1995 The carbonic anhydrase domain of receptor tyrosine phosphatase beta is a functional ligand for the axonal cell recognition molecule contactin. Cell 359 7628014
2005 Human plasma N-glycoproteome analysis by immunoaffinity subtraction, hydrazide chemistry, and mass spectrometry. Journal of proteome research 350 16335952
2007 What is an epigenetic transgenerational phenotype? F3 or F2. Reproductive toxicology (Elmsford, N.Y.) 345 17949945
2007 Huntingtin interacting proteins are genetic modifiers of neurodegeneration. PLoS genetics 325 17500595
2003 F3/contactin acts as a functional ligand for Notch during oligodendrocyte maturation. Cell 305 14567914
2013 Loci associated with N-glycosylation of human immunoglobulin G show pleiotropy with autoimmune diseases and haematological cancers. PLoS genetics 292 23382691
2011 A directed protein interaction network for investigating intracellular signal transduction. Science signaling 258 21900206
1989 The mouse neuronal cell surface protein F3: a phosphatidylinositol-anchored member of the immunoglobulin superfamily related to chicken contactin. The Journal of cell biology 258 2474555
1993 The F3/11 cell adhesion molecule mediates the repulsion of neurons by the extracellular matrix glycoprotein J1-160/180. Neuron 232 7678967
2019 A randomized, placebo-controlled trial of emricasan in patients with NASH and F1-F3 fibrosis. Journal of hepatology 198 31887369
1999 Ataxia and abnormal cerebellar microorganization in mice with ablated contactin gene expression. Neuron 190 10595523
2007 Ba/F3 cells and their use in kinase drug discovery. Current opinion in oncology 188 17133113
2015 Contactin 1 IgG4 associates to chronic inflammatory demyelinating polyneuropathy with sensory ataxia. Brain : a journal of neurology 159 25808373
2005 Epidermal growth factor-independent transformation of Ba/F3 cells with cancer-derived epidermal growth factor receptor mutants induces gefitinib-sensitive cell cycle progression. Cancer research 155 16204070
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