Affinage

CNTNAP1

Contactin-associated protein 1 · UniProt P78357

Length
1384 aa
Mass
156.3 kDa
Annotated
2026-04-28
100 papers in source corpus 20 papers cited in narrative 20 extracted findings

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

CNTNAP1 (Caspr) is a transmembrane glycoprotein of the neurexin superfamily that serves as the central axonal organizer of paranodal septate-like junctions, establishing the membrane diffusion barrier required for saltatory nerve conduction. CNTNAP1 forms a cis complex with contactin (F3), which is required for its exit from the endoplasmic reticulum and delivery to the plasma membrane via a non-conventional, Golgi-independent pathway; CNTNAP1 in turn regulates contactin glycoprocessing and restricts its ability to bind the glial receptor neurofascin-155 (NF155), which mediates trans-axoglial adhesion at paranodes (PMID:10769038, PMID:14676309, PMID:11839274, PMID:12972410). The cytoplasmic domain of CNTNAP1 binds protein 4.1B through a conserved GNP motif, anchoring the paranodal complex to the actin cytoskeleton; this interaction is specifically required not for paranodal localization itself but for generating the barrier that excludes Kv1 potassium channels from the paranode into the juxtaparanodal domain (PMID:12082082, PMID:20164332). Loss-of-function mutations in CNTNAP1 cause a severe human disorder featuring arthrogryposis multiplex congenita, hypomyelinating leukodystrophy, and profoundly reduced nerve conduction velocity, with ultrastructural absence of paranodal transverse bands identical to those seen in Caspr-null mice (PMID:24319099, PMID:27818385).

Mechanistic history

Synthesis pass · year-by-year structured walk · 12 steps
  1. 1997 High

    The identity and localization of the axonal component of paranodal septate-like junctions was unknown; immunoelectron microscopy identified Caspr (CNTNAP1) as a transmembrane glycoprotein concentrated specifically at these junctions and associated with the axon cytoskeleton, establishing the first molecular handle on paranodal organization.

    Evidence Immunoelectron microscopy, detergent extraction, and immunofluorescence in myelinating cultures and sciatic nerve tissue

    PMID:9396755

    Open questions at the time
    • No functional consequence of Caspr loss was known
    • Binding partners on the glial side were unidentified
    • Mechanism of Caspr targeting to paranodes was unknown
  2. 2000 High

    How Caspr reaches the cell surface and is targeted to paranodes was unclear; reconstitution experiments showed that Caspr is retained in the ER when expressed alone and requires cis association with the GPI-anchored molecule contactin (F3) for plasma membrane delivery via lipid raft microdomains, establishing the obligate heteromeric nature of the complex.

    Evidence Transfection in CHO and neuroblastoma cells, surface biotinylation, lipid raft fractionation, co-immunoprecipitation, and myelinating coculture perturbation

    PMID:10769038 PMID:11069942

    Open questions at the time
    • The glial trans-binding partner was still unidentified
    • In vivo loss-of-function had not been tested
    • The trafficking route beyond ER exit was not defined
  3. 2001 High

    Whether Caspr is essential for nerve function in vivo was untested; Caspr knockout mice showed complete failure of paranodal junction formation, displacement of Kv1 channels into paranodal regions, and severely reduced conduction velocity, proving Caspr is indispensable for axonal domain organization and saltatory conduction.

    Evidence Caspr knockout mouse with immunofluorescence, electron microscopy, and electrophysiology

    PMID:11395000

    Open questions at the time
    • The mechanism of Kv1 channel exclusion (direct barrier vs. indirect) was not resolved
    • Cytoplasmic anchoring mechanism was not addressed
    • Human disease relevance was not yet established
  4. 2002 High

    The glial receptor completing the trans-paranodal adhesion complex was unknown; binding assays and myelination inhibition experiments identified neurofascin-155 (NF155) as the glial partner that directly interacts with the axonal Caspr–contactin complex, completing the molecular model of the paranodal junction.

    Evidence Cell binding assay with transfected cells, pull-down from brain lysates, myelinating coculture inhibition

    PMID:11839274

    Open questions at the time
    • Structural basis of the NF155–Caspr/contactin interaction was unknown
    • Whether NF155 binding is sufficient for junction formation in vivo was not tested
  5. 2002 High

    How the paranodal complex is stabilized at the membrane was unclear; transgenic rescue and domain-deletion experiments showed that the Caspr cytoplasmic domain binds protein 4.1B via a conserved GNP motif and that this interaction prevents internalization, establishing the cytoskeletal anchor of the paranodal complex.

    Evidence Transgenic rescue in Caspr-null mice, co-clustering assays, internalization assays in transfected cells, co-immunoprecipitation from brain

    PMID:12082082 PMID:12542678

    Open questions at the time
    • Whether 4.1B binding contributes to the Kv1 channel diffusion barrier was not separated from junction retention
    • Downstream cytoskeletal linkage to actin was inferred but not directly shown
  6. 2003 High

    The mechanism by which Caspr regulates its partner contactin was unknown; biochemical analysis revealed that Caspr directs expression of a low-molecular-weight, ER-type glycoform of contactin that cannot bind NF155, and that the Caspr–contactin complex traffics to the surface via a brefeldin A-insensitive, Golgi-independent pathway, explaining how Caspr controls both partner processing and the unconventional route to the paranodal membrane.

    Evidence Endoglycosidase H sensitivity assays, brefeldin A treatment, calnexin interaction, Caspr knockout mouse glycoform analysis, truncation mutants

    PMID:12972410 PMID:14676309

    Open questions at the time
    • The identity of the non-conventional trafficking carrier was not determined
    • How NF155 binding is ultimately restored at the paranode after surface delivery was not explained
  7. 2003 Medium

    Whether Caspr has additional trans-binding partners beyond NF155 was open; cell binding assays suggested that oligodendroglial Nogo-A interacts directly with Caspr at paranodes and that Caspr also associates with schwannomin/merlin via its cytoplasmic GNP motif, expanding the potential signaling repertoire of Caspr.

    Evidence CHO cell binding to Nogo-66 substrates, co-immunoprecipitation, GST pull-down from brain

    PMID:12558984 PMID:14592966

    Open questions at the time
    • Nogo-A–Caspr interaction was shown only in a single lab with overexpression
    • Functional consequence of schwannomin–Caspr binding at paranodes is undefined
    • Neither interaction has been validated genetically in vivo
  8. 2009 High

    Whether Caspr functions outside myelinated axons was unknown; analysis of Caspr-null mice revealed that Caspr is required for structural integrity of calyceal synaptic junctions at vestibular hair cells and for clustering of the K+ channel KCNQ4, while the shambling truncating mutation confirmed that the transmembrane and cytoplasmic domains are essential for all paranodal functions.

    Evidence Caspr knockout and shambling mutant mice, freeze-fracture EM, immunolabeling, electrophysiology

    PMID:19279247 PMID:19816196

    Open questions at the time
    • Whether Caspr uses the same molecular partners (contactin, NF155) at vestibular synapses was not determined
    • Calyceal junction phenotype has not been linked to vestibular behavioral deficits
  9. 2010 High

    Whether the 4.1B-binding function of Caspr is separable from its junction-assembly function was untested; transgenic rescue with a Caspr mutant lacking only the 4.1B-binding site showed that this mutant localizes normally to paranodes and recruits contactin and NF155, but fails to exclude Kv1 channels, demonstrating that 4.1B anchoring specifically generates the paranodal diffusion barrier.

    Evidence Transgenic rescue of Caspr-null mice with Caspr-Δ4.1 mutant, immunofluorescence

    PMID:20164332

    Open questions at the time
    • The biophysical mechanism by which 4.1B creates the diffusion barrier is unknown
    • Whether other 4.1 family members partially compensate was not tested
  10. 2013 High

    Whether CNTNAP1 loss causes human disease was unresolved; whole-exome sequencing in four unrelated families identified homozygous frameshift CNTNAP1 mutations causing severe arthrogryposis multiplex congenita with profoundly reduced nerve conduction and ultrastructural paranodal defects identical to Caspr-null mice, establishing a direct human disease link.

    Evidence Whole-exome sequencing, transmission electron microscopy of nerve biopsy, nerve conduction studies in patients

    PMID:24319099

    Open questions at the time
    • Genotype–phenotype correlation across different mutation types was limited
    • Whether any residual Caspr function exists in hypomorphic alleles was unknown
  11. 2014 High

    The relationship between Caspr and Caspr2 in axolemmal organization was unclear; double knockout mice revealed that the two proteins together maintain both radial (internodal) and longitudinal (nodal) organization, with compensatory masking of some defects in single knockouts.

    Evidence Caspr/Caspr2 double knockout mouse, immunofluorescence, electron microscopy

    PMID:25378149

    Open questions at the time
    • Molecular basis of radial domain organization by Caspr is unknown
    • Whether Caspr and Caspr2 interact physically was not addressed
  12. 2017 Medium

    An unexpected developmental role for Caspr was identified: Caspr is expressed in cortical radial glia and cooperates with the Notch intracellular domain to repress Hes1 transcription, thereby regulating the timing of neuron-to-astrocyte fate switching during cortical development.

    Evidence Caspr knockout mouse, in utero electroporation, Hes1 shRNA rescue, BrdU labeling

    PMID:26740489

    Open questions at the time
    • This role is from a single lab and has not been independently replicated
    • How a paranodal adhesion molecule accesses nuclear Notch signaling is mechanistically unexplained
    • Whether CNTNAP1 patient mutations affect cortical development was not examined

Open questions

Synthesis pass · forward-looking unresolved questions
  • Key unresolved questions include: the structural basis of the Caspr–contactin–NF155 ternary complex, the biophysical mechanism by which the Caspr–4.1B interaction creates a membrane diffusion barrier, the identity of the non-conventional trafficking carrier used by the Caspr–contactin complex, and the full genotype–phenotype spectrum of CNTNAP1 mutations in humans.
  • No atomic-resolution structure of the paranodal complex exists
  • Mechanism of diffusion barrier formation is entirely unknown at the biophysical level
  • The non-conventional ER-to-surface pathway has not been molecularly defined

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0098631 cell adhesion mediator activity 4 GO:0008092 cytoskeletal protein binding 3
Localization
GO:0005886 plasma membrane 4 GO:0005856 cytoskeleton 3 GO:0005783 endoplasmic reticulum 2
Pathway
R-HSA-112316 Neuronal System 4 R-HSA-1500931 Cell-Cell communication 4 R-HSA-1266738 Developmental Biology 1
Partners
CNTN1EPB41L3NF2NFASCPRNPRTN4
Complex memberships
Caspr–contactin paranodal complexCaspr–contactin–NF155 axoglial junction complex

Evidence

Reading pass · 20 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
1997 Caspr (CNTNAP1) is a transmembrane glycoprotein homologous to Neurexin IV that localizes specifically to paranodal septate-like junctions between axons and myelinating glia, where it is poorly extracted by nonionic detergents, indicating association with the axon cytoskeleton at these junctions. Immunoelectron microscopy, detergent extraction, immunofluorescence in myelinating cultures and tissue The Journal of cell biology High 9396755
2000 Caspr forms a cis complex with contactin in paranodal regions; contactin is required to target the Caspr/contactin complex to paranodal junctions via extracellular interactions with myelinating glia, and treatment with RPTPbeta-Fc blocks paranodal localization of the complex. Co-immunoprecipitation, co-extraction from neurons and myelin preparations, sucrose gradient fractionation, myelinating coculture perturbation assay The Journal of neuroscience High 11069942
2000 Caspr requires association with F3/contactin (a GPI-anchored adhesion molecule) for surface transport; Caspr is retained in the endoplasmic reticulum when transfected alone, and F3 co-expression promotes plasma membrane delivery and recruitment of Caspr into Triton X-100-insoluble lipid raft microdomains; the GPI anchor plus FNIII repeats and Ig domains of F3 are all required for this cooperative effect. Transfection in CHO and neuroblastoma cells, confocal microscopy, cell surface biotinylation, co-immunoprecipitation, lipid raft fractionation The Journal of cell biology High 10769038
2001 Mice lacking Caspr (NCP1) fail to form normal paranodal junctions; contactin is undetectable at paranodes, K+ channels are displaced from juxtaparanodal into paranodal domains, and peripheral nerve conduction velocity is severely reduced, establishing Caspr as essential for axonal domain organization and saltatory conduction. Caspr knockout mouse, immunofluorescence, electrophysiology, electron microscopy Neuron High 11395000
2002 The extracellular domain of the glial isoform neurofascin NF155 binds specifically to the axonal Caspr/paranodin-contactin complex on transfected cells and from brain lysates in vitro; NF155 antibodies and its extracellular domain inhibit myelination in cocultures, establishing NF155 as the glial receptor for the Caspr-contactin axoglial complex. Cell binding assay (transfected cells), in vitro pull-down from brain lysates, myelinating coculture inhibition assay Current biology : CB High 11839274
2002 The cytoplasmic domain of Caspr is required for retention of the Caspr-contactin complex at the paranodal junction; a short sequence in the cytoplasmic domain mediates binding to the cytoskeletal protein 4.1B, and deletion of this 4.1B-binding site accelerates internalization of a Caspr-contactin chimera from the cell surface. Transgenic mouse rescue experiments, immunoelectron microscopy, co-clustering assays, internalization assay in transfected cells The Journal of cell biology High 12082082
2003 Caspr inhibits NF155 binding to contactin by associating with contactin during biosynthesis and directing expression of a low-molecular-weight, endoglycosidase H-sensitive isoform of contactin at the cell membrane; deletion of Caspr in mice shifts contactin from the LMw to the HMw glycoform, demonstrating that Caspr regulates contactin processing and transport. Co-expression in transfected cells, endoglycosidase H sensitivity assay, Caspr knockout mouse, binding assays The Journal of cell biology High 14676309
2003 The conserved intracellular juxtamembrane GNP motif of Caspr/paranodin binds protein 4.1B (and 4.1R); 4.1B co-immunoprecipitates with Caspr in brain homogenates and accumulates progressively at paranodes during postnatal development, linking Caspr to the actin-based cytoskeleton. GST pull-down, co-immunoprecipitation from brain, immunofluorescence during postnatal development The European journal of neuroscience High 12542678
2003 The paranodal Caspr-F3/contactin complex traffics to the cell surface via a non-conventional, Golgi-independent (brefeldin A-insensitive) pathway; N-glycosylation and calnexin-mediated quality control in the ER are required for surface delivery, and the ectodomain of Caspr mediates ER retention when expressed alone. Brefeldin A treatment, endoglycosidase H sensitivity, calnexin interaction assay, truncation mutants in transfected neuroblastoma cells The Journal of biological chemistry High 12972410
2003 Nogo-A, an oligodendroglial protein, localizes to paranodes and interacts in trans with axonal Caspr at CNS paranodes; CHO cells co-transfected with Caspr and F3 (but not F3 alone) bind specifically to Nogo-66-coated substrates, and this binding persists after PI-PLC removal of GPI-linked F3, indicating a direct Nogo-66/Caspr interaction. Nogo-A and Caspr both co-immunoprecipitate with Kv1 channels, implicating this interaction in K+ channel localization. Cell binding assay with transfected CHO cells, PI-PLC treatment, co-immunoprecipitation, immunofluorescence in pathological mouse models The EMBO journal Medium 14592966
2003 Caspr/paranodin associates with the tumor suppressor schwannomin/merlin through binding of the schwannomin FERM domain to the Caspr GNP motif; the two proteins co-immunoprecipitate from brain extracts and are both associated with integrin beta1, with Caspr increasing the schwannomin-integrin beta1 association. GST pull-down, co-immunoprecipitation from brain and transfected cells, dysmyelinated (jimpy) mouse model Journal of neurochemistry Medium 12558984
2009 Caspr is required for the structural integrity of calyceal synaptic junctions at vestibular hair cells and for clustering of the K+ channel KCNQ4 at the postsynaptic membrane; Caspr knockout mice show irregular membrane separation at calyceal synapses and diffuse KCNQ4 distribution. Caspr knockout mouse, freeze-fracture electron microscopy, immunolabeling, ultrastructural analysis The Journal of neuroscience High 19279247
2009 A truncating shambling (shm) mutation in Caspr (frameshift causing loss of transmembrane and cytoplasmic domains) disrupts paranodal junctions, causes aberrant localization of voltage-gated ion channels, reduces expression of contactin and neurofascin-155, and reduces saltatory conduction velocity, confirming transmembrane/cytoplasmic domain necessity for Caspr paranodal function. Positional cloning, immunohistochemistry, electron microscopy, electrophysiology in mutant mice Journal of neuropathology and experimental neurology High 19816196
2010 Caspr interaction with protein 4.1B is required for the generation of an efficient membrane barrier at the paranodal junction; Caspr mutants lacking the 4.1B-binding sequence (Caspr-d4.1) localize to the paranodal junction and recruit contactin and NF155, but fail to exclude Kv1 channels from paranodes, demonstrating that the Caspr-4.1B interaction is necessary for the barrier function. Transgenic rescue of Caspr-null mice with d4.1 mutant, immunofluorescence The Journal of neuroscience High 20164332
2010 Cellular prion protein (PrP) directly binds to Caspr and inhibits Reelin-mediated proteolytic shedding of Caspr from the neuronal cell surface; increased surface Caspr potentiates Caspr-mediated inhibition of neurite outgrowth, while PrP deficiency reduces surface Caspr and enhances neurite outgrowth and axon regeneration in vivo. Co-immunoprecipitation, cell surface Caspr quantification, neurite outgrowth assay, spinal cord injury model in PrP-deficient mice The Journal of neuroscience Medium 20610764
2013 Homozygous frameshift mutations in CNTNAP1 cause a severe form of arthrogryposis multiplex congenita with markedly reduced motor nerve conduction velocity (<10 m/s) and electron microscopy-confirmed severe abnormalities at nodes of Ranvier and myelinated axons in patients, establishing CNTNAP1 as essential for paranodal domain organization and saltatory conduction in humans. Whole exome sequencing, transmission electron microscopy of sciatic nerve biopsy, nerve conduction studies Human molecular genetics High 24319099
2014 Caspr and Caspr2 together are required for both radial (mesaxonal internodal line) and longitudinal (nodal domain) organization of the axolemma; double Caspr/Caspr2 null mice show dispersed Kv1 channel aggregates along the axolemma and widened nodes of Ranvier, revealing compensatory roles of the two proteins. Double knockout mouse generation, immunofluorescence, electron microscopy The Journal of neuroscience High 25378149
2016 CNTNAP1 mutations in patients cause characteristic ultrastructural lesions at paranodes: absence of transverse bands, loss of myelin loop-axolemma attachment, and hypomyelination; these lesions are identical to those in Caspr-null mice, confirming the essential role of CNTNAP1 in forming transverse bands that stabilize paranodal axo-glial junctions in humans. Nerve biopsy with electron microscopy in patients with compound heterozygous CNTNAP1 mutations Journal of neuropathology and experimental neurology High 27818385
2017 Caspr is expressed by radial glial neural progenitor cells in the developing cerebral cortex and regulates the timing of neuron versus astrocyte generation; Caspr-deficient mice show delayed neuronal production and premature astrogenesis. Caspr cooperates with the intracellular domain of Notch to repress Hes1 transcription, and shRNA knockdown of Hes1 rescues the progenitor specification defect. Caspr knockout mouse, in utero electroporation, Hes1 shRNA rescue, BrdU labeling, gene expression analysis Cerebral cortex Medium 26740489
2017 CNTNAP1 mutations cause severe CNS hypomyelinating leukodystrophy and peripheral neuropathy with or without arthrogryposis; nerve biopsy shows lack of paranodal transverse bands and widened paranodal junctional gaps, consistent with CNTNAP1's role in paranodal junction formation. Whole-exome sequencing, MRI, nerve biopsy with electron microscopy, neurophysiology in patients from two unrelated families Neurology. Genetics High 28374019

Source papers

Stage 0 corpus · 100 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2001 Axon-glia interactions and the domain organization of myelinated axons requires neurexin IV/Caspr/Paranodin. Neuron 466 11395000
1996 P210 and P190(BCR/ABL) induce the tyrosine phosphorylation and DNA binding activity of multiple specific STAT family members. The Journal of biological chemistry 410 8940193
1999 The P190, P210, and P230 forms of the BCR/ABL oncogene induce a similar chronic myeloid leukemia-like syndrome in mice but have different lymphoid leukemogenic activity. The Journal of experimental medicine 408 10224280
1992 Primary structure and cellular localization of chicken brain myosin-V (p190), an unconventional myosin with calmodulin light chains. The Journal of cell biology 335 1469047
1992 Molecular cloning of cDNAs encoding the GAP-associated protein p190: implications for a signaling pathway from ras to the nucleus. Cell 333 1581965
1997 The axonal membrane protein Caspr, a homologue of neurexin IV, is a component of the septate-like paranodal junctions that assemble during myelination. The Journal of cell biology 308 9396755
2002 Neurofascin is a glial receptor for the paranodin/Caspr-contactin axonal complex at the axoglial junction. Current biology : CB 249 11839274
1993 rho family GTPase activating proteins p190, bcr and rhoGAP show distinct specificities in vitro and in vivo. The EMBO journal 223 8262058
2000 Contactin-associated protein (Caspr) and contactin form a complex that is targeted to the paranodal junctions during myelination. The Journal of neuroscience : the official journal of the Society for Neuroscience 212 11069942
2001 p190 RhoGAP is the principal Src substrate in brain and regulates axon outgrowth, guidance and fasciculation. Nature cell biology 207 11283609
2003 Rnd proteins function as RhoA antagonists by activating p190 RhoGAP. Current biology : CB 195 12842009
2000 The adhesion signaling molecule p190 RhoGAP is required for morphogenetic processes in neural development. Development (Cambridge, England) 183 11044403
2001 Regulating axon branch stability: the role of p190 RhoGAP in repressing a retraction signaling pathway. Cell 178 11672527
1995 BCR/ABL P210 and P190 cause distinct leukemia in transgenic mice. Blood 159 8541551
2007 Angiopoietin-1 requires p190 RhoGAP to protect against vascular leakage in vivo. The Journal of biological chemistry 156 17562701
1995 Functional detection of MDR1/P170 and MRP/P190-mediated multidrug resistance in tumour cells by flow cytometry. British journal of cancer 152 7669559
2016 Auto-antibodies to contactin-associated protein 1 (Caspr) in two patients with painful inflammatory neuropathy. Brain : a journal of neurology 146 27474220
1991 Significance of the P210 versus P190 molecular abnormalities in adults with Philadelphia chromosome-positive acute leukemia. Blood 134 1932753
1999 Regulation of p190 Rho-GAP by v-Src is linked to cytoskeletal disruption during transformation. Journal of cell science 133 10036244
2003 Caspr regulates the processing of contactin and inhibits its binding to neurofascin. The Journal of cell biology 124 14676309
2008 The PAR-6 polarity protein regulates dendritic spine morphogenesis through p190 RhoGAP and the Rho GTPase. Developmental cell 119 18267090
2003 Protein 4.1B associates with both Caspr/paranodin and Caspr2 at paranodes and juxtaparanodes of myelinated fibres. The European journal of neuroscience 114 12542678
1999 Interaction of c-Jun amino-terminal kinase interacting protein-1 with p190 rhoGEF and its localization in differentiated neurons. The Journal of biological chemistry 113 10574993
1998 Phosphotyrosine (p-Tyr)-dependent and -independent mechanisms of p190 RhoGAP-p120 RasGAP interaction: Tyr 1105 of p190, a substrate for c-Src, is the sole p-Tyr mediator of complex formation. Molecular and cellular biology 113 9819392
1995 p190-B, a new member of the Rho GAP family, and Rho are induced to cluster after integrin cross-linking. The Journal of biological chemistry 112 8537347
2000 The glycosylphosphatidyl inositol-anchored adhesion molecule F3/contactin is required for surface transport of paranodin/contactin-associated protein (caspr). The Journal of cell biology 111 10769038
1992 Biochemical and immunological characterization of p190-calmodulin complex from vertebrate brain: a novel calmodulin-binding myosin. The Journal of cell biology 111 1378447
2001 Treatment of Bcr/Abl-positive acute lymphoblastic leukemia in P190 transgenic mice with the farnesyl transferase inhibitor SCH66336. Blood 107 11222386
2003 Changes in the expression and localization of the paranodal protein Caspr on axons in chronic multiple sclerosis. Brain : a journal of neurology 101 12805111
2013 Mutations in CNTNAP1 and ADCY6 are responsible for severe arthrogryposis multiplex congenita with axoglial defects. Human molecular genetics 100 24319099
1984 Processing, polymorphism, and biological significance of P190, a major surface antigen of the erythrocytic forms of Plasmodium falciparum. Molecular and biochemical parasitology 96 6205267
2010 Organization of myelinated axons by Caspr and Caspr2 requires the cytoskeletal adapter protein 4.1B. The Journal of neuroscience : the official journal of the Society for Neuroscience 93 20164332
2001 Tyrosine phosphorylation of p190 RhoGAP by Fyn regulates oligodendrocyte differentiation. Journal of neurobiology 93 11536198
2002 Fear memory formation involves p190 RhoGAP and ROCK proteins through a GRB2-mediated complex. Neuron 88 12441060
2002 Retention of a cell adhesion complex at the paranodal junction requires the cytoplasmic region of Caspr. The Journal of cell biology 87 12082082
2000 RAFTK/Pyk2 tyrosine kinase mediates the association of p190 RhoGAP with RasGAP and is involved in breast cancer cell invasion. Oncogene 87 10713673
2004 Thy-1 regulates fibroblast focal adhesions, cytoskeletal organization and migration through modulation of p190 RhoGAP and Rho GTPase activity. Experimental cell research 86 15093746
2017 Differential signaling networks of Bcr-Abl p210 and p190 kinases in leukemia cells defined by functional proteomics. Leukemia 80 28111465
2002 Caspr3 and caspr4, two novel members of the caspr family are expressed in the nervous system and interact with PDZ domains. Molecular and cellular neurosciences 79 12093160
2005 p190 Rho-GTPase activating protein associates with plexins and it is required for semaphorin signalling. Journal of cell science 78 16188938
1998 The function of the p190 Rho GTPase-activating protein is controlled by its N-terminal GTP binding domain. The Journal of biological chemistry 78 9852136
2004 CaspR: a web server for automated molecular replacement using homology modelling. Nucleic acids research 76 15215460
2006 Protein tyrosine phosphatase receptor type Z is involved in hippocampus-dependent memory formation through dephosphorylation at Y1105 on p190 RhoGAP. Neuroscience letters 74 16513268
1987 A naturally occurring gene encoding the major surface antigen precursor p190 of Plasmodium falciparum lacks tripeptide repeats. The EMBO journal 74 3327688
2000 Molecular analysis of lineage-specific chimerism and minimal residual disease by RT-PCR of p210(BCR-ABL) and p190(BCR-ABL) after allogeneic bone marrow transplantation for chronic myeloid leukemia: increasing mixed myeloid chimerism and p190(BCR-ABL) detection precede cytogenetic relapse. Blood 73 10753848
1997 Aberrant Ras regulation and reduced p190 tyrosine phosphorylation in cells lacking p120-Gap. Molecular and cellular biology 68 9121432
2001 Phosphorylation of p190 on Tyr1105 by c-Src is necessary but not sufficient for EGF-induced actin disassembly in C3H10T1/2 fibroblasts. Journal of cell science 62 11309200
1997 Structural determinants required for the interaction between Rho GTPase and the GTPase-activating domain of p190. The Journal of biological chemistry 62 9407060
2003 The paranodal complex of F3/contactin and caspr/paranodin traffics to the cell surface via a non-conventional pathway. The Journal of biological chemistry 61 12972410
1992 Restricted oncogenicity of BCR/ABL p190 in transgenic mice. Cancer research 61 1643646
2014 Neuronal Ig/Caspr recognition promotes the formation of axoaxonic synapses in mouse spinal cord. Neuron 60 24411736
1988 Major surface antigen p190 of Plasmodium falciparum: detection of common epitopes present in a variety of plasmodia isolates. The EMBO journal 60 2452082
2005 AMN107, a novel aminopyrimidine inhibitor of p190 Bcr-Abl activation and of in vitro proliferation of Philadelphia-positive acute lymphoblastic leukemia cells. Cancer 59 16078266
1998 Regulation of RhoA GTP hydrolysis by the GTPase-activating proteins p190, p50RhoGAP, Bcr, and 3BP-1. Biochemistry 59 9548756
1997 A BCR-ABL(p190) fusion gene made by homologous recombination causes B-cell acute lymphoblastic leukemias in chimeric mice with independence of the endogenous bcr product. Blood 59 9310467
1995 Phosphorylation of the multidrug resistance associated protein gene encoded protein P190. Biochemistry 59 7880829
1988 Nonpolymorphic regions of p190, a protein of the Plasmodium falciparum erythrocytic stage, contain both T and B cell epitopes. Journal of immunology (Baltimore, Md. : 1950) 59 2452192
2010 p190 RhoGTPase-activating protein links the β1 integrin/caveolin-1 mechanosignaling complex to RhoA and actin remodeling. Arteriosclerosis, thrombosis, and vascular biology 54 21051664
1997 The GTPase and Rho GAP domains of p190, a tumor suppressor protein that binds the M(r) 120,000 Ras GAP, independently function as anti-Ras tumor suppressors. Cancer research 53 9192829
1993 Increased levels of p21ras-GTP and enhanced DNA synthesis accompany elevated tyrosyl phosphorylation of GAP-associated proteins, p190 and p62, in c-src overexpressors. Oncogene 51 7681161
2020 Characterization of p190-Bcr-Abl chronic myeloid leukemia reveals specific signaling pathways and therapeutic targets. Leukemia 49 33168949
2003 Nogo-A at CNS paranodes is a ligand of Caspr: possible regulation of K(+) channel localization. The EMBO journal 49 14592966
1995 Two SH2 domains of p120 Ras GTPase-activating protein bind synergistically to tyrosine phosphorylated p190 Rho GTPase-activating protein. The Journal of biological chemistry 49 7629101
1994 p190 RhoGAP, the major RasGAP-associated protein, binds GTP directly. Molecular and cellular biology 49 7935432
2000 p190-A, a human tumor suppressor gene, maps to the chromosomal region 19q13.3 that is reportedly deleted in some gliomas. Gene 48 11054565
1998 Expression of p210 and p190 BCR-ABL due to alternative splicing in chronic myelogenous leukaemia. British journal of haematology 46 9858221
2006 Inactivation of Rho GTPases by p190 RhoGAP reduces human pancreatic cancer cell invasion and metastasis. Cancer science 45 16776779
2018 Loss of Pax5 Exploits Sca1-BCR-ABLp190 Susceptibility to Confer the Metabolic Shift Essential for pB-ALL. Cancer research 44 29490943
2001 Crkl enhances leukemogenesis in BCR/ABL P190 transgenic mice. Cancer research 44 11245441
2010 Cellular form of prion protein inhibits Reelin-mediated shedding of Caspr from the neuronal cell surface to potentiate Caspr-mediated inhibition of neurite outgrowth. The Journal of neuroscience : the official journal of the Society for Neuroscience 42 20610764
2003 p190-B RhoGAP regulates mammary ductal morphogenesis. Molecular endocrinology (Baltimore, Md.) 42 12637587
2002 BCR/ABL p210, p190 and p230 fusion genes in 250 Mexican patients with chronic myeloid leukaemia (CML). Clinical and laboratory haematology 42 12067277
2017 Differential signaling through p190 and p210 BCR-ABL fusion proteins revealed by interactome and phosphoproteome analysis. Leukemia 41 28210003
2010 Analysis of genomic breakpoints in p190 and p210 BCR-ABL indicate distinct mechanisms of formation. Leukemia 40 20703256
2006 P190-B Rho GTPase-activating protein overexpression disrupts ductal morphogenesis and induces hyperplastic lesions in the developing mammary gland. Molecular endocrinology (Baltimore, Md.) 39 16469769
2006 p190-RhoGAP as an integral component of the Tiam1/Rac1-induced downregulation of Rho. Biological chemistry 39 16542153
2006 Resistance to imatinib of bcr/abl p190 lymphoblastic leukemia cells. Cancer research 39 16707466
1992 Sequence variation in the tripeptide repeats and T cell epitopes in P190 (MSA-1) of Plasmodium falciparum from field isolates. Molecular and biochemical parasitology 39 1373473
2012 Vav3 collaborates with p190-BCR-ABL in lymphoid progenitor leukemogenesis, proliferation, and survival. Blood 38 22692505
2014 Caspr and caspr2 are required for both radial and longitudinal organization of myelinated axons. The Journal of neuroscience : the official journal of the Society for Neuroscience 37 25378149
2009 Disposition of axonal caspr with respect to glial cell membranes: Implications for the process of myelination. Journal of neuroscience research 37 19170162
2017 p190-B RhoGAP and intracellular cytokine signals balance hematopoietic stem and progenitor cell self-renewal and differentiation. Nature communications 36 28176763
2000 Reduced oncogenicity of p190 Bcr/Abl F-actin-binding domain mutants. Blood 36 10979970
2000 P190-B, a Rho-GTPase-activating protein, is differentially expressed in terminal end buds and breast cancer. Cell growth & differentiation : the molecular biology journal of the American Association for Cancer Research 35 10939588
2012 Rnd1 and Rnd3 targeting to lipid raft is required for p190 RhoGAP activation. Molecular biology of the cell 34 22357615
2007 Increased resistance to a farnesyltransferase inhibitor by N-cadherin expression in Bcr/Abl-P190 lymphoblastic leukemia cells. Leukemia 34 17392819
2007 Crosstalk between the p190-B RhoGAP and IGF signaling pathways is required for embryonic mammary bud development. Developmental biology 34 17662267
2007 Nilotinib treatment in mouse models of P190 Bcr/Abl lymphoblastic leukemia. Molecular cancer 33 17958915
2009 The septate junction protein caspr is required for structural support and retention of KCNQ4 at calyceal synapses of vestibular hair cells. The Journal of neuroscience : the official journal of the Society for Neuroscience 32 19279247
2009 A novel Caspr mutation causes the shambling mouse phenotype by disrupting axoglial interactions of myelinated nerves. Journal of neuropathology and experimental neurology 32 19816196
2003 Protein tyrosine phosphatase PTP20 induces actin cytoskeleton reorganization by dephosphorylating p190 RhoGAP in rat ovarian granulosa cells stimulated with follicle-stimulating hormone. Molecular endocrinology (Baltimore, Md.) 31 12554790
2017 Caspr Controls the Temporal Specification of Neural Progenitor Cells through Notch Signaling in the Developing Mouse Cerebral Cortex. Cerebral cortex (New York, N.Y. : 1991) 30 26740489
2003 Association of Caspr/paranodin with tumour suppressor schwannomin/merlin and beta1 integrin in the central nervous system. Journal of neurochemistry 29 12558984
2002 Philadelphia chromosome-positive chronic myeloid leukemia expressing p190(BCR-ABL). Internal medicine (Tokyo, Japan) 29 12521212
1991 HLA polymorphism and T cell recognition of a conserved region of p190, a malaria vaccine candidate. International immunology 29 1718405
2016 Contactin-Associated Protein 1 (CNTNAP1) Mutations Induce Characteristic Lesions of the Paranodal Region. Journal of neuropathology and experimental neurology 28 27818385
2010 The anaphase-promoting complex/cyclosome activator Cdh1 modulates Rho GTPase by targeting p190 RhoGAP for degradation. Molecular and cellular biology 28 20530197
1991 Establishment of a lymphoblastoid cell line, SD-1, expressing the p190 bcr-abl chimaeric protein. Leukemia 28 1847983
2017 CNTNAP1 mutations cause CNS hypomyelination and neuropathy with or without arthrogryposis. Neurology. Genetics 27 28374019
1996 Progression from myelodysplastic syndrome to acute lymphoblastic leukaemia with Philadelphia chromosome and p190 BCR-ABL transcript. British journal of haematology 27 8639433