Affinage

CNTNAP1

Contactin-associated protein 1 · UniProt P78357

Length
1384 aa
Mass
156.3 kDa
Annotated
2026-06-09
100 papers in source corpus 21 papers cited in narrative 21 extracted findings
Cross-family judge vs UniProt: Affinage preferred faithfulness: 7/7 claims corpus-supported (100%)

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

CNTNAP1 (Caspr/paranodin) is an axonal transmembrane glycoprotein that builds and maintains the septate-like paranodal axoglial junction required for saltatory nerve conduction (PMID:9396755, PMID:11395000). At the paranode it forms a cis complex with the GPI-anchored adhesion molecule contactin (F3), which is required to release Caspr from the ER, deliver it to the cell surface via a non-conventional Golgi-independent pathway, and recruit it into lipid raft microdomains (PMID:10769038, PMID:12972410); reciprocally, Caspr governs contactin glycoform processing, generating a low-molecular-weight paranodal isoform (PMID:14676309). The surface Caspr-contactin complex engages the glial neurofascin isoform NF155 in trans, the interaction that drives paranodal assembly during myelination (PMID:11839274, PMID:19170162). The cytoplasmic juxtamembrane GNP motif of Caspr anchors the complex to the axonal cytoskeleton through the FERM-domain protein 4.1B (and 4.1R), and this linkage retains the complex at the junctional axolemma and establishes the membrane diffusion barrier that excludes Kv1 channels from the paranode and keeps nodal/juxtaparanodal domains properly partitioned (PMID:12082082, PMID:12542678, PMID:20164332). Genetic loss of Caspr in mice abolishes paranodal junction formation, mislocalizes K+ channels, and slows nerve conduction, with Caspr2 able to partially compensate for its barrier function (PMID:11395000, PMID:25378149). Beyond myelination, Caspr supports calyceal synapse integrity and KCNQ4 clustering at vestibular hair cells (PMID:19279247) and, in radial glial progenitors, cooperates with the Notch intracellular domain to repress Hes1 and control the temporal switch from neurogenesis to astrogenesis (PMID:26740489). In humans, homozygous and compound heterozygous CNTNAP1 loss-of-function mutations cause severe hypomyelinating neuropathy with arthrogryposis multiplex congenita, markedly reduced motor nerve conduction, and paranodal ultrastructural lesions that recapitulate the mouse knockout (PMID:24319099, PMID:27818385).

Mechanistic history

Synthesis pass · year-by-year structured walk · 10 steps
  1. 1997 High

    Establishing where Caspr resides defined the structural problem it solves: it is an axonal glycoprotein concentrated at the septate-like paranodal junction and tethered to the cytoskeleton there.

    Evidence Immunoelectron microscopy and detergent-extraction assays on myelinating cultures and nervous tissue

    PMID:9396755

    Open questions at the time
    • No binding partners identified at this stage
    • Functional role inferred from localization, not tested
  2. 2000 High

    Identifying contactin as both a binding partner and a trafficking chaperone answered how Caspr reaches the cell surface and is targeted to the paranode.

    Evidence Co-IP, sucrose gradient fractionation, surface biotinylation in neurons/myelin, plus co-transfection with F3 deletion constructs showing ER retention rescue and lipid raft recruitment

    PMID:10769038 PMID:11069942

    Open questions at the time
    • Glial trans-receptor for the complex not yet identified
    • Mechanism of paranodal vs nodal isoform sorting incompletely defined
  3. 2001 High

    Genetic knockout demonstrated that Caspr is causally required for paranodal junction formation, ion channel partitioning, and saltatory conduction, not merely a marker.

    Evidence Caspr-null mouse with immunofluorescence, immunoEM, and nerve conduction velocity measurement

    PMID:11395000

    Open questions at the time
    • Molecular basis of barrier function not yet dissected
    • Cytoplasmic vs ectodomain contributions unresolved
  4. 2002 High

    Defining NF155 as the glial receptor and the cytoplasmic domain plus 4.1B as the cytoskeletal anchor explained how the complex is held in trans at the junction and retained at the axolemma.

    Evidence Cell-based binding and brain-lysate pulldown for NF155, coculture myelination inhibition; transgenic cytoplasmic-domain-deletion rescue and clustering/internalization assays for 4.1B

    PMID:11839274 PMID:12082082

    Open questions at the time
    • Whether 4.1B linkage specifically gates ion channel exclusion not yet shown
    • Stoichiometry of trans complex unknown
  5. 2003 High

    A cluster of biochemical studies resolved the trafficking pathway, the reciprocal control of contactin glycoforms, the 4.1R/4.1B-binding GNP motif, and additional cytoplasmic partners (schwannomin/merlin, beta1 integrin) and an axonal trans-partner (Nogo-A).

    Evidence Brefeldin A/EndoH/N-glycosylation/calnexin analyses, EndoH and Caspr-null glycoform analysis, GST pulldown and brain co-IP, PI-PLC binding assays

    PMID:12542678 PMID:12558984 PMID:12972410 PMID:14592966 PMID:14676309

    Open questions at the time
    • Functional consequence of merlin/integrin association not directly demonstrated [#11]
    • Nogo-A link to Kv1 channel positioning is correlative [#10]
  6. 2010 High

    Separating the 4.1B-binding sequence from the rest of Caspr showed that the cytoskeletal linkage—rather than complex assembly per se—is what creates the diffusion barrier excluding Kv1 channels.

    Evidence Transgenic Caspr-d4.1 rescue in Caspr-null mice with ion channel immunofluorescence

    PMID:20164332

    Open questions at the time
    • Biophysical nature of the diffusion barrier not directly measured
    • Whether 4.1B alone is sufficient for barrier formation unknown
  7. 2009 High

    Myelination-independent and live-imaging studies extended Caspr's role to calyceal synapse integrity/KCNQ4 clustering and revealed NF155-tracked helical Caspr distribution during paranode assembly.

    Evidence Caspr-null freeze-fracture EM and KCNQ4 immunolabeling; shambling frameshift mutant phenotyping; time-lapse myelinating culture imaging

    PMID:19170162 PMID:19279247 PMID:19816196

    Open questions at the time
    • Mechanism of KCNQ4 clustering by Caspr not defined
    • Direct NF155 binding not assayed in the imaging study [#20]
  8. 2013 High

    Human genetics established CNTNAP1 as a disease gene, showing that loss of function causes severe congenital hypomyelinating neuropathy and arthrogryposis with paranodal pathology mirroring the mouse.

    Evidence Whole exome sequencing of multiple families, nerve biopsy TEM, nerve conduction studies, zebrafish morpholino knockdown

    PMID:24319099

    Open questions at the time
    • Genotype-phenotype correlation across mutation types not fully resolved
  9. 2014 High

    Double knockout revealed that Caspr2 partially compensates for Caspr's barrier function and that both are required for radial Kv1 channel organization in peripheral axons.

    Evidence caspr-/-/caspr2-/- double-knockout mice with immunofluorescence

    PMID:25378149

    Open questions at the time
    • Molecular basis of Caspr2 compensation unknown
  10. 2017 Medium

    A developmental role was uncovered in which Caspr controls the neurogenesis-to-astrogenesis switch in cortical progenitors through Notch/Hes1 repression, distinct from its paranodal function.

    Evidence Caspr-null mice, in utero electroporation, Hes1 shRNA epistasis rescue, transcriptional reporters

    PMID:26740489

    Open questions at the time
    • Single-lab study
    • How a junctional adhesion protein engages Notch signaling mechanistically is unclear

Open questions

Synthesis pass · forward-looking unresolved questions
  • How Caspr's diverse functions—paranodal barrier formation, contactin glycoform control, synaptic ion channel clustering, and Notch-dependent progenitor fate—are coordinated and whether they share a unifying biochemical mechanism remains unresolved.
  • No structural model of the trans complex
  • Mechanism connecting cytoplasmic signaling roles to the adhesion ectodomain undefined

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0060090 molecular adaptor activity 3 GO:0098631 cell adhesion mediator activity 3 GO:0008092 cytoskeletal protein binding 2
Localization
GO:0005886 plasma membrane 3 GO:0005783 endoplasmic reticulum 2 GO:0005856 cytoskeleton 2
Pathway
R-HSA-112316 Neuronal System 2 R-HSA-1643685 Disease 2 GO:0140110 transcription regulator activity 1 R-HSA-1266738 Developmental Biology 1
Partners
CNTN1EPB41EPB41L3NF155NFASCNLGNPRNPRTN4
Complex memberships
Caspr-contactin paranodal complexparanodal axoglial junction

Evidence

Reading pass · 21 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
1997 Caspr (CNTNAP1) is an axonal transmembrane glycoprotein homologous to Drosophila Neurexin IV that localizes specifically to the septate-like paranodal junctions between axons and paranodal loops of myelinating glia, as demonstrated by immunoelectron microscopy. Caspr is resistant to nonionic detergent extraction, indicating association with the axon cytoskeleton at these junctions. Immunoelectron microscopy, detergent extraction, immunofluorescence on myelinating cultures and peripheral/central nervous system tissue The Journal of cell biology High 9396755
2000 Caspr forms a cis complex with contactin in paranodal regions and juxtamesaxon. The two proteins co-extract, co-precipitate, and co-fractionate as a high-molecular-weight complex from neurons, myelinating cultures, and myelin preparations. A PI-PLC-resistant, lower-molecular-weight isoform of contactin is specifically associated with Caspr at paranodes, while a higher-molecular-weight contactin isoform at nodes is not Caspr-associated, indicating that Caspr determines the paranodal targeting of contactin. Blocking glial receptor RPTPβ inhibits paranodal targeting of the complex. Co-immunoprecipitation, sucrose gradient fractionation, cell surface biotinylation, myelinating coculture treatment with RPTPβ-Fc The Journal of neuroscience High 11069942
2001 Genetic knockout of Caspr (NCP1) in mice abolishes normal paranodal junction formation, renders paranodal loops disorganized, causes contactin to become undetectable at paranodes, and displaces K+ channels from juxtaparanodal into paranodal domains. Loss of Caspr also severely reduces peripheral nerve conduction velocity. This demonstrates a critical role for Caspr in axonal domain delineation and saltatory conduction. Caspr knockout mouse model, immunofluorescence, immunoelectron microscopy, electrophysiology (nerve conduction velocity) Neuron High 11395000
2000 Surface transport of Caspr (paranodin) to the plasma membrane requires co-expression with the GPI-anchored adhesion molecule F3/contactin. Caspr is retained in the ER when transfected alone. Co-transfection with F3 delivers Caspr to the plasma membrane and recruits it into Triton X-100-insoluble lipid raft microdomains. The Ig domains of F3 mediate its association with Caspr, and both the GPI anchor and the fibronectin type III repeats of F3 are required cooperatively for this effect. Co-transfection in CHO and neuroblastoma cells, confocal microscopy, cell surface biotinylation, co-immunoprecipitation with F3 deletion constructs, detergent fractionation The Journal of cell biology High 10769038
2002 The glial isoform NF155 of neurofascin binds specifically to the Caspr–contactin axonal complex. The extracellular domain of NF155 binds to transfected cells expressing Caspr–contactin at the cell surface and pulls down the complex from brain lysates in vitro. NF155 antibodies and soluble NF155 extracellular domain inhibit myelination in cocultures, establishing NF155 as the glial receptor for the paranodal Caspr–contactin complex. Cell-based binding assay (transfected HEK cells), in vitro pulldown 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 paranodal junctions. Transgenic mice expressing a Caspr mutant lacking its intracellular domain show the truncated protein mislocated within the axon rather than at the junctional axolemma. A short sequence in the cytoplasmic domain mediates binding to the cytoskeletal protein 4.1B. Clustering of contactin on the cell surface induces coclustering of Caspr and immobilized 4.1B at the plasma membrane, and deletion of the 4.1B-binding site accelerates internalization of a Caspr–contactin chimera. Transgenic mouse rescue experiments, immunoelectron microscopy, co-immunoprecipitation, cell clustering assay, internalization assay The Journal of cell biology High 12082082
2003 Caspr regulates the intracellular processing of contactin. Coexpression of Caspr with contactin during biosynthesis produces a low-molecular-weight, endoglycosidase H-sensitive contactin isoform that remains at the cell surface associated with Caspr but is unable to bind NF155. NF155 binds directly to contactin alone, but this interaction is inhibited when Caspr is co-expressed. Genetic deletion of Caspr in mice shifts contactin from the LMw to the HMw glycoform. Co-transfection, endoglycosidase H digestion, co-immunoprecipitation, Caspr-null mouse analysis The Journal of cell biology High 14676309
2003 The conserved intracellular juxtamembrane GNP motif of Caspr/paranodin binds FERM-domain-containing proteins 4.1R and 4.1B. Protein 4.1B co-immunoprecipitates with Caspr in brain homogenates and accumulates progressively at paranodes during postnatal development, following the developmental concentration of Caspr at paranodes in both central and peripheral myelinated axons. GST pulldown, co-immunoprecipitation from brain homogenates, immunohistochemistry during postnatal development The European journal of neuroscience High 12542678
2010 Caspr's interaction with protein 4.1B via its cytoplasmic domain is required for efficient membrane barrier function at the paranodal junction (PNJ). Transgenic Caspr-d4.1 mutant lacking the 4.1-binding sequence localizes to the PNJ and recruits contactin and NF155, but Kv1 channels are aberrantly detected at paranodes, indicating that the Caspr–4.1B interaction is needed to exclude Kv1 channels from the paranodal domain. Transgenic rescue in Caspr-null mice, immunofluorescence, confocal microscopy The Journal of neuroscience High 20164332
2003 The paranodal Caspr–F3/contactin complex traffics to the cell surface via a non-conventional Golgi-independent pathway. When Caspr is transfected alone, it is retained in the ER; ER retention is governed by the ectodomain. Cell surface delivery requires N-glycosylation and calnexin-mediated quality control. When complexed with F3, the glycoproteins are endoglycosidase H-sensitive and brefeldin A-insensitive at the cell surface, and recruited to lipid rafts. Brefeldin A treatment, EndoH digestion, N-glycosylation inhibition, lectin-chaperone (calnexin) analysis, confocal microscopy, chimeric construct analysis The Journal of biological chemistry High 12972410
2003 Nogo-A, an oligodendroglial protein concentrated at CNS paranodes, interacts directly with axonal Caspr in trans. CHO cells co-transfected with Caspr and F3 bind specifically to Nogo-66 peptide substrates, and this binding persists after PI-PLC removal of GPI-anchored F3, indicating a direct Nogo-66/Caspr interaction. Nogo-A and Caspr co-immunoprecipitate with Kv1.1 and Kv1.2 channels; in paranodal junction-defective pathological models, Nogo-A congregation is reduced and Kv1 channels shift toward paranodes. Cell-based binding assay with 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 via the FERM domain of schwannomin binding to the Caspr GNP motif, and with β1 integrin. All three proteins co-immunoprecipitate from brain extracts. Caspr enhances the association between β1 integrin and schwannomin. In jimpy dysmyelinating mice with deficient paranodal junctions, interactions among these three proteins are profoundly altered. GST pulldown, co-immunoprecipitation from brain homogenates and transfected COS-7 cells, jimpy mouse analysis Journal of neurochemistry Medium 12558984
2009 Caspr is required for structural integrity of calyceal synapses at vestibular hair cells and for clustering of KCNQ4 K+ channels at the postsynaptic membrane. In Caspr knockout mice, the separation between hair cell and afferent neuron membranes is irregularly increased, and KCNQ4 fails to cluster at the postsynaptic membrane, instead distributing diffusely along the calyceal membrane. Freeze-fracture electron microscopy, immunolabeling, Caspr knockout mouse analysis The Journal of neuroscience High 19279247
2009 A novel frameshift mutation in Caspr (shambling mouse) causing loss of transmembrane and cytoplasmic domains abolishes paranodal junction formation and causes axonal transport defects (large mitochondria, abnormal organelle accumulation at paranodes), reduced expression of Caspr, contactin, and NF155 at paranodes, aberrant localization of voltage-gated ion channels at the nodal/paranodal axolemma, and reduced saltatory conduction velocity. Positional cloning, immunohistochemistry, electron microscopy, electrophysiology in mutant mice Journal of neuropathology and experimental neurology High 19816196
2010 Cellular prion protein (PrP) directly binds Caspr and inhibits Reelin-mediated proteolytic shedding of Caspr from the neuronal cell surface. This increases surface Caspr levels and potentiates Caspr's inhibitory effect on neurite outgrowth. PrP-deficient neurons have reduced surface Caspr and enhanced neurite outgrowth in vitro; PrP-deficient mice show more efficient axon regeneration following spinal cord injury. Co-immunoprecipitation (direct binding of PrP to Caspr), neurite outgrowth assays, surface Caspr quantification, PrP knockout mouse analysis, in vivo spinal cord injury model The Journal of neuroscience Medium 20610764
2013 Homozygous frameshift mutations in CNTNAP1 in humans cause severe arthrogryposis multiplex congenita with markedly reduced motor nerve conduction velocity (<10 m/s) and transmission electron microscopy-confirmed severe abnormalities in nodes of Ranvier width and myelinated axon ultrastructure, establishing CNTNAP1/Caspr as essential for paranodal junction integrity and saltatory conduction in humans. Whole exome sequencing, nerve biopsy with transmission electron microscopy, nerve conduction studies, zebrafish morpholino knockdown Human molecular genetics High 24319099
2014 Caspr4, in a coreceptor complex with contactin5/NB2 on proprioceptive sensory terminals, interacts with NrCAM/CHL1 on GABAergic spinal interneurons to direct high-density accumulation of inhibitory GABAergic boutons at sensory terminals. Genetic elimination of NB2 (contactin5) disproportionately strips inhibitory boutons from high-density GABApre-sensory synapses. Genetic knockout (NB2-null mice), immunofluorescence, synaptic density quantification in spinal cord Neuron Medium 24411736
2014 Both Caspr and Caspr2 are required for the radial organization of Kv1 channels along the inner mesaxon and circumferential ring in peripheral myelinated axons. In mice lacking both Caspr and Caspr2, Kv1 channels form large aggregates dispersed along the axolemma rather than clustered at the internodal line. Additionally, deletion of both proteins causes widening of nodes of Ranvier, showing that Caspr2 (present at paranodes in Caspr-null mice) can partially compensate for Caspr's barrier function. Double-knockout mouse generation (caspr-/-/caspr2-/-), immunofluorescence, confocal microscopy The Journal of neuroscience High 25378149
2016 CNTNAP1 mutations in humans produce characteristic ultrastructural lesions: absence of transverse bands at paranodal axoglial junctions, loss of attachment between myelin loops and axolemma, and elongated Schwann cell processes dissociating the membranes at the node of Ranvier—lesions exclusively in the region where Caspr-1 is located, recapitulating caspr-1-null mouse pathology. Nerve biopsy with electron microscopy in compound heterozygous CNTNAP1 mutation patients, comparison with caspr-null mice Journal of neuropathology and experimental neurology High 27818385
2017 Caspr is expressed by radial glial neural progenitor cells and controls the temporal specification of neuronal versus astrocyte fate in the developing mouse cerebral cortex. Loss of Caspr delays neuronal production and induces precocious astrogenesis. At the molecular level, Caspr cooperates with the intracellular domain of Notch to repress transcription of the Notch effector Hes1. ShRNA knockdown of Hes1 rescues the abnormal neurogenesis and astrogenesis in Caspr-deficient mice. Caspr knockout mouse analysis, in utero electroporation, immunofluorescence, shRNA knockdown of Hes1, transcriptional reporter assays Cerebral cortex Medium 26740489
2009 During myelination, NF155 on oligodendrocyte processes acts as the glial partner responsible for paranodal Caspr distribution: Caspr is recruited to the cell surface at the axon–oligodendrocyte contact zone, where it undergoes a helical distribution that mirrors the turns of the overlying myelin sheath, consistent with trans-interaction with NF155 tracking the spiraling membrane. Time-lapse imaging and immunofluorescence in myelinating cultures, developmental time-course analysis Journal of neuroscience research Medium 19170162

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 468 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 411 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 409 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 224 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 180 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 147 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 125 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 113 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
2013 Mutations in CNTNAP1 and ADCY6 are responsible for severe arthrogryposis multiplex congenita with axoglial defects. Human molecular genetics 102 24319099
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
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 94 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 81 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 80 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 75 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
2014 Neuronal Ig/Caspr recognition promotes the formation of axoaxonic synapses in mouse spinal cord. Neuron 61 24411736
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
1998 Regulation of RhoA GTP hydrolysis by the GTPase-activating proteins p190, p50RhoGAP, Bcr, and 3BP-1. Biochemistry 60 9548756
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
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
2020 Characterization of p190-Bcr-Abl chronic myeloid leukemia reveals specific signaling pathways and therapeutic targets. Leukemia 51 33168949
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
2003 Nogo-A at CNS paranodes is a ligand of Caspr: possible regulation of K(+) channel localization. The EMBO journal 50 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
2018 Loss of Pax5 Exploits Sca1-BCR-ABLp190 Susceptibility to Confer the Metabolic Shift Essential for pB-ALL. Cancer research 45 29490943
2006 Inactivation of Rho GTPases by p190 RhoGAP reduces human pancreatic cancer cell invasion and metastasis. Cancer science 45 16776779
2001 Crkl enhances leukemogenesis in BCR/ABL P190 transgenic mice. Cancer research 44 11245441
2002 BCR/ABL p210, p190 and p230 fusion genes in 250 Mexican patients with chronic myeloid leukaemia (CML). Clinical and laboratory haematology 43 12067277
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
2010 Analysis of genomic breakpoints in p190 and p210 BCR-ABL indicate distinct mechanisms of formation. Leukemia 42 20703256
2003 p190-B RhoGAP regulates mammary ductal morphogenesis. Molecular endocrinology (Baltimore, Md.) 42 12637587
2012 Vav3 collaborates with p190-BCR-ABL in lymphoid progenitor leukemogenesis, proliferation, and survival. Blood 39 22692505
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
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
1994 Late-appearing Philadelphia chromosome in a patient with acute nonlymphocytic leukaemia derived from myelodysplastic syndrome: detection of P210- and P190-type bcr/abl fusion gene transcripts at the leukaemic stage. British journal of haematology 37 7524618
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
1997 Establishment of a novel human myeloid leukaemia cell line (HNT-34) with t(3;3)(q21;q26), t(9;22)(q34;q11) and the expression of EVI1 gene, P210 and P190 BCR/ABL chimaeric transcripts from a patient with AML after MDS with 3q21q26 syndrome. British journal of haematology 35 9266939
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
2016 Contactin-Associated Protein 1 (CNTNAP1) Mutations Induce Characteristic Lesions of the Paranodal Region. Journal of neuropathology and experimental neurology 29 27818385
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
2017 CNTNAP1 mutations cause CNS hypomyelination and neuropathy with or without arthrogryposis. Neurology. Genetics 28 28374019
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

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