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1 requires the presence of both fyn kinase and contactin.
2 odal cell adhesion molecules neurofascin and contactin.
3 espite efficient association with Nav1.2 and contactin.
4 teracts with the fibronectin-like domains of contactin.
5 binding to the neural cell adhesion molecule contactin.
6 ia homophilic cell adhesion, fyn kinase, and contactin.
7  evidence indicates that paranodal proteins (contactin 1, contactin-associated protein 1, and neurofa
8 se genes chosen for further study, including contactin 1, myozenin 2, and ubiquitin-conjugating enzym
9 uloneuropathy (CIDP) shows autoantibodies to contactin (1).
10                                  We identify Contactin-1 (Cntn1) as an AIS cell surface protein.
11              Two patients' sera precipitated contactin-1 (CNTN1), and 1 precipitated both CNTN1 and c
12 inst the paranodal proteins neurofascin-155, contactin-1 (CNTN1), contactin-associated protein-1 (Cas
13 n Golgi and granule cells and the absence of Contactin-1 also results in deficits in inhibitory synap
14             We believe the identification of contactin-1 as a key cell-surface protein for PNN struct
15                           High reactivity to contactin-1 by ELISA was found in four patients with chr
16                          We document dynamic Contactin-1 expression on oligodendrocytes in vivo, and
17     These multiple roles distinguish central Contactin-1 functions from its specific role at paranode
18 dence for multiple and critical functions of Contactin-1 in central myelin.
19 phoshpacan to primary cortical neurons, that contactin-1 is the glycosylphosphatidylinositol-linked p
20 c, and attenuated the expression of MMP9 and contactin-1 metastatic factors.
21                       These data reveal that Contactin-1 regulates both myelin formation and organiza
22 uch as epithelial cell adhesion molecule and contactin-1, and upregulated proinflammatory proteins, s
23 ture of patients with autoantibodies against contactin-1, identified from a cohort with chronic infla
24 of an Ig superfamily cell adhesion molecule, Contactin-1, in Golgi and granule cells and the absence
25                                         Anti-contactin-1-associated neuropathy does not meet morpholo
26                                              Contactin-1-deficiency disrupted paranodal junction form
27 ses uncovered significant hypomyelination in Contactin-1-deficient central nerves, with up to 60% mye
28                        We conclude that anti-contactin-1-related neuropathy constitutes a presumably
29 as confirmed by immunoblot assay, binding to contactin-1-transfected human embryonic kidney cells, bi
30  used ELISA to detect autoantibodies against contactin-1.
31 ainst nodal proteins such as neurofascin and contactin-1.
32 Nfasc155 to complex with its axonal partners contactin-1/CASPR1 or induce target internalization.
33 teraction of CASPR2 with its binding partner contactin 2 in vitro and were internalized after binding
34 l projections requires the adhesion molecule Contactin 2.
35                                              Contactin-2 (CNTN2), a member of the immunoglobulin supe
36 rate upregulation of Purkinje-enriched genes Contactin-2 and Scn5a and downregulation of K(+) channel
37 both CASPR2 and LGI1 antibodies (3 also with contactin-2 antibodies).
38 ioma inactivated 1 protein in 55 sera and to contactin-2 in five sera, four of which were also positi
39 xpressed in the hippocampus; and (iii) Tag-1/contactin-2 that associates with contactin-associated pr
40 B and AMPA receptors and to LGI1, CASPR2 and Contactin-2, components of the voltage-gated potassium c
41 ptor (NMDAR), VGKC-complex, LGI1, CASPR2 and contactin-2, GlyR, D1R, D2R, AMPAR, GABA(B)R and glutami
42 complex-associated proteins LGI1, CASPR2 and contactin-2.
43 xpression patterns in mouse sSC: cadherin 7, contactin 3, netrin G2, cadherin 6, protocadherin 20, re
44  G (RPTPgamma/PTPRG) interacts in vitro with contactin-3-6 (CNTN3-6), a group of glycophosphatidylino
45  based on our demonstration of disruption of Contactin 4 (CNTN4) in a patient with ASD; the recent fi
46 on for 3p deletion syndrome and disrupts the Contactin 4 (CNTN4) mRNA transcript at 3p26.2-3p26.3.
47          Here we show that in the absence of contactin 4 (CNTN4) or one of its binding partners, amyl
48  In the developing retinotectal system, APP, contactin 4 and NgCAM are expressed in the retina and te
49 e identification of two associated proteins: contactin 4 and NgCAM.
50 g fragment, CTFalpha, were modulated by both contactin 4 and NgCAM.
51  revealed regulatory effects of both APP and contactin 4 on NgCAM-dependent growth of cultured retina
52 owth factor receptor, coagulation factor Xa, contactin 4, kynureninase, neurogenic locus notch homolo
53                                              Contactin-4 (CNTN4) is a complex cell adhesion molecule
54 xpression of a homophilic adhesion molecule, Contactin 5 (Cntn5).
55 al multivariable model found three proteins (Contactin-5 [CNTN5], Low affinity immunoglobulin gamma F
56 events, significantly modified the effect of Contactin-5 and Complement factor B on risk of CVD.
57                                              Contactin, a cell adhesion/recognition molecule of the i
58  cells failed to extend neurites in vitro on contactin, a known ligand for Nr-CAM expressed in the ce
59 -) mice in the absence of the Nfasc155-Caspr-Contactin adhesion complex.
60 ellular domain of the cell adhesion molecule contactin (also called F3 or F11), which binds to the ex
61                                              Contactin (also known as F3, F11) is a surface glycoprot
62  alone, similar to that shown previously for contactin and beta2.
63                                         Both contactin and Caspr are uniformly expressed at high leve
64                  These results indicate that contactin and Caspr function independently during myelin
65   We have investigated the potential role of contactin and contactin-associated protein (Caspr) in th
66 s comprised of the neuronal heterocomplex of contactin and contactin-associated protein and the myeli
67 l adhesion molecules, including neurofascin, contactin and contactin-associated protein, can be linke
68 We further demonstrate that the signals from contactin and integrin are integrated by differential ph
69          We propose that the upregulation of contactin and its colocalization with Na(v)1.3 in axotom
70 onal interactions among proteins of the APP, contactin and L1CAM families, with general implications
71 l studies show a transient colocalization of contactin and Na(+) channels at new nodes of Ranvier for
72                                              Contactin and Na(+) channels can be reciprocally coimmun
73 ndent of its other binding partners, such as Contactin and Neuroglian and the midline glia protein Wr
74 dy, we characterized beta1 interactions with contactin and Nf186 in greater detail and investigated i
75 cts homophilically and heterophilically with contactin and Nf186.
76  inhibitor of HDAC8, restored acetylation of contactin and reduced expression of those proteins.
77  protein with the C domain (beta C) binds to contactin and supports neuronal adhesion and neurite gro
78 ivity was directed against the Ig domains of contactin and was dependent on N-glycans.
79 ts in the mislocalization of neurofascin155, contactin, and Caspr, and the aberrant localization of K
80               We also show that Neurexin IV, Contactin, and Neuroglian are coexpressed in the periphe
81 stingly, the murine homologs of Neurexin IV, Contactin, and Neuroglian are expressed at the paranodal
82                    Mutations in neurexin IV, contactin, and neuroglian result in the disruption of bl
83  paranodal junction components (i.e., Caspr, contactin, and NF155), and apposes the inner mesaxon of
84 s similar to GlialCAM, tenascin, neuregulin, contactin, and protease kinase C inhibitors are present
85 s inhibited by antibodies against Nr-CAM and contactin, and these cell adhesion molecules formed a co
86 ion relationships for beta1 association with contactin, ankyrin, and Nav1.2.
87 k for investigating how the misregulation of Contactin-APP interactions might contribute to neuronal
88 hey also support the model that misregulated Contactin-APP interactions might provoke aberrant activa
89               By defining the normal role of Contactin-APP signaling during development, these studie
90  Strikingly, the oligomannose type sugars of contactin are required for association with its glial pa
91 l. present the axonal cell adhesion molecule contactin as a functional Notch ligand, and suggest inte
92 ular domain (ECD) of NRG3 identified Caspr3 (contactin associate-like protein 3) as a binding partner
93                In the elderly, anti-LGI1 and contactin associated protein like 2 (CASPR2) antibody-as
94                                         Anti-contactin associated protein receptor 2 (CASPR2) encepha
95     Homozygous loss-of-function mutations in Contactin Associated Protein-like 2 (CNTNAP2) are strong
96                              Variants of the contactin associated protein-like 2 (Cntnap2) gene are r
97 utism susceptibility candidate 2 (AUTS2) and Contactin Associated Protein-Like 2 (CNTNAP2) in a child
98 ing distinct clinical populations, implicate contactin associated protein-like 2 (CNTNAP2) in aspects
99 trios and found significant association with Contactin Associated Protein-Like 2 (CNTNAP2), a strong
100                                              Contactin associated protein-like 2 (CNTNAP2), in which
101 stigated the potential role of contactin and contactin-associated protein (Caspr) in the axonal-glial
102                                    Paranodin/contactin-associated protein (Caspr), a paranodal protei
103 erized node development in mice deficient in contactin-associated protein (Caspr), an integral juncti
104 r the membrane and synaptic targeting of the contactin-associated protein (Caspr/paranodin) and for t
105                                  We identify Contactin-associated protein 1 (Caspr1) as an AMPA recep
106 1 (CNTN1), and 1 precipitated both CNTN1 and contactin-associated protein 1 (CASPR1).
107 oltage-dependent anion channel 1 (VDAC1) and contactin-associated protein 1 (CNTNAP1), reduced Abeta
108 icates that paranodal proteins (contactin 1, contactin-associated protein 1, and neurofascin-155) are
109 try, which resulted in the identification of contactin-associated protein 2 (CASPR2) as a major antig
110 ich, glioma-inactivated protein 1 (LGI1) and contactin-associated protein 2 (Caspr2).
111 leucine-rich glioma inactivated 1 (LGI1) and contactin-associated protein 2 (CASPR2).
112                             Mutations in the contactin-associated protein 2 (CNTNAP2) gene encoding C
113  the neuronal heterocomplex of contactin and contactin-associated protein and the myelin protein neur
114                                       CASPR (contactin-associated protein) and K(v)1.2 channels were
115           We previously reported that Caspr (contactin-associated protein) is a major axonal constitu
116 ecules, including neurofascin, contactin and contactin-associated protein, can be linked to phenotypi
117 oteins neurofascin-155, contactin-1 (CNTN1), contactin-associated protein-1 (Caspr1), or nodal forms
118 leucine-rich glioma-inactivated 1 (LGI1) and contactin-associated protein-2 (CASPR2), are found in pa
119 f these syndromes; furthermore, detection of contactin-associated protein-2 antibodies should help id
120 ucine-rich, glioma inactivated 1 protein and contactin-associated protein-2 as the major targets of p
121 to Kv1 subunits were found in three sera, to contactin-associated protein-2 in 19 sera, to leucine-ri
122 ed potassium channels in brain extracts: (i) contactin-associated protein-2 that is localized at the
123 (iii) Tag-1/contactin-2 that associates with contactin-associated protein-2.
124                      Of the 19 patients with contactin-associated protein-antibody-2, 10 had neuromyo
125 etion of various proteins in mice, including contactin-associated protein-like 2 (Caspr2) and transie
126 leucine-rich glioma inactivated-1 (LGI1) and contactin-associated protein-like 2 (CASPR2) antibodies,
127 leucine-rich glioma-inactivated 1 (LGI1) and contactin-associated protein-like 2 (CASPR2) antibodies.
128                       Autoantibodies against contactin-associated protein-like 2 (CASPR2) are observe
129 he N-methyl-D-aspartate receptor (NMDAR) and contactin-associated protein-like 2 (CASPR2) in maternal
130                                              Contactin-associated protein-like 2 (Caspr2) is a neurex
131                                              Contactin-associated protein-like 2 (CASPR2) is encoded
132 licated genes has been CNTNAP2, encoding for contactin-associated protein-like 2 (CASPR2), a multidom
133 leucine-rich glioma-inactivated 1 (LGI1) and contactin-associated protein-like 2 (CASPR2), and specie
134 ro to the C6 monoclonal antibody, binding to contactin-associated protein-like 2 (Caspr2), display ab
135 or leucine-rich glioma-inactivated 1 (LGI1), contactin-associated protein-like 2 (CASPR2), N-methyl-d
136 utcomes and associated prognostic factors in contactin-associated protein-like 2 (CASPR2)-antibody di
137 mmune checkpoints, focusing on patients with contactin-associated protein-like 2 (CASPR2)-autoantibod
138 ioma-inactivated 1 (LGI1)-IgG associated and contactin-associated protein-like 2 (CASPR2)-IgG associa
139 ne-rich glioma inactivated protein 1 (LGI1), contactin-associated protein-like 2 (CASPR2)], the prodr
140                                              Contactin-associated protein-like 2 (CNTNAP2) encodes fo
141            Loss-of-function mutations in the contactin-associated protein-like 2 (CNTNAP2) gene are c
142         Mutations in the human gene encoding contactin-associated protein-like 2 (CNTNAP2) have been
143  deficits in certain social responses in the contactin-associated protein-like 2 (Cntnap2) mouse mode
144 se models that are genetically deficient for contactin-associated protein-like 2 (Cntnap2)(5), fragil
145       We identified a common polymorphism in contactin-associated protein-like 2 (CNTNAP2), a member
146        We found antibodies against antigens, contactin-associated protein-like 2 in 11 patients, unch
147 e-rich glioma inactivated 1 and five against contactin-associated protein-like 2), as well as 10 case
148 teins (leucine-rich glioma-inactivated 1 and contactin-associated protein-like 2), glycine receptor,
149 tification of a specific receptor of Nell-1, contactin-associated protein-like 4 (Cntnap4), for osteo
150  is indicated by a complete lack of neurexin/contactin-associated protein/paranodin clustering in par
151 ephalitis associated with antibodies against contactin-associated proteinlike 2 (CASPR2) is presumabl
152           We describe the cloning of a novel contactin-associated transmembrane receptor (p190/Caspr)
153 pt in the patients with tumours, who all had contactin-associated-2 protein antibodies.
154 evel of colocalization of Na(+) channels and contactin at nodes both during development and in the ad
155         Importantly, we showed that the anti-contactin autoantibodies induced alteration of paranodal
156 one patient was selectively directed against contactin bearing mannose-rich N-glycans.
157                                         Thus contactin binds directly to Na(v)1.9/NaN and participate
158 results show that the cell adhesion molecule contactin binds directly to Na(v)1.9/NaN and recruits te
159 a (RPTPbeta), a potential glial receptor for contactin, blocks the localization of the Caspr/contacti
160      These results provide new evidence that Contactins can function as authentic ligands for APP fam
161 e nodes of Ranvier is reduced, but Na(v)1.6, contactin, caspr 1, and K(v)1 channels are all localized
162 The known molecular components of paranodes--contactin, Caspr, and neurofascin 155--are not clustered
163               The binding of RPTPbeta to the contactin-Caspr complex could provide a mechanism for ce
164                            Engagement of the contactin-Caspr complex with RPTPbeta may thus regulate
165 ients prevented adhesive interaction between contactin.Caspr and NF155.
166                               The complex of contactin.Caspr.neurofascin-155 (NF155) enables the form
167                                              Contactin clusters at the paranodal axolemma during Schw
168 at two sequentially expressed members of the contactin (CNTN) family of adhesion molecules, TAG1 and
169 immunoglobulin repeats of the members of the contactin (CNTN) family of neural recognition molecules.
170 ed neurite outgrowth is abrogated in Fyn and contactin (Cntn) null CGNs.
171                                              Contactins (CNTNs) are neural cell adhesion molecules th
172                       Here, we asked whether contactins (Cntns), six homologs of Sdks and Dscams, are
173                             Na(v)1.9/NaN and contactin co-immunoprecipitate from dorsal root ganglia
174                   In this study we show that contactin coimmunoprecipitates with Na(v)1.3 from postna
175                           We now report that contactin colocalizes and forms a cis complex with Caspr
176 e conclude, therefore, that a novel integrin/contactin complex coordinates signals from extracellular
177 tactin, blocks the localization of the Caspr/contactin complex to the paranodes.
178  whereas NF155, which binds the axonal Caspr/contactin complex, is located at the paranodal junction
179 oding the critical paranodal proteins Caspr, contactin (Cont), and the myelinating glia-specific isof
180               These results demonstrate that contactin controls axonal and dendritic interactions of
181 ty and identify PPF and LTD, but not LTP, as contactin-dependent processes.
182 or beta1 (TGFbeta1)-induced deacetylation of contactin, EMT, phosphorylation of Smad3, STAT3, and bet
183                    We report that GPI-linked contactin enables the formation of the paranodal septate
184 spr may function as a signaling component of contactin, enabling recruitment and activation of intrac
185 se hamster ovary cells with Na(v)1.9/NaN and contactin enhances the surface expression of the sodium
186                                    Caspr and contactin exist as a complex in rat brain and are bound
187                                              Contactin/F3, a cell adhesion molecule, has been shown t
188 ch provides new evidence that members of the Contactin family function as authentic ligands for APP a
189 nteract with any of the other members of the contactin family.
190 rising glial Neurofascin155 and axonal Caspr/Contactin flanks mature nodes [2].
191 of the N and C termini of Na(v)1.3 pull down contactin from lysates of transfected HEK 293 cells.
192                         Enzymatic removal of contactin from the cell surface of cotransfected cells d
193 e developing nervous system, we have ablated contactin gene expression in mice.
194 channel Na(v)1.2alpha and beta1 subunits and contactin have threefold to fourfold higher peak Na(+) c
195 7/L1CAM in sensory neuron PHC binds to RIG-6/contactin in AVG.
196 glycosylphosphatidyl inositol (GPI)-anchored contactin in hippocampal CA1 synaptic plasticity.
197                                  Ablation of contactin in mutant mice disrupts junctional attachment
198  small interfering RNA-mediated knockdown of contactin in oligodendrocytes.
199 orylation of the inhibitory Tyr-531, whereas contactin increased phosphorylation of both Tyr-531 and
200      Transfection of HEK-Na(v)1.3 cells with contactin increases the amplitude of the current threefo
201 , consistent with previous work showing that Contactins interact with APP family proteins in other sy
202 imeras were used to assign putative sites of contactin interaction to two regions of the beta1 Ig loo
203 ifferent subunits from cell lines shows that contactin interacts specifically with the beta1 subunit.
204                                        Thus, contactin is a crucial part in the machinery that contro
205                                              Contactin is a noncanonical Notch receptor ligand that m
206  issue of the JCI, Nakahara et al. show that Contactin is abundantly expressed on demyelinated axons
207 demonstrate that the Ig superfamily molecule contactin is associated in oligodendrocytes with integri
208                                              Contactin is downregulated along the entire myelinated n
209             Molecular analyses indicate that contactin is essential for the membrane and synaptic tar
210                       In the nervous system, contactin is expressed by neurons, oligodendrocytes, and
211 uggest that a preformed complex of Caspr and contactin is targeted to the paranodal junctions via ext
212                                              Contactin is undetectable in the paranodes, and K(+) cha
213  Finally, we show that, similar to Na(v)1.3, contactin is upregulated in axotomized DRG neurons and a
214                          Neurons express two contactin isoforms that differ in their extent of glycos
215 nce of L1-Fc, the extracellular portion of a contactin ligand expressed on axons, enhanced survival a
216                                              Contactin may thus significantly influence the functiona
217 g this assay, we have now identified Manduca Contactin (MsContactin) as an endogenous ligand for APPL
218                              Analysis of the contactin-/- mutant cerebellum revealed defects in granu
219                                              Contactin-/- mutants displayed a severe ataxic phenotype
220                                          The contactin mutation does not affect sodium channel cluste
221         To investigate precisely the role of contactin N-glycans, we have mutated each of the nine co
222 s, whereas a higher-molecular-weight form of contactin, not associated with Caspr, is present in cent
223 uggest that binding of glial RPTPbeta to the contactin/Nr-CAM complex is important for neurite growth
224           Besides, our study also implicated Contactins-NYAPs-WAVE1 pathway in ASD pathogenesis.
225 inositol (GPI)-anchored recognition molecule contactin on neuronal cells leading to neurite outgrowth
226 he glial membrane and a complex of Caspr and contactin on the axon.
227 a(v)1.2alpha alone, Na(v)1.2/beta1, Na(v)1.2/contactin, or Na(v)1.2/beta1/beta2.
228                  These results indicate that contactin plays a selective role in synaptic plasticity
229  sites (N467Q/N473Q/N494Q) in Ig domain 5 of contactin prevented soluble NF155-Fc binding.
230 ctions among multiple members of the APP and contactin protein families.
231          In sciatic nerve, the expression of contactin, receptor protein tyrosine phosphatase beta, a
232 ent Axonal Glycoprotein 1 (TAG1 or CNTN2), a contactin-related adhesion molecule, plays a central rol
233 t not beta2, interacts heterophilically with contactin, resulting in increased levels of cell surface
234                                              Contactin selectively supports paired-pulse facilitation
235 udy, we mapped the molecular determinants of contactin targeted by the autoantibodies.
236 in turtle, the glial:neuron adhesion protein contactin, the Rac GTPase-activating protein tumbleweed,
237  These results suggest that the targeting of contactin to different axonal domains may be determined,

 
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