ライフサイエンスコーパス: contactin

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 Two patients' sera precipitated contactin-1 (CNTN1), and 1 precipitated both CNTN1 and c

11 n Golgi and granule cells and the absence of Contactin-1 also results in deficits in inhibitory synap

12 High reactivity to contactin-1 by ELISA was found in four patients with chr

13 We document dynamic Contactin-1 expression on oligodendrocytes in vivo, and

14 These multiple roles distinguish central Contactin-1 functions from its specific role at paranode

15 dence for multiple and critical functions of Contactin-1 in central myelin.

16 c, and attenuated the expression of MMP9 and contactin-1 metastatic factors.

17 These data reveal that Contactin-1 regulates both myelin formation and organiza

18 ture of patients with autoantibodies against contactin-1, identified from a cohort with chronic infla

19 of an Ig superfamily cell adhesion molecule, Contactin-1, in Golgi and granule cells and the absence

20 Anti-contactin-1-associated neuropathy does not meet morpholo

21 Contactin-1-deficiency disrupted paranodal junction form

22 ses uncovered significant hypomyelination in Contactin-1-deficient central nerves, with up to 60% mye

23 We conclude that anti-contactin-1-related neuropathy constitutes a presumably

24 as confirmed by immunoblot assay, binding to contactin-1-transfected human embryonic kidney cells, bi

25 used ELISA to detect autoantibodies against contactin-1.

26 rate upregulation of Purkinje-enriched genes Contactin-2 and Scn5a and downregulation of K(+) channel

27 both CASPR2 and LGI1 antibodies (3 also with contactin-2 antibodies).

28 ioma inactivated 1 protein in 55 sera and to contactin-2 in five sera, four of which were also positi

29 xpressed in the hippocampus; and (iii) Tag-1/contactin-2 that associates with contactin-associated pr

30 B and AMPA receptors and to LGI1, CASPR2 and Contactin-2, components of the voltage-gated potassium c

31 ptor (NMDAR), VGKC-complex, LGI1, CASPR2 and contactin-2, GlyR, D1R, D2R, AMPAR, GABA(B)R and glutami

32 complex-associated proteins LGI1, CASPR2 and contactin-2.

33 xpression patterns in mouse sSC: cadherin 7, contactin 3, netrin G2, cadherin 6, protocadherin 20, re

34 G (RPTPgamma/PTPRG) interacts in vitro with contactin-3-6 (CNTN3-6), a group of glycophosphatidylino

35 based on our demonstration of disruption of Contactin 4 (CNTN4) in a patient with ASD; the recent fi

36 on for 3p deletion syndrome and disrupts the Contactin 4 (CNTN4) mRNA transcript at 3p26.2-3p26.3.

37 Here we show that in the absence of contactin 4 (CNTN4) or one of its binding partners, amyl

38 In the developing retinotectal system, APP, contactin 4 and NgCAM are expressed in the retina and te

39 e identification of two associated proteins: contactin 4 and NgCAM.

40 g fragment, CTFalpha, were modulated by both contactin 4 and NgCAM.

41 revealed regulatory effects of both APP and contactin 4 on NgCAM-dependent growth of cultured retina

42 Contactin-4 (CNTN4) is a complex cell adhesion molecule

43 xpression of a homophilic adhesion molecule, Contactin 5 (Cntn5).

44 Contactin, a cell adhesion/recognition molecule of the i

45 cells failed to extend neurites in vitro on contactin, a known ligand for Nr-CAM expressed in the ce

46 -) mice in the absence of the Nfasc155-Caspr-Contactin adhesion complex.

47 ellular domain of the cell adhesion molecule contactin (also called F3 or F11), which binds to the ex

48 Contactin (also known as F3, F11) is a surface glycoprot

49 alone, similar to that shown previously for contactin and beta2.

50 Both contactin and Caspr are uniformly expressed at high leve

51 These results indicate that contactin and Caspr function independently during myelin

52 We have investigated the potential role of contactin and contactin-associated protein (Caspr) in th

53 s comprised of the neuronal heterocomplex of contactin and contactin-associated protein and the myeli

54 l adhesion molecules, including neurofascin, contactin and contactin-associated protein, can be linke

55 We further demonstrate that the signals from contactin and integrin are integrated by differential ph

56 We propose that the upregulation of contactin and its colocalization with Na(v)1.3 in axotom

57 onal interactions among proteins of the APP, contactin and L1CAM families, with general implications

58 l studies show a transient colocalization of contactin and Na(+) channels at new nodes of Ranvier for

59 Contactin and Na(+) channels can be reciprocally coimmun

60 ndent of its other binding partners, such as Contactin and Neuroglian and the midline glia protein Wr

61 dy, we characterized beta1 interactions with contactin and Nf186 in greater detail and investigated i

62 cts homophilically and heterophilically with contactin and Nf186.

63 protein with the C domain (beta C) binds to contactin and supports neuronal adhesion and neurite gro

64 ivity was directed against the Ig domains of contactin and was dependent on N-glycans.

65 ts in the mislocalization of neurofascin155, contactin, and Caspr, and the aberrant localization of K

66 We also show that Neurexin IV, Contactin, and Neuroglian are coexpressed in the periphe

67 stingly, the murine homologs of Neurexin IV, Contactin, and Neuroglian are expressed at the paranodal

68 Mutations in neurexin IV, contactin, and neuroglian result in the disruption of bl

69 paranodal junction components (i.e., Caspr, contactin, and NF155), and apposes the inner mesaxon of

70 s inhibited by antibodies against Nr-CAM and contactin, and these cell adhesion molecules formed a co

71 ion relationships for beta1 association with contactin, ankyrin, and Nav1.2.

72 k for investigating how the misregulation of Contactin-APP interactions might contribute to neuronal

73 hey also support the model that misregulated Contactin-APP interactions might provoke aberrant activa

74 By defining the normal role of Contactin-APP signaling during development, these studie

75 Strikingly, the oligomannose type sugars of contactin are required for association with its glial pa

76 l. present the axonal cell adhesion molecule contactin as a functional Notch ligand, and suggest inte

77 Homozygous loss-of-function mutations in Contactin Associated Protein-like 2 (CNTNAP2) are strong

78 Variants of the contactin associated protein-like 2 (Cntnap2) gene are r

79 utism susceptibility candidate 2 (AUTS2) and Contactin Associated Protein-Like 2 (CNTNAP2) in a child

80 ing distinct clinical populations, implicate contactin associated protein-like 2 (CNTNAP2) in aspects

81 trios and found significant association with Contactin Associated Protein-Like 2 (CNTNAP2), a strong

82 Contactin associated protein-like 2 (CNTNAP2), in which

83 stigated the potential role of contactin and contactin-associated protein (Caspr) in the axonal-glial

84 Paranodin/contactin-associated protein (Caspr), a paranodal protei

85 erized node development in mice deficient in contactin-associated protein (Caspr), an integral juncti

86 r the membrane and synaptic targeting of the contactin-associated protein (Caspr/paranodin) and for t

87 We identify Contactin-associated protein 1 (Caspr1) as an AMPA recep

88 1 (CNTN1), and 1 precipitated both CNTN1 and contactin-associated protein 1 (CASPR1).

89 oltage-dependent anion channel 1 (VDAC1) and contactin-associated protein 1 (CNTNAP1), reduced Abeta

90 icates that paranodal proteins (contactin 1, contactin-associated protein 1, and neurofascin-155) are

91 try, which resulted in the identification of contactin-associated protein 2 (CASPR2) as a major antig

92 ich, glioma-inactivated protein 1 (LGI1) and contactin-associated protein 2 (Caspr2).

93 leucine-rich glioma inactivated 1 (LGI1) and contactin-associated protein 2 (CASPR2).

94 Mutations in the contactin-associated protein 2 (CNTNAP2) gene encoding C

95 the neuronal heterocomplex of contactin and contactin-associated protein and the myelin protein neur

96 CASPR (contactin-associated protein) and K(v)1.2 channels were

97 We previously reported that Caspr (contactin-associated protein) is a major axonal constitu

98 ecules, including neurofascin, contactin and contactin-associated protein, can be linked to phenotypi

99 leucine-rich glioma-inactivated 1 (LGI1) and contactin-associated protein-2 (CASPR2), are found in pa

100 f these syndromes; furthermore, detection of contactin-associated protein-2 antibodies should help id

101 ucine-rich, glioma inactivated 1 protein and contactin-associated protein-2 as the major targets of p

102 to Kv1 subunits were found in three sera, to contactin-associated protein-2 in 19 sera, to leucine-ri

103 ed potassium channels in brain extracts: (i) contactin-associated protein-2 that is localized at the

104 (iii) Tag-1/contactin-2 that associates with contactin-associated protein-2.

105 Of the 19 patients with contactin-associated protein-antibody-2, 10 had neuromyo

106 etion of various proteins in mice, including contactin-associated protein-like 2 (Caspr2) and transie

107 Autoantibodies against contactin-associated protein-like 2 (CASPR2) are observe

108 he N-methyl-D-aspartate receptor (NMDAR) and contactin-associated protein-like 2 (CASPR2) in maternal

109 Contactin-associated protein-like 2 (CASPR2) is encoded

110 licated genes has been CNTNAP2, encoding for contactin-associated protein-like 2 (CASPR2), a multidom

111 leucine-rich glioma-inactivated 1 (LGI1) and contactin-associated protein-like 2 (CASPR2), and specie

112 ro to the C6 monoclonal antibody, binding to contactin-associated protein-like 2 (Caspr2), display ab

113 or leucine-rich glioma-inactivated 1 (LGI1), contactin-associated protein-like 2 (CASPR2), N-methyl-d

114 ne-rich glioma inactivated protein 1 (LGI1), contactin-associated protein-like 2 (CASPR2)], the prodr

115 Contactin-associated protein-like 2 (CNTNAP2) encodes fo

116 Mutations in the human gene encoding contactin-associated protein-like 2 (CNTNAP2) have been

117 deficits in certain social responses in the contactin-associated protein-like 2 (Cntnap2) mouse mode

118 We identified a common polymorphism in contactin-associated protein-like 2 (CNTNAP2), a member

119 We found antibodies against antigens, contactin-associated protein-like 2 in 11 patients, unch

120 teins (leucine-rich glioma-inactivated 1 and contactin-associated protein-like 2), glycine receptor,

121 is indicated by a complete lack of neurexin/contactin-associated protein/paranodin clustering in par

122 We describe the cloning of a novel contactin-associated transmembrane receptor (p190/Caspr)

123 pt in the patients with tumours, who all had contactin-associated-2 protein antibodies.

124 evel of colocalization of Na(+) channels and contactin at nodes both during development and in the ad

125 Importantly, we showed that the anti-contactin autoantibodies induced alteration of paranodal

126 one patient was selectively directed against contactin bearing mannose-rich N-glycans.

127 Thus contactin binds directly to Na(v)1.9/NaN and participate

128 results show that the cell adhesion molecule contactin binds directly to Na(v)1.9/NaN and recruits te

129 a (RPTPbeta), a potential glial receptor for contactin, blocks the localization of the Caspr/contacti

130 These results provide new evidence that Contactins can function as authentic ligands for APP fam

131 e nodes of Ranvier is reduced, but Na(v)1.6, contactin, caspr 1, and K(v)1 channels are all localized

132 The known molecular components of paranodes--contactin, Caspr, and neurofascin 155--are not clustered

133 The binding of RPTPbeta to the contactin-Caspr complex could provide a mechanism for ce

134 Engagement of the contactin-Caspr complex with RPTPbeta may thus regulate

135 ients prevented adhesive interaction between contactin.Caspr and NF155.

136 The complex of contactin.Caspr.neurofascin-155 (NF155) enables the form

137 Contactin clusters at the paranodal axolemma during Schw

138 at two sequentially expressed members of the contactin (CNTN) family of adhesion molecules, TAG1 and

139 immunoglobulin repeats of the members of the contactin (CNTN) family of neural recognition molecules.

140 ed neurite outgrowth is abrogated in Fyn and contactin (Cntn) null CGNs.

141 Here, we asked whether contactins (Cntns), six homologs of Sdks and Dscams, are

142 Na(v)1.9/NaN and contactin co-immunoprecipitate from dorsal root ganglia

143 In this study we show that contactin coimmunoprecipitates with Na(v)1.3 from postna

144 We now report that contactin colocalizes and forms a cis complex with Caspr

145 e conclude, therefore, that a novel integrin/contactin complex coordinates signals from extracellular

146 tactin, blocks the localization of the Caspr/contactin complex to the paranodes.

147 oding the critical paranodal proteins Caspr, contactin (Cont), and the myelinating glia-specific isof

148 These results demonstrate that contactin controls axonal and dendritic interactions of

149 ty and identify PPF and LTD, but not LTP, as contactin-dependent processes.

150 We report that GPI-linked contactin enables the formation of the paranodal septate

151 spr may function as a signaling component of contactin, enabling recruitment and activation of intrac

152 se hamster ovary cells with Na(v)1.9/NaN and contactin enhances the surface expression of the sodium

153 Caspr and contactin exist as a complex in rat brain and are bound

154 Contactin/F3, a cell adhesion molecule, has been shown t

155 ch provides new evidence that members of the Contactin family function as authentic ligands for APP a

156 nteract with any of the other members of the contactin family.

157 rising glial Neurofascin155 and axonal Caspr/Contactin flanks mature nodes [2].

158 of the N and C termini of Na(v)1.3 pull down contactin from lysates of transfected HEK 293 cells.

159 Enzymatic removal of contactin from the cell surface of cotransfected cells d

160 e developing nervous system, we have ablated contactin gene expression in mice.

161 channel Na(v)1.2alpha and beta1 subunits and contactin have threefold to fourfold higher peak Na(+) c

162 7/L1CAM in sensory neuron PHC binds to RIG-6/contactin in AVG.

163 glycosylphosphatidyl inositol (GPI)-anchored contactin in hippocampal CA1 synaptic plasticity.

164 Ablation of contactin in mutant mice disrupts junctional attachment

165 small interfering RNA-mediated knockdown of contactin in oligodendrocytes.

166 orylation of the inhibitory Tyr-531, whereas contactin increased phosphorylation of both Tyr-531 and

167 Transfection of HEK-Na(v)1.3 cells with contactin increases the amplitude of the current threefo

168 , consistent with previous work showing that Contactins interact with APP family proteins in other sy

169 imeras were used to assign putative sites of contactin interaction to two regions of the beta1 Ig loo

170 ifferent subunits from cell lines shows that contactin interacts specifically with the beta1 subunit.

171 Thus, contactin is a crucial part in the machinery that contro

172 Contactin is a noncanonical Notch receptor ligand that m

173 issue of the JCI, Nakahara et al. show that Contactin is abundantly expressed on demyelinated axons

174 demonstrate that the Ig superfamily molecule contactin is associated in oligodendrocytes with integri

175 Contactin is downregulated along the entire myelinated n

176 Molecular analyses indicate that contactin is essential for the membrane and synaptic tar

177 In the nervous system, contactin is expressed by neurons, oligodendrocytes, and

178 uggest that a preformed complex of Caspr and contactin is targeted to the paranodal junctions via ext

179 Contactin is undetectable in the paranodes, and K(+) cha

180 Finally, we show that, similar to Na(v)1.3, contactin is upregulated in axotomized DRG neurons and a

181 Neurons express two contactin isoforms that differ in their extent of glycos

182 nce of L1-Fc, the extracellular portion of a contactin ligand expressed on axons, enhanced survival a

183 Contactin may thus significantly influence the functiona

184 g this assay, we have now identified Manduca Contactin (MsContactin) as an endogenous ligand for APPL

185 Analysis of the contactin-/- mutant cerebellum revealed defects in granu

186 Contactin-/- mutants displayed a severe ataxic phenotype

187 The contactin mutation does not affect sodium channel cluste

188 To investigate precisely the role of contactin N-glycans, we have mutated each of the nine co

189 s, whereas a higher-molecular-weight form of contactin, not associated with Caspr, is present in cent

190 uggest that binding of glial RPTPbeta to the contactin/Nr-CAM complex is important for neurite growth

191 Besides, our study also implicated Contactins-NYAPs-WAVE1 pathway in ASD pathogenesis.

192 inositol (GPI)-anchored recognition molecule contactin on neuronal cells leading to neurite outgrowth

193 he glial membrane and a complex of Caspr and contactin on the axon.

194 a(v)1.2alpha alone, Na(v)1.2/beta1, Na(v)1.2/contactin, or Na(v)1.2/beta1/beta2.

195 These results indicate that contactin plays a selective role in synaptic plasticity

196 sites (N467Q/N473Q/N494Q) in Ig domain 5 of contactin prevented soluble NF155-Fc binding.

197 ctions among multiple members of the APP and contactin protein families.

198 In sciatic nerve, the expression of contactin, receptor protein tyrosine phosphatase beta, a

199 ent Axonal Glycoprotein 1 (TAG1 or CNTN2), a contactin-related adhesion molecule, plays a central rol

200 t not beta2, interacts heterophilically with contactin, resulting in increased levels of cell surface

201 Contactin selectively supports paired-pulse facilitation

202 udy, we mapped the molecular determinants of contactin targeted by the autoantibodies.

203 These results suggest that the targeting of contactin to different axonal domains may be determined,