ライフサイエンスコーパス: NCAM

1 NCAM and polySia are expressed and developmentally regul

2 NCAM and ST8SiaII mRNA transcripts peaked by embryonic d

3 NCAM enhanced ephrin-A5-induced EphA3 autophosphorylatio

4 NCAM forms a complex between its terminal domains Ig1 an

5 NCAM is upregulated during the remodeling period of hype

6 NCAM upregulation induces the formation of novel signali

7 NCAM was localized to the epithelium, stroma, and stroma

8 NCAM-dependent Pak1 activation was abolished after lipid

9 NCAM-EC transgenic mice exhibited a striking reduction i

10 NCAM-mediated clustering of EphA3 was essential for ephr

11 Five NCAM isoforms including NCAM-120, NCAM-180 and three soluble NCAM isoforms with low molecu

12 or the synaptic targeting of presynaptic 140 NCAM but that the localization of presynaptic 180 NCAM o

13 but that the localization of presynaptic 180 NCAM occurs via a different mechanism.

14 these candidates, four targets (i.e. TIMP-2, NCAM-1, JAM-C, and tissue factor (TF)) were selected for

15 , we asked whether peripherally administered NCAM peptide mimetics penetrate the brain and alter the

16 is study, we show that impaired LTP in adult NCAM-deficient (NCAM(-/-)) mice is restored by increasin

17 ess plating of gold into the nanopores of an NCAM (Au-NCAM).

18 alylation and enhanced O-glycosylation of an NCAM- olfactory cell adhesion molecule chimera, and inse

19 Proton transfer through an NCAM into microchannels is reduced for pore diameters, d

20 ule analyses further indicate that apCAM and NCAM are species homologs likely performing similar func

21 their role in enzyme autopolysialylation and NCAM-specific polysialylation.

22 on are indicated by decreased E-cadherin and NCAM expression and by ineffective differentiation in re

23 f the cell surface proteins, EpCAM/CD326 and NCAM/CD56.

24 for the best-understood CAMs--L1, CHL1, and NCAM--important for neuronal migration and axon guidance

25 nts responsible for human PrP(C) (HuPrP) and NCAM interaction using stimulated emission depletion (ST

26 sed neuronal markers such as Tuj1, Map2, and NCAM.

27 contrasts with the mouse, where polySia and NCAM expression are restricted to multipotent hematopoie

28 TrkB and NCAM gene expression in laser capture microdissected tas

29 TrkB and NCAM may be therapeutic targets for aggressive neuroendo

30 vation and on failures in both wild-type and NCAM 180 null junctions supported this pathway, and seri

31 Another NCAM peptide mimetic, FGL(L), had acute anxiogenic effec

32 notochord, and paraxial mesoderm as well as NCAM and XMyoD expression.

33 the Fab'-Au-NCAM relative to the control Au-NCAM.

34 an 20-fold after passing through the Fab'-Au-NCAM relative to the control Au-NCAM.

35 ng of gold into the nanopores of an NCAM (Au-NCAM).

36 The affinity-tagged Au-NCAM can be incorporated into microfluidic devices to al

37 An antibody is then immobilized on the Au-NCAM via gold-thiol chemistry as a thiolated fragment of

38 ibodies, which mimic the interaction between NCAM and its extracellular ligands.

39 the polyST, ST8SiaIV/PST, specifically binds NCAM and that this binding requires the FN1 domain.

40 compete with SW2 cell ST8SiaIV/PST and block NCAM polysialylation.

41 ylation site, decreases or completely blocks NCAM polysialylation.

42 Additionally, both NCAM and polySia were detected on embryonic corneal and

43 ansferase domain of ST8Sia IV decreased both NCAM polysialylation and autopolysialylation in parallel

44 fragment adhesion and the strengths of both NCAM bonds shows that the domain deletions considered in

45 in-A5 induced co-clustering of surface-bound NCAM and EphA3 in GABAergic cortical interneurons in cul

46 tion and suppress differentiation induced by NCAM.

47 PSA modulates cell interactions mediated by NCAM and other adhesion molecules.

48 replacing three identical regions shared by NCAM and OCAM FN1, (500)PSSP(503) (PSSP), (526)GGVPI(530

49 nuclear import of PSA-lacking and -carrying NCAM fragments.

50 is we verified that the nuclear PSA-carrying NCAM fragment increases mRNA and protein expression of n

51 In the nucleus, the PSA-carrying NCAM fragment interacts via PSA with PC4 and cofilin, wh

52 Here, we show that a PSA-carrying NCAM fragment is generated at the plasma membrane by mat

53 sults indicate that the nuclear PSA-carrying NCAM fragment is generated by distinct and functionally

54 that the nuclear import of the PSA-carrying NCAM fragment is mediated by positive cofactor 4 and cof

55 pression on human NK cells the role of CD56 (NCAM) in human NK cell cytotoxic function has not been d

56 tophysin compared with chromogranin and CD56/NCAM.

57 In non-immune cells, NCAM can induce signaling, mediate adhesion, and promote

58 combinations of markers, suggest that CK19+/NCAM+ cells are transitional cells in the biliary lineag

59 ast, similarly denervated muscles in Hb9(cre)NCAM(flx) mice failed to recover the force lost due to t

60 remained at extrasynaptic regions in Hb9(cre)NCAM(flx) mice rather than being distributed, as occurs

61 -4 weeks post-partial denervation in Hb9(cre)NCAM(flx) mice, while another 25% were partially reinner

62 ions of NMJs in partially denervated Hb9(cre)NCAM(flx) soleus muscles, one with high (mature) quantal

63 Extrasynaptic SVs in Hb9(cre)NCAM(flx) sprouts were associated with L-type voltage-de

64 es in mice lacking presynaptic NCAM (Hb9(cre)NCAM(flx)).

65 8Sia IV with alanine substantially decreased NCAM-specific polysialylation while only partially impac

66 nces and the acidic patch residues decreases NCAM-polyST binding, whereas replacing the GGVPI and NGK

67 w that impaired LTP in adult NCAM-deficient (NCAM(-/-)) mice is restored by increasing the activity o

68 Western blot analyses were used to determine NCAM expression and polysiaylation in embryonic, hatchli

69 by a charge reversal mutation that disrupted NCAM/EphA3 association, emphasizing the importance of th

70 putative FGFR1-binding segments, one in each NCAM FN3 domain, are situated close to the domain interf

71 iaIV/PST substantially reduces or eliminates NCAM polysialylation, respectively.

72 multiple residues are involved in the enzyme-NCAM interaction.

73 rly, stem/progenitor surface markers (EpCAM, NCAM, CD133, CXCR4), and sometimes weakly adult liver, b

74 Five NCAM isoforms including NCAM-120, NCAM-180 and three sol

75 tein interaction region that is critical for NCAM recognition and polysialylation by the polysialyltr

76 ansferases do not require the Ig5 domain for NCAM recognition, their ability to engage with this doma

77 ll adhesion molecule (NCAM) is essential for NCAM-mediated neurite outgrowth.

78 e residues may be particularly important for NCAM polysialylation.

79 e compared the PBR sequence requirements for NCAM, neuropilin-2 (NRP-2), and synaptic cell adhesion m

80 vation of RhoA GTPase, indicating a role for NCAM in activating EphA3 signaling through clustering.

81 Immunofluorescence staining for NCAM and polySia was conducted on cryosections of embryo

82 Other polysiaylated proteins aside from NCAM were also detected by Western blot analysis.

83 and cofilin was reduced in growth cones from NCAM-deficient neurons, which was accompanied by decreas

84 While PSA removal from NCAM by spinal intrathecal injection of endoneuraminidas

85 Whether and how NCAM per se affects GABAergic synapse development is unk

86 We solved the crystal structure of human NCAM FN1 and found that, in addition to a unique acidic

87 n LTP that could be fully restored by DCS in NCAM(+/+) mice but only partially restored in NCAM(-/-)

88 mate mice and abolished the rescue by DCS in NCAM(-/-) mice, suggesting that the effects of DCS are m

89 rons included basket interneurons evident in NCAM-EC transgenic mice intercrossed with a reporter lin

90 n, whereas Arg(93) specifically functions in NCAM recognition.

91 ose carrying the polysialylated N-glycans in NCAM substantially decrease or eliminate polysialylation

92 nsferase catalytic motifs may be involved in NCAM recognition, but not overall enzyme activity.

93 N2A subtype reduced LTP to the same level in NCAM(-/-) and wild-type (NCAM(+/+)) littermate mice and

94 insufficient contribution of GluN to LTD in NCAM(-/-) mice was also compensated for by DCS.

95 dues (Ser and Asn) in analogous positions in NCAM Ig5.

96 ed fear conditioning levels were restored in NCAM(-/-) mice by administration of DCS before condition

97 CAM(+/+) mice but only partially restored in NCAM(-/-) mice.

98 ace patch and alpha-helix that play roles in NCAM polysialylation.

99 ed in NRP-2 and SynCAM 1 recognition than in NCAM recognition.

100 Five NCAM isoforms including NCAM-120, NCAM-180 and three soluble NCAM isoforms with

101 er permeability and gap junctions, increased NCAM expression and produced haemorrhagic angiogenesis i

102 nd microscopic model assumes two independent NCAM-NCAM bonds, and more accurately describes the break

103 inserting non-conserved OCAM sequences into NCAM Ig5, including an "extra" N-glycosylation site, dec

104 d that the nuclear PSA-carrying and -lacking NCAM fragments affect expression of different genes.

105 PSA indicates that PSA-carrying and -lacking NCAM play different functional roles in the nervous syst

106 2 group F member 6, whereas the PSA-lacking NCAM fragment increases mRNA and protein expression of l

107 polysialylation but not that of full-length NCAM, suggesting that the two proteins are interacting d

108 ysialic acid to FN1 O-glycans in full-length NCAM.

109 al Ig5-FN1 substrate but also of full-length NCAM.

110 rst time (to our knowledge) that apCAM, like NCAM, is indeed a homophilic cell adhesion molecule.

111 Furthermore, like NCAM, apCAM exhibits two distinct bonds in the trans con

112 g cell marker MASH1, nor the neuronal marker NCAM.

113 Nanocapillary array membranes (NCAMs), comprised of thin (d approximately 5-10 microm)

114 Nanocapillary array membranes (NCAMs), consisting of thin (5 microm < d < 20 microm) me

115 ier of polysialic acid (PSA) which modulates NCAM functions of neural cells at the cell surface.

116 ubclasses, the neural cell adhesion molecule NCAM and the L1 family of adhesion molecules, which shar

117 d FACS for the neural cell adhesion molecule NCAM on differentiated PDiPS cells before transplantatio

118 n carrier, the neural cell adhesion molecule NCAM, play important roles in many nervous system functi

119 loop (FGL) of neural cell adhesion molecule (NCAM) (5 microg, i.c.v.) into the lateral ventricle of r

120 Since neural cell adhesion molecule (NCAM) activates FGF receptors, we asked whether peripher

121 antibodies to neural cell adhesion molecule (NCAM) and ATP receptor P2X3.

122 The neural cell adhesion molecule (NCAM) and the receptor tyrosine kinase EphA3 regulate th

123 dominantly on neural cell adhesion molecule (NCAM) during development of the vertebrate nervous syste

124 e function of neural cell adhesion molecule (NCAM) expression in motor neurons during axonal sproutin

125 id not affect Neural Cell Adhesion Molecule (NCAM) expression or Schwann cell migration in vitro.

126 actors, the neuronal cell adhesion molecule (NCAM) has been studied in vivo, but the structural basis

127 added to the neural cell adhesion molecule (NCAM) in the Golgi by PST or STX polysialyltransferase.

128 Neural cell adhesion molecule (NCAM) is a cell surface adhesion glycoprotein that plays

129 ling molecule neural cell adhesion molecule (NCAM) is a downstream target of NeuroD1, whose impaired

130 tor (FGFR) by neural cell adhesion molecule (NCAM) is essential for NCAM-mediated neurite outgrowth.

131 The neural cell adhesion molecule (NCAM) is the major carrier of polysialic acid (PSA) whic

132 The neural cell adhesion molecule (NCAM) is the major substrate for the polysialyltransfera

133 Neural cell adhesion molecule (NCAM) is the predominant carrier of the unusual glycan p

134 e lacking all neural cell adhesion molecule (NCAM) isoforms or only the 180 isoform demonstrated that

135 c acid on the neural cell adhesion molecule (NCAM) modulates cell-cell adhesion and signaling, is req

136 The neural cell adhesion molecule (NCAM) plays an important role in nervous system developm

137 The Neural cell adhesion molecule (NCAM) plays an important role in regulation of nervous s

138 cation of the neural cell adhesion molecule (NCAM) produced by the polysialyltransferases ST8SIA2 and

139 required for neural cell adhesion molecule (NCAM) recognition and subsequent polysialylation.

140 arried by the neural cell adhesion molecule (NCAM) regulates the timing of their maturation.

141 orthologue of neural cell adhesion molecule (NCAM), as a physiologically significant and specific inh

142 cule (EpCAM), neural cell adhesion molecule (NCAM), cytokeratin (CK) 19, albumin +/-, and are negativ

143 cation of the neural cell adhesion molecule (NCAM), polySia is produced by the polysialyltransferases

144 ncluding CD56/neural cell adhesion molecule (NCAM), promoted phagocytosis in human SCLC cell lines th

145 alized with neuronal cell adhesion molecule (NCAM), suggesting that these TRCs may have synaptic cont

146 found on the neural cell adhesion molecule (NCAM), where it is synthesized on N-glycans by either of

147 , we used the neural cell adhesion molecule (NCAM), which was recently shown to form two independent

148 cumulation of neural cell adhesion molecule (NCAM)-positive myofibres, and an accumulation of pyknoti

149 proportion of neural cell adhesion molecule (NCAM)-positive satellite cells; (iv) improved muscle oxi

150 (Ig5) of the neural cell adhesion molecule (NCAM).

151 lySTs) is the neural cell adhesion molecule (NCAM).

152 strate is the neural cell adhesion molecule (NCAM).

153 tein scaffold neural cell adhesion molecule (NCAM).

154 modifying the neural cell adhesion molecule (NCAM).

155 tached to the neural cell adhesion molecule (NCAM).

156 soform of the neural cell adhesion molecule (NCAM).

157 he vertebrate neural cell adhesion molecule (NCAM); however, whether apCAM exhibits similar binding p

158 M stabilizing neural cell adhesion molecule (NCAM-120).

159 transmembrane neural cell adhesion molecule (NCAM-EC) is shed as a soluble fragment at elevated level

160 cule [EpCAM], neural cell adhesion molecule [NCAM], epithelial growth factor receptor [EGFR]), and in

161 nal reveals that the cell-adhesion molecule, NCAM, is at the heart of crosstalk between E-cadherin lo

162 lycans of the neural cell adhesion molecule, NCAM, is critical for brain development and plays roles

163 added to the neural cell adhesion molecule, NCAM.

164 mbers are the neural cell adhesion molecules NCAM and L1, which were the first to be shown to be esse

165 (polySia) on neural cell adhesion molecules (NCAM).

166 ymal interactions during skin morphogenesis (NCAM, versican, and alkaline phosphatase) were all sever

167 In 12-month-old NCAM(-/-), but not NCAM(+/+) mice, there was a decline in LTP compared with

168 ch correlate with reduced cleavage of NrCAM, NCAM and other ADAM10 substrates.

169 fferential gene expression evoked by nuclear NCAM fragments without and with PSA indicates that PSA-c

170 onstrated higher basal locomotor activity of NCAM-EC mice and enhanced responses to amphetamine and (

171 s study, it was demonstrated that binding of NCAM and EphA3 occurred between the NCAM Ig2 domain and

172 nd Pak1 activity were inhibited in brains of NCAM-deficient mice.

173 Thus, several deficiencies of NCAM(-/-) mice can be ameliorated by enhancing GluN2A-me

174 gh the removal of PSA by genetic deletion of NCAM also results in a smaller OB and a swollen RMS, the

175 We find that depletion of NCAM, inhibition of the dynein-NCAM180 interaction, or d

176 Impaired differentiation of NCAM- or ST8SIA2-negative oligodendrocyte precursors sug

177 The distributions of NCAM and polySia in cornea and on corneal nerves suggest

178 cognize an acidic patch in the FN1 domain of NCAM but also must contact sequences in the Ig5 domain f

179 the fibronectin type 3 (FN3)-like domains of NCAM as being important for these activities.

180 e form of Fyn kinase rescues, the effects of NCAM knockdown.

181 d that human NK cells modulate expression of NCAM and the degree of polymerization of its polySia gly

182 e first fibronectin type III repeat (FN1) of NCAM is required for polysialylation of the N-glycans on

183 e first fibronectin type III repeat (FN1) of NCAM is required for polyST recognition and the polysial

184 e first fibronectin type III repeat (FN1) of NCAM is required for the polysialylation of N-glycans on

185 second fibronectin type III repeat (FN2) of NCAM cannot replace FN1.

186 ts with the polysialic-acid-modified form of NCAM reveal that, at physiological ionic strength, the c

187 as been considered as the Aplysia homolog of NCAM.

188 on the fifth immunoglobulin domain (Ig5) of NCAM requires the presence of specific sequences in the

189 An isoform of NCAM (CD56) on natural killer (NK) cells is the only pro

190 in response to the extracellular ligands of NCAM.

191 However, loss of NCAM once the synapses are already formed did not show a

192 to the hinge seen in electron micrographs of NCAM.

193 eening to search for new binding partners of NCAM and identified p21-activated kinase 1 (Pak1).

194 The polysialylation of NCAM N-glycans decreases cell adhesion and alters signal

195 for the protein-specific polysialylation of NCAM.

196 These findings suggest that the presence of NCAM without PSA plays a role in the dispersion process,

197 of the NCAM ectodomain and the regulation of NCAM adhesion by post-translational modification.

198 hat the first fibronectin type III repeat of NCAM (FN1) was necessary for the polysialylation of the

199 in the first fibronectin type III repeat of NCAM are required for the polysialylation of N-glycans o

200 The first fibronectin type III repeat of NCAM, FN1, is necessary for the polysialylation of N-gly

201 results suggested that elevated shedding of NCAM perturbs synaptic connectivity of GABAergic interne

202 pCAM bonds are quite different from those of NCAM.

203 To evaluate the capability of NCAMs to support pH gradients, the proton transport prop

204 radients, the proton transport properties of NCAMs were studied using laser scanning confocal fluores

205 In 12-month-old NCAM(-/-), but not NCAM(+/+) mice, there was a decline i

206 hly conserved C-terminal (KENESKA) domain on NCAM that is required to maintain effective transmission

207 PolySia levels on NCAM in adult mice were reduced significantly upon admin

208 Deficits in PSA and/or NCAM expression cause impairments in hippocampal long-te

209 Using single-cell genetics to knock out NCAM in individual basket interneurons in mouse cortical

210 Polysialylated NCAM (PSA-NCAM) and perineuronal nets, highly glycosylat

211 Polysialylated NCAM is critical for brain development and plays roles i

212 , requiring an initial polysialyltransferase-NCAM protein-protein interaction.

213 tead is correlated with a decrease in polyST-NCAM binding.

214 hese observations indicate that postsynaptic NCAM is required for the synaptic targeting of presynapt

215 g soleus muscles in mice lacking presynaptic NCAM (Hb9(cre)NCAM(flx)).

216 unit expansion in the absence of presynaptic NCAM.

217 We propose that presynaptic NCAM bridges a critical link between the SV cycle and th

218 rious cellular markers; doublecortin and PSA-NCAM as the early neuronal marker, NeuN to identify matu

219 Therefore, the number of DCX and PSA-NCAM immunoreactive cells in the piriform cortex were qu

220 large reduction in the number of DCX and PSA-NCAM immunoreactive cells in the piriform cortex, simila

221 hildren, most PL cells are immature (DCX+PSA-NCAM+), and during adolescence many transition into matu

222 cells in the SVZ, such as doublecortin, PSA-NCAM, beta-tubulin, Dlx2, or GFAP.

223 tion as has been reported for endogenous PSA-NCAM.

224 o be immature granule neurons expressing PSA-NCAM, calretinin, and Prox-1.

225 nded distribution of the new-cell marker PSA-NCAM (polysialylated form of neural cell adhesion molecu

226 ialylated neural cell adhesion molecule (PSA-NCAM) are associated with structural plasticity in the a

227 rm of the neural cell adhesion molecule (PSA-NCAM) functions broadly, serving to mediate synaptic pla

228 ialylated neural cell adhesion molecule (PSA-NCAM) in adult spinal substantia gelatinosa also express

229 d form of neural cell adhesion molecule (PSA-NCAM) is expressed by these cells, and has been shown to

230 -carrying neural cell adhesion molecule (PSA-NCAM) with MARCKS and co-immunostaining of MARCKS and PS

231 ialylated neural cell adhesion molecule (PSA-NCAM).

232 Polysialylated NCAM (PSA-NCAM) and perineuronal nets, highly glycosylated molecul

233 ral progenitor cell development (nestin, PSA-NCAM, NeuN, and Tuj1) but did not colocalize with marker

234 id)EGFR(high)PlexinB2(high)CD24(-/low)O4/PSA-NCAM(-/low)Ter119/CD45(-) (GEPCOT) cells.

235 Depletion of PSA-NCAM in the ventromedial prefrontal cortex was sufficien

236 Moreover, the expression of PSA-NCAM is reduced by depression, and conversely enhanced b

237 owed that extracellularly applied PSA or PSA-NCAM and intracellularly expressed MARCKS-GFP are in clo

238 addition of fluorescently labeled PSA or PSA-NCAM to live CHO cells or hippocampal neurons expressing

239 These data indicate that PSA-NCAM-mediated neuroplasticity is necessary for antidepre

240 ary for antidepressant action; therefore PSA-NCAM represents an interesting, and novel, target for ph

241 pete with endogenous ST8SiaIV/PST and reduce NCAM polysialylation in SW2 small cell lung carcinoma ce

242 utopolysialylation but significantly reduced NCAM polysialylation.

243 (580)NGKG(583) (NGKG), dramatically reduces NCAM polysialylation.

244 A related NCAM peptide mimetic, FGL(S), had antidepressant effects

245 olecule (OCAM) was able to partially replace NCAM FN1.

246 ysialylated protein, could partially replace NCAM FN1.

247 Western blot analysis revealed NCAM was polysialylated and its expression developmental

248 Also, the location of singly NCAM-positive cells in DRs suggests that they may be bip

249 Both membrane-associated and soluble NCAM isoforms are expressed in chick corneas.

250 cluding NCAM-120, NCAM-180 and three soluble NCAM isoforms with low molecular weights (87-96 kDa) wer

251 In stroma, NCAM expression shifted from anterior to posterior strom

252 imulation of cultured neurons with surrogate NCAM ligands leads to the generation and nuclear import

253 Here we demonstrate that NCAM and ST8SIA2 promote oligodendrocyte differentiation

254 ic developmental time periods, we found that NCAM loss during perisomatic synapse formation impairs t

255 Our combined observations thus indicate that NCAM activates Pak1 to drive actin polymerization to pro

256 Results indicate that NCAM peptide mimetics penetrate the brain and support th

257 Evidence indicates that NCAM polysialylation is highly protein-specific, requiri

258 We show that NCAM interacts with Pak1 in growth cones of neurons.

259 after lipid raft disruption, suggesting that NCAM promotes Pak1 activation in the lipid raft environm

260 The NCAM peptide mimetic, plannexin, acutely increased and c

261 about the interaction between HuPrP and the NCAM fibronectin domain, and revealed a new role of PrP(

262 e-synaptic cacophony Ca(2+) channels and the NCAM-like adhesion molecule, Fasciclin II, take part in

263 ted only a very weak interaction between the NCAM FN3 tandem and soluble FGFR1 proteins expressed in

264 nding of NCAM and EphA3 occurred between the NCAM Ig2 domain and EphA3 cysteine-rich domain (CRD).

265 at is normalized for nucleosome density, the NCAM (normalized chromatin accessibility to MNase) assay

266 sed of complementary charged residues in the NCAM Ig2 domain (Arg-156 and Lys-162) and the EphA3 CRD

267 Moreover, the NCAM antibody triggers calmodulin-dependent activation o

268 tural insights into the configuration of the NCAM ectodomain and the regulation of NCAM adhesion by p

269 uPrP N terminus and the second module of the NCAM fibronectin type-3 domain.

270 Here we report the crystal structure of the NCAM FN3 domain tandem, which reveals an acutely bent do

271 ustering of EphA3 through interaction of the NCAM Ig2 domain and the EphA3 CRD, stimulating EphA3 aut

272 we have solved the crystal structure of the NCAM Ig5-FN1 tandem.

273 e also produced by selective deletion of the NCAM-180 isoform.

274 sociation, emphasizing the importance of the NCAM/EphA3 binding interface for cluster formation.

275 residues for substrate recognition, that the NCAM-recognizing PBR sites in ST8Sia-II and ST8Sia-IV in

276 Thus, the NCAM-FGFR1 interaction at the cell surface is likely to

277 tail, which binds with high affinity to the NCAM fibronectin type-3 domain.

278 lybasic regions that might interact with the NCAM acidic patch or the growing polysialic acid chain.

279 ere is interest in H+-transport across these NCAMs because there is significant practical interest in

280 In contrast to NCAM, little is known on the biosynthesis of polySia on

281 In contrast to NCAM-deficient, ST8SiaII-deficient, or ST8SiaIV-deficien

282 Although PST(Nm) was able to add PSA to NCAM, most of its product was attached to other cell sur

283 and inserting other FN1 sequences unique to NCAM, predominantly the acidic patch, created a new poly

284 neurons is induced by a function-triggering NCAM antibody and a peptide comprising the effector doma

285 the O-glycan polysialylation of a truncated NCAM protein, and replacing the alpha-helix or QVQ shift

286 o the same level in NCAM(-/-) and wild-type (NCAM(+/+)) littermate mice and abolished the rescue by D

287 e contractile force of muscles in wild-type (NCAM(+/+)) mice recovered completely 2 weeks after 75% o

288 and functional similarities with vertebrate NCAM and therefore has been considered as the Aplysia ho

289 When NCAM of cell A and of cell B connect to each other throu

290 increased in the HT-lo/diss variant, whereas NCAM-1, JAM-C, and TF levels were increased in the HT-hi

291 This study delineates a mechanism in which NCAM promotes ephrin-A5-dependent clustering of EphA3 th

292 anding of the molecular mechanisms via which NCAM influences differentiation of neurons, we used a ye

293 g a new pattern of migration associated with NCAM-dependent differentiation.

294 the 140 isoform was targeted on contact with NCAM-/- myotubes.

295 -96 kDa) were present in chick corneas, with NCAM-120 being the predominate isoform.

296 ovel signaling complexes that correlate with NCAM-dependent focal adhesion assembly, migration, and c

297 en isolated growth cones were incubated with NCAM function triggering antibodies, which mimic the int

298 PrP(C) co-localizes with NCAM in mouse hippocampal neurons, and this interaction

299 Staining with NCAM, CK19, and HepPar1 has revealed a distinctly bipola

300 uggesting that conformational changes within NCAM may modulate FGFR1 activation.