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 Additionally, NCAM-EC mice were impaired in contextual and cued fear c

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 measurements with both full-length NCAM and NCAM mutants that lack different immunoglobulin (Ig) dom

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

29 TrkB and NCAM gene expression in laser capture microdissected tas

30 TrkB and NCAM may be therapeutic targets for aggressive neuroendo

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

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 tophysin compared with chromogranin and CD56/NCAM.

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

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

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

59 -4 weeks post-partial denervation in Hb9(cre)NCAM(flx) mice, while another 25% were partially reinner

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

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

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

63 8Sia IV with alanine substantially decreased NCAM-specific polysialylation while only partially impac

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

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

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

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

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

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

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

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

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

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

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

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

76 e residues may be particularly important for NCAM polysialylation.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

99 and extracellular matrix proteins, including NCAM and collagen II (Col2a1) in the limb bud.

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

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

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

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

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

105 2 group F member 6, whereas the PSA-lacking NCAM fragment increases mRNA and protein expression of l

106 ule force measurements with both full-length NCAM and NCAM mutants that lack different immunoglobulin

107 f the rupture forces between the full-length NCAM extracellular domains revealed two binding events,

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

152 tein scaffold neural cell adhesion molecule (NCAM).

153 modifying the neural cell adhesion molecule (NCAM).

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

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

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

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

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

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

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

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

162 added to the neural cell adhesion molecule, NCAM.

163 erases is 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 meters that describe the energy landscape of NCAM-NCAM bonds.

191 in response to the extracellular ligands of NCAM.

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

193 The homophilic binding mechanism of NCAM is still a subject of debate on account of findings

194 to the hinge seen in electron micrographs of NCAM.

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

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

197 for the protein-specific polysialylation of NCAM.

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

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

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

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

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

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

204 pCAM bonds are quite different from those of NCAM.

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

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

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

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

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

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

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

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

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

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

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

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

217 unit expansion in the absence of presynaptic NCAM.

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

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

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

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

222 In contrast, PSA-NCAM, calbindin and GAD67 immunohistochemistry did not r

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

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

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

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

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

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

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

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

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

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

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

245 ysialylated protein, could partially replace NCAM FN1.

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

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

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

249 velopment and function of expressing soluble NCAM-EC from the neuron-specific enolase promoter in the

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

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

258 urface-force measurements, which showed that NCAM forms two spatially distinct bonds between opposed

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

278 The NCAMs studied here are characterized by a positive zeta

279 H+] in microfluidic channels adjacent to the NCAMs yield information regarding diffusive and electrok

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

296 -96 kDa) were present in chick corneas, with NCAM-120 being the predominate isoform.

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

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

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

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

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