ライフサイエンスコーパス: MAG

1 MAG (0-2.5wt%) had no remarkable impact on the chemical

2 MAG binds NgR2 directly and with greater affinity than N

3 MAG can display clarithromycin resistance through the in

4 MAG inhibition of axon outgrowth in some neurons is reve

5 MAG percentage was maximum (7mol%) at lower water activi

6 MAG significantly decreased the interfacial tension of S

7 "MAG" PTLs for ionotropic and metabotropic glutamate rece

8 MAG's preferred ligands are derivatives of the monosialy

9 MAG, a member of the Siglec family of sialic acid-bindin

10 MAG-PEI25 reached a maximum adsorption capacity of 6.11

11 iated glycoprotein to proteolipid protein 1 (MAG:PLP1) ratio, which declines in chronically hypoperfu

12 ain that results in sn-2 monoacylglycerol (2-MAG) rather than LPA as the major product.

13 At low concentrations of 2-MAG (<50 microm), the major acylation product by DGAT1 w

14 TAG; however, increased concentrations of 2-MAG (50-200 microm) resulted in decreased TAG formation.

15 The possible roles of 2-MAGs as intermediates in cutin synthesis are discussed.

16 ) of an acylglycerol mixture (containing 67% MAGs) produced by enzymatic glycerolysis of sardine oil

17 h sidearm phosphorylation and demonstrates a MAG-mediated pathogenic effect of the anti-MAG antibody

18 d modulate alternative exon inclusion from a MAG minigene reporter.

19 rts binding of the myelin inhibitors Nogo-A, MAG (myelin-associated glycoprotein), and OMgp (oligoden

20 eoglycans and the myelin inhibitors (Nogo-A, MAG, and OMgp).

21 Three molecules, Nogo-A, MAG, and OMgp, are produced by oligodendrocytes and shar

22 e inhibitory proteins in CNS myelin: Nogo-A, MAG, and OMgp.

23 ith anti-MAG demyelinating polyneuropathy (A-MAG-DP).

24 Thirteen A-MAG-DP patients were randomized to rituximab and 13 to p

25 irst drug that improves some patients with A-MAG-DP in a controlled study.

26 -Cys(336) is deleted and followed by a 13 aa MAG-binding motif of the NgR2 stalk, shows superior bind

27 MASS1 RNAi or a specific inhibitor abrogates MAG up-regulation.

28 ique" domain are necessary for high-affinity MAG binding.

29 Although MAG:PLP1 tended to be lowest in cortex from patients wit

30 shows superior binding of OMgp, Nogo-66, and MAG compared with wild-type NgR1 or NgR2.

31 The physical properties of DAG and MAG in the SSO may be related to the chemical stability

32 We also examined the influence of DAG and MAG on the physical properties of SSO.

33 p (oligodendrocyte-myelin glycoprotein), and MAG (myelin-associated glycoprotein).

34 t the adhesive interactions between MUC1 and MAG are of biological significance in pancreatic cancer

35 asion showed the expression of both MUC1 and MAG.

36 me the inhibitory effects of both myelin and MAG for cortical, hippocampal, and DRG neurons.

37 ent in two major myelin inhibitors, Nogo and MAG, and their common receptor NgR1 (or NgR).

38 nal levels are commonly regulated by NT3 and MAG.

39 This NT3- and MAG-dependent axonal mRNA transport requires activation

40 NgR1 supports binding of Nogo-66, OMgp, and MAG.

41 The release of FFAs and MAGs from TAGs proceeded faster than their incorporation

42 of triacylglycerides, formation of FFAs and MAGs, and micellar incorporation of carotenoids, FFAs an

43 ellar incorporation of carotenoids, FFAs and MAGs.

44 Anti-MAG (myelin-associated glycoprotein) neuropathy is a dis

45 At month 8, IgM was reduced by 34% and anti-MAG titers by 50%.

46 immunological surrogate mouse model for anti-MAG neuropathy producing high levels of anti-MAG IgM was

47 toward an antigen-specific therapy for anti-MAG neuropathy.

48 th anti-myelin-associated glycoprotein (anti-MAG) neuropathy, an autoimmune disease of the peripheral

49 improved patients were those with high anti-MAG titers and most severe sensory deficits at baseline.

50 evidence of a treatment effect for IgM anti-MAG neuropathy and diabetic amyotrophy (radiculoplexus n

51 IgM levels, anti-MAG titers, B cells, antigen-presenting cells, and immun

52 enicity and demyelinating properties of anti-MAG autoantibodies are well established, current treatme

53 a correlation between the reduction of anti-MAG IgM levels and clinical improvement, an immunologica

54 MAG neuropathy producing high levels of anti-MAG IgM was developed.

55 selectively neutralizing the pathogenic anti-MAG antibodies with carbohydrate-based ligands mimicking

56 a MAG-mediated pathogenic effect of the anti-MAG antibody in peripheral nerves.

57 led study of rituximab in patients with anti-MAG demyelinating polyneuropathy (A-MAG-DP).

58 Patients with anti-MAG neuropathy showed substantial clonal expansions of b

59 binds to sialic acid in the same linkage as MAG.

60 iosides in the absence of inhibitors such as MAG is also shown to inhibit neurite outgrowth in cultur

61 hly expressed on adhesion molecules, such as MAG, present in myelinated nerve fibers.

62 f endogenous regeneration inhibitors such as MAG.

63 hibition of RGCs; however, it does attenuate MAG inhibition of cerebellar granule neurons.

64 ovide insights into how interactions between MAG and members of the Nogo receptor family function to

65 Finally, we show that hnRNPA1 binds MAG pre-mRNA and modulates alternative inclusion of MAG

66 itors and promotes neurite outgrowth on both MAG and CNS myelin substrates.

67 ardless of the NgR1 genotype, membrane-bound MAG strongly inhibits neurite outgrowth of primary cereb

68 Conversely, the repulsion conferred by MAG or netrin-1 on adult growth cones is mediated by pro

69 Growth cone repulsion induced by MAG was accompanied by localized Ca2+ signals on the sid

70 e bidirectional turning responses induced by MAG.

71 ly, NgR1(-/-) RGCs are strongly inhibited by MAG.

72 ty of neurotrophins, overcomes inhibition by MAG and myelin.

73 ulture and in vivo to overcome inhibition by MAG and that spermidine can promote optic nerve regenera

74 GF-like neurotrophins overcome inhibition by MAG by activating tyrosine kinase receptors.

75 he ability of cAMP to overcome inhibition by MAG in culture involves the upregulation of the enzyme a

76 AMP and putrescine to overcome inhibition by MAG is abolished in the presence of roscovitine, a Cdk i

77 ng lesion effect in overcoming inhibition by MAG is initially dependent on ongoing polyamine synthesi

78 y BDNF is required to overcome inhibition by MAG, and that activated Erk transiently inhibits phospho

79 trescine's ability to overcome inhibition by MAG.

80 verexpressing p35 can overcome inhibition by MAG.

81 In contrast to DRGNs, in CGNs MAG inhibition was exclusively via gangliosides, whereas

82 ever, only the chimeric molecules containing MAG Ig-5 inhibited neurite outgrowth.

83 the concentration of triacylglycerols, DAG, MAG and free fatty acids (FFA) and the concentration of

84 aired trafficking of plasma membrane-derived MAG through the endolysosomal system in primary cells an

85 biodistribution, mercapto-acetyl diglycine (MAG(2)) was compared with diethylenetriaminepentaacetic

86 AGs reveals two high-coverage, low-diversity MAGs from Piccard enriched in unique genes related to th

87 c nerve explants and then acutely eliminated MAG function along the nerve using chromophore-assisted

88 that hydrolyzes sialic acids and eliminates MAG-sialoglycan binding.

89 activity or membrane depolarization enhanced MAG-induced Ca2+ signals and converted growth cone repul

90 or scalable production of n-3 PUFAs enriched MAGs as potential food emulsifier and ingredient.

91 in the acyltransferase function but exhibits MAG and LPC hydrolase activities.

92 A focal MAG gradient induced polarized endocytosis and concomita

93 role for Nogo-A and synergistic actions for MAG and OMgp, presumably through shared receptors.

94 stinct and cell type-specific mechanisms for MAG-elicited growth inhibition.

95 re we show that NgR2 is a novel receptor for MAG and acts selectively to mediate MAG inhibitory respo

96 gated whether MUC1 is a counter-receptor for MAG and if their interaction contributed to pancreatic p

97 ors (NgRs) as exclusive axonal receptors for MAG.

98 The receptors responsible for MAG inhibition of neurite outgrowth varied with nerve ce

99 These results suggest a novel role for MAG/myelin in poor SC-myelin interaction and identify p7

100 on of NgR2, but not NgR1, are sufficient for MAG binding, and when expressed in neurons, exhibit cons

101 ing was neither necessary nor sufficient for MAG to bring about inhibition of neurite outgrowth.

102 of the in vitro TAG synthesis initiated from MAG is mediated by DGAT1 in Caco-2 cell and rat intestin

103 nd that triacylglycerol (TAG) synthesis from MAG by DGAT1 does not behave according to classic Michae

104 ic lesions of multifocal atrophic gastritis (MAG) and intestinal metaplasia (IM) have occurred.

105 reconstruct 73 metagenome-assembled genomes (MAGs) from two geochemically distinct vent fields in the

106 and maturation of the male accessory gland (MAG) in the red flour beetle, Tribolium castaneum.

107 lucose was converted to monoacetone glucose (MAG), and a single (2)H and (13)C NMR spectrum of MAG pr

108 e and its conversion to monoacetone glucose (MAG).

109 yelin marker [myelin associate glycoprotein (MAG)].

110 A, OMgp, and myelin-associated glycoprotein (MAG) and has been proposed to function as the ligand-bin

111 Myelin-associated glycoprotein (MAG) binds to the nerve cell surface and inhibits nerve

112 contain the myelin-associated glycoprotein (MAG) but not P(0) or proteolipid protein (PLP), the stru

113 covered that myelin-associated glycoprotein (MAG) expression is dramatically decreased in Frings mice

114 umulation of myelin-associated glycoprotein (MAG) in LAMP1(+)perinuclear vesicles that fail to migrat

115 irectly with myelin associated glycoprotein (MAG) in myelin, resulting in reduced activation of growt

116 Myelin-associated glycoprotein (MAG) is a potent inhibitor of axonal regeneration.

117 Myelin-associated glycoprotein (MAG) is a sialic acid-binding Ig-family lectin that func

118 Myelin-associated glycoprotein (MAG) is an abundant myelin protein that inhibits neurite

119 vous system, myelin-associated glycoprotein (MAG) on residual myelin binds to receptors on axons, inh

120 (OMgp), and myelin-associated glycoprotein (MAG) to mediate neurite outgrowth inhibition by these li

121 Myelin-associated glycoprotein (MAG), a membrane-bound protein expressed on oligodendroc

122 nstrate that myelin-associated glycoprotein (MAG), a well known inhibitor of neurite outgrowth, inhib

123 ogo/Nogo-66, myelin-associated glycoprotein (MAG), and oligodendrocyte myelin glycoprotein (OMgp).

124 e inhibitor, myelin-associated glycoprotein (MAG), binds to sialoglycans and other receptors on axons

125 gradient of myelin-associated glycoprotein (MAG), cAMP acts by modulating MAG-induced Ca2+ signaling

126 nous lectin, myelin-associated glycoprotein (MAG), is reported to bind to axonal gangliosides (GD1a a

127 olecule, the myelin-associated glycoprotein (MAG), located in the adaxonal plasmalemma of myelin-prod

128 tors such as myelin-associated glycoprotein (MAG), Nogo-A, and oligodendrocyte-myelin glycoprotein.

129 lin, such as myelin-associated glycoprotein (MAG), play an important role in preventing regeneration

130 lin, such as myelin-associated glycoprotein (MAG), represent major obstacles to axonal regeneration f

131 nts encoding myelin-associated glycoprotein (MAG), which generates two protein isoforms that associat

132 n induced by myelin-associated glycoprotein (MAG).

133 3 (NT3) and myelin-associated glycoprotein (MAG).

134 tion such as myelin-associated glycoprotein (MAG).

135 netrin-1 and myelin-associated glycoprotein (MAG).

136 (JAM-C) and myelin-associated glycoprotein (MAG).

137 lin, such as myelin-associated glycoprotein (MAG).

138 Myelin-associated glycoprotein (MAG, Siglec-4) is one of several endogenous axon regener

139 -1beta) and myelin-associated glycoproteins (MAG, Nogo).

140 val advantage of multiple arterial grafting (MAG) vs the standard use of left internal thoracic arter

141 ry isolated coronary artery bypass grafting (MAG, n = 5580; LITA+SVG, n = 14496) in the province of B

142 embers of the Mycobacterium abscessus group (MAG) cause lung, soft tissue, and disseminated infection

143 tional resistance, as well as slowly growing MAG strains and also strains displaying an inducible res

144 Soluble NgR2 has MAG antagonistic capacity and promotes neuronal growth o

145 However, MAG:PLP1 showed a significant negative correlation with

146 When applied acutely, however, MAG-Fc and OMgp-Fc induce a modest degree of growth cone

147 d expression of NgR2 is sufficient to impart MAG inhibition to neonatal sensory neurons.

148 These findings implicate MAG as an important component of the myelin-derived inhi

149 The decline in MAG:PLP1 strongly suggests pathological hypoperfusion of

150 In contrast, decreases in MAG expression and severe demyelination at the soma of S

151 e relative roles of gangliosides and NgRs in MAG-mediated inhibition of neurite outgrowth from three

152 We show here that incisures are present in MAG-null and absent from P(0)-null PNS internodes.

153 that SPD is able to concentrate n-3 PUFAs in MAG form by distilling at proper TE e.g. 125 degrees C,

154 more, peptides corresponding to sequences in MAG Ig-5, but not Ig-4 or Sn Ig-5, are able to block inh

155 C marker S100 and MBP expressions increased; MAG, GFAP, and SCMP expressions were very low.

156 oes not result in a substantial release of L-MAG (large MAG) inhibition.

157 that from wild-type mice, but myelin lacking MAG and OMgp is indistinguishable from control.

158 ult in a substantial release of L-MAG (large MAG) inhibition.

159 tgrowth almost as effectively as full-length MAG.

160 ptor for MAG and acts selectively to mediate MAG inhibitory responses.

161 The MILLIPLEX-MAG Rat cytokine-chemokine magnetic bead array was used

162 glycoprotein (MAG), cAMP acts by modulating MAG-induced Ca2+ signaling.

163 e fatty acids, FFAs, and monoacylglycerides, MAGs) during in vitro digestion of oil-in-water emulsion

164 tic activity for acylating monoacylglycerol (MAG).

165 f diacylglycerol (DAG) and monoacylglycerol (MAG) on the oxidative stability of stripped soybean oil

166 yzes the acylation of both monoacylglycerol (MAG) and diacylglycerol (DAG) to generate DAG and TAG, r

167 s revealed the presence of monoacylglycerol (MAG) and lysophosphatidylcholine (LPC) hydrolytic activi

168 Pretreatment with the monoacylglycerol (MAG) lipase inhibitor JZL-184 also reduced affective dis

169 aroyl lactylate (SSL) and monoacylglycerols (MAG) and Bacillus stearothermophilus maltogenic alpha-am

170 diacylglycerols (DAG) and monoacylglycerols (MAG) with a high content of polyunsaturated fatty acids

171 Production of monoacylglycerols (MAGs) rich in omega-3 polyunsaturated fatty acids (n-3 P

172 Antibodies against the MPZ, MAG, S100, and SCMP proteins immunostained along pericor

173 rs of axonal regeneration present in myelin--MAG, Nogo, and OMgp--all interact with the same receptor

174 nd flow cytometry, and this occurred in NAG, MAG and IM.

175 d substrata adsorbed with full-length native MAG extracted from purified myelin.

176 A soluble proteolytic fragment of native MAG, dMAG, also inhibited neurite outgrowth.

177 Consistent with its role as a neuronal MAG receptor, NgR2 is an axonassociated glycoprotein.

178 DGAT1 (IC(50) of human DGAT1: 16.6+/-4.0 nM (MAG as substrate) and 1499+/-318 nM (DAG as substrate);

179 Nogo, MAG and OMgp are three prototypical myelin inhibitors th

180 Nogo, MAG, and OMgp are myelin-associated proteins that bind t

181 f myelin-associated inhibitors such as Nogo, MAG, and OMgp.

182 which we have identified, do not bind Nogo, MAG, OMgp or NgR.

183 ical NgR signaling from myelin-derived Nogo, MAG, and OMgp consolidates the neural circuitry establis

184 icity, is a high-affinity receptor for Nogo, MAG, and OMgp.

185 proteins present in myelin, including Nogo, MAG, and oligodendrocyte-myelin glycoprotein (OMgp), hav

186 of the three major myelin inhibitors, Nogo, MAG, and OMgp, in injury-induced axonal growth, includin

187 Three proteins in mature myelin (Nogo, MAG, and OMgp) have been purported to be critical in cau

188 Three proteins found in myelin--Nogo, MAG, and OMgp--inhibit axon regeneration in vitro and bi

189 at the binding of soluble fragments of Nogo, MAG and NgR to cell-surface NgR requires the entire leuc

190 The myelin-derived proteins Nogo, MAG and OMgp limit axonal regeneration after injury of t

191 Three myelin proteins, Nogo, MAG (myelin-associated glycoprotein), and OMgp (oligoden

192 Our data indicate that while Nogo, MAG, and OMgp may modulate axon sprouting, they do not p

193 ration beyond the injury site in either Nogo/MAG/NgR1 triple mutants or NgR1 single mutants.

194 tially rescues neurite inhibition by Nogo66, MAG, OMgp, and myelin in cultured neurons.

195 erebral amyloid angiopathy, neither VEGF nor MAG:PLP1 correlated significantly with the severity of s

196 We here showed that SSL but not MAG delays wheat starch hydrolysis by BStA.

197 VEGF but not MAG:PLP1 increased with Alzheimer's disease severity, as

198 r that selectively inhibits the acylation of MAG by DGAT1 (IC(50) of human DGAT1: 16.6+/-4.0 nM (MAG

199 The addition of MAG (0.5wt%) suppressed the effectiveness of alpha-tocop

200 Subsequent 2H and 13C NMR analysis of MAG from normal volunteers after ingestion of 2H2O and [

201 f glycans and glycan mimetics as blockers of MAG-mediated axon outgrowth inhibition.

202 CALI of MAG permitted significant regrowth of retinal axons past

203 In contrast, labeling of CALI of MAG-treated crushed optic nerve showed significant retin

204 s and subgroups support the consideration of MAG for a broader spectrum of patients who are undergoin

205 iency was thought to underlie the defects of MAG splicing in the qk(v) mutant.

206 In contrast, deletion of MAG and OMgp stimulates neither axonal growth nor enhanc

207 show that the first three Ig-like domains of MAG bind with high affinity and in a sialic acid-depende

208 OLs completely rescues the dysregulation of MAG splicing without increasing expression or nuclear ab

209 ing I (QKI) leads to severe dysregulation of MAG splicing.

210 The ectodomain of MAG is comprised of five Ig-like domains and uses neuron

211 dbcAMP), can block the inhibitory effects of MAG and myelin.

212 inhibitory and repulsive turning effects of MAG in vitro.

213 ay mediate some of the inhibitory effects of MAG.

214 viously shown to bind an intronic element of MAG and modulate alternative exon inclusion from a MAG m

215 We show that when a truncated form of MAG missing Ig domains 1 and 2 is expressed by Chinese h

216 maturation of MAG by promoting the growth of MAG cells.

217 The growth of MAG was impaired after double-stranded RNA (dsRNA)-media

218 Domains Ig3-Ig5 of MAG are sufficient to inhibit neurite outgrowth but fail

219 -mRNA and modulates alternative inclusion of MAG exons.

220 Conversely, specific inhibition of MAG or sialyl-T MUC1 partially blocked adhesion.

221 ed potent monovalent sialoside inhibitors of MAG using a novel screening platform.

222 ral HNK-1 epitope blocked the interaction of MAG with pathogenic IgM antibodies from patient sera but

223 The acute loss of MAG function can promote significant axon growth across

224 g through IIS pathway regulate maturation of MAG by promoting the growth of MAG cells.

225 ilar effects on the growth and maturation of MAG.

226 pathways to regulate myelination by means of MAG protein stability in myelin-forming cells of the aud

227 nsistent with C1q-mediated neutralization of MAG.

228 compare the safety and long-term outcomes of MAG vs LITA+SVG among overall and selected subgroups of

229 A smaller percentage of MAG inhibition of DRGN outgrowth was via gangliosides, e

230 the binding pocket in the 2 photoisomers of MAG and (ii) the degree of clamshell closure that is pos

231 arginine 118 in the extracellular portion of MAG, but it is independent of Nogo signaling in the axon

232 enhance neurite outgrowth in the presence of MAG.

233 romotes neurite outgrowth in the presence of MAG.

234 The size of MAG increased from day 1 to day 5 post-adult emergence (

235 This increase in the size of MAG is contributed by an increase in cell size, but not

236 and a single (2)H and (13)C NMR spectrum of MAG provided the following metabolic data (all in units

237 MASS1 inhibits the ubiquitylation of MAG, thus enhancing the stability of this protein, and t

238 A synthesized short version of MAG turns the channel on in either the cis or trans stat

239 on emulsion presented a higher conversion of MAGs to FFAs during digestion, which led to a higher con

240 with 91% purity and 94% overall recovery of MAGs.

241 tic capacity and promotes neuronal growth on MAG and CNS myelin substrate in vitro.

242 oot ganglion neurons show enhanced growth on MAG compared to wild-type controls.

243 , DRG-cAMP returns to control, but growth on MAG/myelin improves and is now PKA independent.

244 ce extend significantly shorter processes on MAG compared with wild-type DRG neurons, and regeneratio

245 We conclude that the inhibition site on MAG is carried by Ig domain 5 and that this site is dist

246 showed that the sialic acid binding site on MAG maps to arginine 118 in Ig domain 1.

247 is, we now map a distinct inhibition site on MAG to Ig domain 5 (Ig-5).

248 ttraction to gradients of cAMP, netrin-1, or MAG is mediated by Epac.

249 evealed that increased expression of MUC1 or MAG enhanced adhesion.

250 Finally, when adding SSL or MAG on top of BStA to starch suspensions, the effect of

251 ssential source of cAMP for BDNF to overcome MAG-dependent inhibition of neurite outgrowth.

252 Mechanistically, MT-I/II ability to overcome MAG-mediated inhibition is transcription-dependent, and

253 quired for dbcAMP and putrescine to overcome MAG-mediated inhibition.

254 iGluR6 using a family of photoiosomerizable MAG (maleimide-azobenzene-glutamate) PTLs that covalentl

255 r myelin genes, such as proteolipid protein, MAG, MBP, and myelin oligodendrocyte glycoprotein, were

256 .1 (4.5-11.7) years for the groups receiving MAG and LITA+SVG, respectively.

257 of blood IgM memory B cells that recognized MAG antigen.

258 echanism in which C1q binding to MAG reduces MAG signaling to neurons, complement C1q blocked both th

259 oss of p75(NTR) is not sufficient to release MAG inhibition of RGCs, but p75(NTR-/-) dorsal root gang

260 t VCN treatment is not sufficient to release MAG inhibition of RGCs; however, it does attenuate MAG i

261 The ability to reverse MAG inhibition with monovalent glycosides encourages fur

262 ese were tested for their ability to reverse MAG-mediated inhibition of axon outgrowth from rat cereb

263 ndicated that blocking gangliosides reversed MAG inhibition.

264 An inhibitor of Rho kinase reversed MAG-mediated inhibition in all nerve cells, whereas a pe

265 tal dynamics after acute exposure to soluble MAG, OMgp, or Nogo-66, but is not required for these lig

266 vation of PKC and Rho in response to soluble MAG.

267 sted the presence of two separate substrate (MAG and LPC)-binding sites in a single polypeptide.

268 Comparison of nine Sulfurovum MAGs reveals two high-coverage, low-diversity MAGs from

269 In neurons NgR1 and NgR2 support MAG binding in a sialic acid-dependent Vibrio cholerae n

270 Compared with LITA+SVG, MAG is associated with reduced mortality, repeated revas

271 Compared with LITA+SVG, MAG was associated with reduced mortality rates (hazard

272 his binding is sialidase-sensitive, and that MAG physically associates with MUC1.

273 We also confirmed here that MAG binds to NgR2, but not to NgR3.

274 This reinforces the hypothesis that MAG is involved in the control of neurofilament spacing

275 Our data indicate that MAG inhibits axon outgrowth via two independent receptor

276 Here we show that MAG binding to cerebellar neurons induces alpha- and the

277 Results showed that MAG binds pancreatic cells expressing MUC1, that this bi

278 s report establishes for the first time that MAG also promotes resistance to axonal injury and preven

279 The MAG-Sn molecules were expressed in CHO cells and all con

280 In frontal cortex the MAG:PLP1 ratio was significantly reduced in Alzheimer's

281 ls on the side of the growth cone facing the MAG source, due to Ca2+ release from intracellular store

282 In DRGNs, most of the MAG inhibition was via NgRs, evidenced by reversal of in

283 hat is possible given the disposition of the MAG linker.

284 cs to probe the molecular composition of the MAG receptor complex in postnatal retinal ganglion cells

285 Modification of the MAG(2) radiometal chelator dramatically altered the upta

286 e, considering the multivalent nature of the MAG-IgM interaction, polylysine polymers of different si

287 ced axon regeneration in proportion to their MAG binding affinities.

288 cules of various combinations of these three MAG Ig domains fused to Ig domains from another Ig famil

289 glycerol was proven to be an alternative to MAG as acyl-group acceptor.

290 is mediated by IgM autoantibodies binding to MAG antigen.

291 -enhancing mechanism in which C1q binding to MAG reduces MAG signaling to neurons, complement C1q blo

292 gamma-secretase activity before exposing to MAG or CNS myelin improves SC migration and survival in

293 ficacy of two-photon (2P) excitation for two MAG molecules using nonlinear spectroscopy.

294 ition of neurite outgrowth by both wild-type MAG and CNS myelin.

295 Of 5580 participants who underwent MAG, 586 (11%) were women and the mean (SD) age was 60 (

296 which remained in an amorphous form, whereas MAG led to strong scattering, indicating the formation o

297 urther work is required to determine whether MAG dysregulation is a cause or consequence of audiogeni

298 diethylenetriaminepentaacetic acid and with MAG(2)-3,400-molecular-weight PEG (PEG(3,400)).

299 ction in EDN1, and positive correlation with MAG:PLP1, in the hypoperfused white matter in Alzheimer'

300 xpectedly, we found that OMgp interacts with MAG with a higher affinity compared with NgR1.