ライフサイエンスコーパス: myelin protein

1 It represents approximately 7% of total myelin protein.

2 characterization of the repertoire of human myelin proteins.

3 cture of myelin, and the expression level of myelin proteins.

4 nct complements of transcription factors and myelin proteins.

5 ndrocytes, including numerous genes encoding myelin proteins.

6 nock-outs (KOs) of the classic MBPs or other myelin proteins.

7 iple layers of bimolecular lipid leaflet and myelin proteins.

8 e-Tooth (CMT) disease caused by mutations in myelin proteins.

9 ainst paralysis induced by immunization with myelin proteins.

10 nectin production, and prevents synthesis of myelin proteins.

11 turn leads to the loss of the corresponding myelin proteins.

12 ific for myelin basic protein (MBP) or other myelin proteins.

13 inating and differentiating cells to express myelin proteins.

14 n identical in vivo hierarchy of these three myelin proteins.

15 lin internodes, as well as the expression of myelin proteins.

16 to overcome neurite outgrowth inhibition by myelin proteins.

17 ubsequent adaptive inflammatory responses to myelin proteins.

18 ng of transfectants that expressed different myelin proteins.

19 ority of T cell hybridomas were specific for myelin protein 0 (P0), which was the principal target of

20 d CNS-specific autoantigens derived from the myelin protein 2',3'-cyclic nucleotide 3'-phosphodiester

21 Reduced levels of the myelin protein 2'-3'-cyclic nucleotide 3'-phosphodiester

22 MT1A) is caused by duplication of peripheral myelin protein 22 (PMP22) and is the most common heredit

23 in the tetraspan membrane protein peripheral myelin protein 22 (PMP22) are known to result in periphe

24 deletions, and point mutations in peripheral myelin protein 22 (PMP22) are linked to several inherite

25 Haploinsufficiency of peripheral myelin protein 22 (PMP22) causes hereditary neuropathy w

26 ve leucine to proline mutation in peripheral myelin protein 22 (PMP22) causes the Trembler-J (TrJ) ne

27 ually caused by overexpression of peripheral myelin protein 22 (PMP22) due to a genomic duplication.

28 irect sequencing of the candidate peripheral myelin protein 22 (PMP22) gene detected a unique G-->C t

29 Alterations in peripheral myelin protein 22 (PMP22) gene expression are associated

30 of 17p11.2 and a deletion of the peripheral myelin protein 22 (PMP22) gene within 17p12 on the homol

31 copy number variant involving the Peripheral Myelin Protein 22 (PMP22) gene, which is located within

32 four novel point mutations in the peripheral myelin protein 22 (PMP22) gene.

33 is linked with duplication of the peripheral myelin protein 22 (PMP22) gene.

34 monly caused by overexpression of peripheral myelin protein 22 (PMP22) in Schwann cells of the periph

35 Since peripheral myelin protein 22 (PMP22) is a key component of myelin s

36 Peripheral myelin protein 22 (PMP22) is a short-lived Schwann cell

37 Peripheral myelin protein 22 (PMP22) is a tetraspan membrane glycop

38 Peripheral myelin protein 22 (PMP22) is an integral membrane protei

39 Peripheral myelin protein 22 (PMP22) is associated with a subset of

40 e is found in the relationship of peripheral myelin protein 22 (PMP22) to Charcot-Marie-Tooth disease

41 Peripheral myelin protein 22 (PMP22) was increased in CMT1A (PMP22

42 ession and cytosolic retention of peripheral myelin protein 22 (PMP22) within Schwann cells (SCs) is

43 utations in the gene encoding the peripheral myelin protein 22 (PMP22), a tetraspan protein in compac

44 Peripheral myelin protein 22 (PMP22), also known as growth arrest-s

45 Peripheral myelin protein 22 (PMP22), another member of the tetrasp

46 he alpha-helical membrane protein peripheral myelin protein 22 (PMP22), the intracellular misfolding

47 xtra copy and increased dosage of peripheral myelin protein 22 (PMP22).

48 ein components of myelin, such as peripheral myelin protein 22 (PMP22).

49 n protein zero gene (MPZ) and the peripheral myelin protein 22 gene (PMP22), appear to make aberrant

50 by an altered copy number of the peripheral myelin protein 22 gene (PMP22), which lies within the cr

51 n on chromosome 11 containing the peripheral myelin protein 22 gene (Pmp22).

52 chromosome 17 which includes the peripheral myelin protein 22 gene (PMP22).

53 e possession of two copies of the peripheral myelin protein 22 gene within the duplicated region on c

54 The occurrence of mutations in peripheral myelin protein 22 is one of the genetic mechanisms assoc

55 the genes encoding protein zero, peripheral myelin protein 22 kDa, and connexin32, all of which are

56 The peripheral myelin protein 22 mutation W28R was associated with CMT1

57 myelin protein zero mutation, 5 a peripheral myelin protein 22 mutation, 1 an early growth response f

58 These genes were peripheral myelin protein 22, decorin, transcription factor AP-1, d

59 alterations of several proteins: peripheral myelin protein 22, myelin protein zero, connexin 32, ear

60 nated by protein zero (P0)(+) and peripheral myelin protein 22-kDa (PMP22)(+) myelin, normally only p

61 myelin protein zero, and two for peripheral myelin protein 22.

62 T1) is caused by mutations in the peripheral myelin protein, 22 kDa (PMP22) gene, protein zero (P0) g

63 The peripheral myelin protein-22 (PMP22) gene is associated with the mo

64 osome 17p11.2, which contains the peripheral myelin protein-22 (PMP22) gene.

65 We investigated whether peripheral nerve myelin protein-22 (PMP22), the gene for which is duplica

66 rom an altered copy number of the peripheral myelin protein-22 gene, PMP22, which maps within the cri

67 chromosome 17p11.2 containing the peripheral myelin protein-22 gene.

68 ts that OSP is a CNS homologue of peripheral myelin protein-22.

69 elination marked by a 40% reduction in major myelin proteins, 30% fewer myelinated axons, a 33% decre

70 hs that formed were shorter, and the rate of myelin protein accumulation was markedly decreased.

71 Lymphocytes respond to myelin proteins after spinal cord injury (SCI) and may c

72 te glycoprotein (MOG) is an encephalitogenic myelin protein and a likely autoantigen in human multipl

73 t mice have a significant reduction in major myelin protein and gene expression.

74 the transcriptional regulation of genes for myelin proteins and by altered distribution of myelin-pr

75 We report herein a bioinformatic analysis of myelin proteins and CSF114(Glc), which led to the identi

76 elinating glial cells synthesize specialized myelin proteins and deposit them in the growing myelin s

77 essed by histology, immunohistochemistry for myelin proteins and electron microscopy coupled with mor

78 These include genes encoding myelin proteins and enzymes required for synthesis of no

79 mmune encephalomyelitis mice stimulated with myelin proteins and may underlie gender differences in s

80 the potential of post-mortem measurement of myelin proteins and mediators of vascular function, to a

81 ous system can be inferred from mutations in myelin proteins and neuropathologies associated with los

82 The Schwann cells expressed low levels of myelin proteins and of Egr2 (also called Krox20), which

83 Three genes encoding for myelin proteins and one for a nuclear protein have been

84 o enhance the generation of OLs that express myelin proteins and reform nodes of Ranvier in the conte

85 The increased expression of myelin proteins and transcription factors associated wit

86 erentiation, decreases their accumulation of myelin proteins, and causes a reversion to less mature s

87 were unable to differentiate and synthesize myelin proteins, and therefore unable to sort and myelin

88 and thyroid hormone-responsive induction of myelin proteins are impaired in Ascl1-/- mutants.

89 myelin membrane structure is destabilized as myelin proteins are lost.

90 ocytes synthesizing abundant levels of other myelin proteins are present in the mutant CNS.

91 locks cAMP-induced expression of Krox 20 and myelin proteins, but induces expression of c-Jun.

92 rified Schwann cells increased expression of myelin proteins, but not Krox20/Egr2, and the levels of

93 g of transfected cells expressing individual myelin proteins, by protein immunoblotting, and by immun

94 s of adrenoleukodystrophy, and that a mutant myelin protein can cause maldistribution of other myelin

95 o abnormalities in intrinsic Schwann cell or myelin proteins, can have clinical manifestations due to

96 teins, showing that the imbalanced supply of myelin proteins causes the disruption of myelin, and exp

97 n protein can cause maldistribution of other myelin proteins, causing dysmyelination, axonal damage,

98 d mice, reduced expression of the structural myelin protein CNP is associated with catatonic signs in

99 f axonal domains, myelin ultrastructure, and myelin protein composition.

100 sing Nrg1-ntfbeta enhanced the expression of myelin proteins, consistent with the expected activation

101 The elevated expression of myelin proteins correlated with a thicker myelin sheath

102 nase (calpain) is believed to participate in myelin protein degradation because known calpain substra

103 lpain) and extent of neurofilament (NFP) and myelin protein degradation were evaluated via Western bl

104 Thus, proteases have been implicated in myelin protein degradation, and recent studies have demo

105 activation of autophagy and the increase in myelin proteins, demonstrating that autophagy is critica

106 BDNF(+/-) mice exhibited decreased levels of myelin proteins during the demyelination and remyelinati

107 virus, CD4(+) T-cell responses against self myelin protein epitopes activated via epitope spreading

108 ion, resulting in a significant reduction in myelin protein expression and myelination of CNS white m

109 normal OL/myelin morphology and dysregulated myelin protein expression in transgenic mice expressing

110 wn of raptor or rictor significantly reduced myelin protein expression in vitro.

111 The decrease in myelin protein expression is associated with an increase

112 uring development and in the adult; however, myelin protein expression was delayed during development

113 Myelin protein expression was restored in SMA Schwann ce

114 An increase in myelin protein expression within lymph nodes during rEAE

115 binant Sox17 prevented Wnt3a from repressing myelin protein expression, and inhibition of Sox17-media

116 ed spontaneous remyelination as evidenced by myelin protein expression, immunostaining, and ultrastru

117 Consistent with these data, myelin protein expression, including myelin basic protei

118 yrosine groups and a subsequent reduction in myelin protein expression.

119 A decrease in myelin proteins expression was visible in several brain

120 uced levels of SMN and failed to express key myelin proteins following differentiation, likely due to

121 entified as the main component of a specific myelin protein fraction consistently increased in MS pre

122 uld not be limited to responses specific for myelin proteins, gender differences in cytokine producti

123 omic rearrangements involving the peripheral myelin protein gene (PMP22) in human chromosome 17p12 ar

124 y neuropathy caused by mutations in the P(0) myelin protein gene on chromosome 1.

125 n, the expression of mRNAs for the two major myelin protein genes, PLP and MBP, could be used to pred

126 Myelin proteins had been thought to be sequestered behin

127 The degradation of myelin proteins has been implicated in destabilization o

128 elination, as the proteolytic degradation of myelin proteins has been observed in disease states.

129 The oral administration of myelin proteins has been used for the successful prevent

130 Recently, however, myelin proteins have been found to be expressed in lymph

131 reated rats also showed a reduction in major myelin protein immunoreactive clusters 7 and 14 days pos

132 al nervous system encoding the most abundant myelin protein in oligodendrocytes, it is also expressed

133 domain of myelin protein zero (P0; the major myelin protein in the peripheral nervous system) that al

134 coincident with the ectopic localization of myelin proteins in kif1b mutant oligodendrocyte cell bod

135 cules traditionally deemphasized in favor of myelin proteins in studies of CNS autoimmunity.

136 atively spliced isoform, DM20, are the major myelin proteins in the CNS, but are also expressed in th

137 and compared with the expression profiles of myelin proteins in the cocultures throughout the myelina

138 is associated with a selective loss of minor myelin proteins, in addition to typical NMO features.

139 he expression of stage specific antigens and myelin proteins including MBP and PLP.

140 system in which T cell reactivity to several myelin proteins, including myelin basic protein (MBP), p

141 res the precise regulation of genes encoding myelin proteins, including PMP22.

142 teasomal degradation of beta-catenin blocked myelin protein induction.

143 MBP is an abundant myelin protein involved in demyelinating diseases, such

144 altered transcript levels of other important myelin proteins leading to a progressive degeneration of

145 RK signaling and restoration of axonal basic myelin protein levels.

146 involves a breakdown in T cell tolerance to myelin proteins like myelin basic protein (MBP).

147 rs, and lesions were defined on the basis of myelin protein loss, the geography and extension of plaq

148 lination were found, defined on the basis of myelin protein loss, the geography and extension of plaq

149 blots and immunohistochemical analysis with myelin protein markers.

150 gest that CD8 T cells and CNS Ags other than myelin proteins may be involved during the MS disease pr

151 ed protein misfolding and aggregation of key myelin proteins may be linked to demyelination and reduc

152 In vivo, a delay in the expression of the myelin protein MBP was observed in the corpus callosum a

153 ific deficit in the translation of the major myelin protein, MBP.

154 dence that autoantibodies against a specific myelin protein mediate target membrane damage in central

155 hanges together with enhanced degradation of myelin protein mRNA may represent a mechanism for differ

156 We hypothesized that QKI binds to myelin protein mRNAs, and the lack of QKI causes posttra

157 sion is regulated in parallel with the major myelin protein mRNAs, encoding MBP and PLP, under a vari

158 exes (TCC) selectively enhances the decay of myelin protein mRNAs.

159 a defect in a gene encoding one of the major myelin proteins (myelin mutants).

160 in the major peripheral nervous system (PNS) myelin protein, myelin protein zero (MPZ), cause Charcot

161 luding that for the most abundant peripheral myelin protein, Myelin protein zero (Mpz).

162 tin and contactin-associated protein and the myelin protein neurofascin 155.

163 Three myelin proteins, Nogo, MAG (myelin-associated glycoprote

164 Three different myelin proteins, Nogo, MAG, and OMgp, inhibit regenerati

165 hat binds three central nervous system (CNS) myelin proteins, Nogo, myelin-associated glycoprotein, a

166 iates the growth-inhibiting effects of three myelin proteins, Nogo, OMgp (oligodendrocyte-myelin glyc

167 erved novel component of myelin called Mp11 (myelin protein of 11 kDa).

168 Mutations in P0 (MPZ), the major myelin protein of the peripheral nervous system, cause t

169 cosylphosphatidylinositol (GPI)-anchored CNS myelin protein, oligodendrocyte-myelin glycoprotein (OMg

170 In addition, LPA increased the expression of myelin protein P(0) in Schwann cells in a Galpha(i)-inde

171 olipid protein is replaced by the peripheral myelin protein P0 and describe a number of early axonal

172 es induced demyelination and lower levels of myelin protein P0 expression were seen in immunoblots af

173 y T cells directed against peptides from the myelin proteins P0, P2, and PMP22.

174 here PLP is replaced by the peripheral nerve myelin protein, P0 (P0-CNS mice).

175 Two myelin proteins, P2 basic protein and P0 glycoprotein, c

176 hought to be mediated by T cells recognizing myelin protein peptides.

177 in humans as well as mice lacking the major myelin protein PLP1.

178 icted targets, among which is the peripheral myelin protein PMP22.

179 related to but distinct from the peripheral myelin protein PMP22.

180 gulate alternative splicing of PLP and DM20, myelin proteins produced by oligodendrocytes (OLs) by se

181 mutation in the gene encoding the major CNS myelin protein, proteolipid protein (PLP1, previously PL

182 e is also given for adrenoleukodystrophy and myelin-protein-related disorders.

183 in proteolipids are not new additions to the myelin protein repertoire, but instead were ancestral sh

184 ity to process antigenic peptide from intact myelin protein results in resistance to EAE and that de

185 multiple sclerosis (MS), the degradation of myelin proteins results in destabilization of the myelin

186 and B cell receptors that recognize the same myelin protein (see the related articles beginning on pa

187 ce a specific increase in ARE mRNAs encoding myelin proteins, showing that the imbalanced supply of m

188 -associated glycoprotein (MAG), Schwann cell myelin protein (SMP), and sialoadhesin, were compared by

189 sociated glycoprotein (MAG) and Schwann cell myelin protein (SMP), had similar and stringent binding

190 Although many studies have characterized myelin protein-specific CD4+ T cells, we have demonstrat

191 of Th1-associated cytokines secreted by CD4+ myelin protein-specific T cells present in the CNS, the

192 vation of self-reactive T cells specific for myelin proteins such as myelin basic protein (MBP).

193 nfluences membrane fluidity, associates with myelin proteins such as myelin proteolipid protein, and

194 the expression of genes encoding structural myelin proteins, such as periaxin, myelin basic protein,

195 of cytoplasmic accumulation of other mutated myelin proteins suggest that diseases affecting myelinat

196 (PSEN1) is highly coexpressed with canonical myelin proteins, suggesting a role for PSEN1 in aspects

197 s required at least 48 h before the onset of myelin protein synthesis in both CNS and PNS.

198 d and myelinated Schwann cells and enhancing myelin protein synthesis in myelinating Schwann cells.

199 ERK2 in the translational control of MBP, a myelin protein that appears critical for ensuring the ti

200 associated glycoprotein (MAG) is an abundant myelin protein that inhibits neurite outgrowth in vitro,

201 s, whereas there was no degradation of other myelin proteins that are not MMP substrates (proteolipid

202 cific for immunodominant epitopes on various myelin proteins that may be involved in either the initi

203 system (CNS) is inhibited by the presence of myelin proteins that prevent axonal regrowth.

204 neutral proteinase (calpain), which degrades myelin proteins, the activity and expression (translatio

205 ins on NgR1 are necessary for binding to the myelin proteins, the exact epitope(s) involved in ligand

206 Because calpain degrades all major myelin proteins, the increased activity and expression o

207 Because these processes are devoid of myelin proteins, they represent a unique compartment of

208 he central nervous system (CNS) and degrades myelin proteins, this endopeptidase has been suggested t

209 educed numbers of NG2+ cells and deficits in myelin proteins throughout development and in the adult,

210 requires the robust and timely production of myelin proteins to generate new myelin sheaths.

211 ies in alternative splicing of MAG and other myelin protein transcripts in the qk mouse is demonstrat

212 We evaluated expression of mRNA for myelin proteins using in situ hybridization with oligonu

213 , its mechanism and association with loss of myelin protein was not elaborated.

214 pe hypersensitivity (DTH) to both virion and myelin proteins was decreased in surviving mice that und

215 processes, whereas the acquisition of mature myelin proteins was unimpeded.

216 Two novel mutations in the gene for P0 myelin protein were also detected.

217 Increases in BDNF, as well as myelin proteins, were observed.

218 Th1 type CD4(+) T cells specific for various myelin proteins which migrate from the periphery to the

219 Previous findings have indicated that myelin proteins, which accumulate following demyelinatio

220 t sciatic nerve, including Periaxin (PRX), a myelin protein whose mutation causes inherited neuropath

221 We also found Periaxin (PRX), a myelin protein whose mutation causes inherited neuropath

222 entry into cell cycle and down-regulation of myelin proteins with a loss of myelin membrane).

223 ediated autoimmune disorder directed against myelin proteins within the CNS.

224 e promoters of specific myelin genes such as myelin protein zero (MPZ) and myelin basic protein (MBP)

225 hesion molecule with the highest homology to myelin protein zero (MPZ) and myelin protein zero-like 2

226 dy light chain variable domain (V(L))(1) and myelin protein zero (MPZ) are representatives of the fun

227 Mutations in myelin protein zero (MPZ) cause Charcot-Marie-Tooth dise

228 nation of the peripheral nervous system, the myelin protein zero (Mpz) gene is induced to produce the

229 have identified five novel mutations in the myelin protein zero (MPZ) gene, encoding the major struc

230 eral neuropathies caused by mutations in the myelin protein zero (MPZ) gene.

231 Myelin protein zero (MPZ) is a member of the immunoglobu

232 Myelin protein zero (MPZ) is the major integral membrane

233 lar genetic testing showed a complex de novo myelin protein zero (MPZ) mutation consisting of a 3bp d

234 he GJB1 gene under the Schwann cell-specific myelin protein zero (Mpz) promoter was generated and del

235 was expressed in transgenic mice using a rat myelin protein zero (Mpz) promoter, which is exclusively

236 ipheral nervous system (PNS) myelin protein, myelin protein zero (MPZ), cause Charcot-Marie-Tooth Dis

237 ability of these cells to induce KROX20 and myelin protein zero (MPZ), localizes NFATC4 to the nucle

238 Mutations in MPZ, the gene encoding myelin protein zero (MPZ), the major protein constituent

239 the most abundant peripheral myelin protein, Myelin protein zero (Mpz).

240 y studies on the cytoplasmic domain of human myelin protein zero (P0) (hP0-cyt) suggest that H-bondin

241 ress the early determinants of their lineage myelin protein zero (P0) and/or fatty acid binding prote

242 r example, deletion of serine 63 (S63del) in myelin protein zero (P0) induces P0 accumulation in the

243 utase active mutant SOD1(G93A) driven by the myelin protein zero (P0) promoter.

244 at neuregulin-1 (NRG1) induces expression of myelin protein zero (P0).

245 Point mutations in the cytoplasmic domain of myelin protein zero (P0; the major myelin protein in the

246 We characterized the mpz gene, which encodes myelin protein zero and is up-regulated in oligodendrogl

247 chwann cell markers, including Pou3f1, Egr2, myelin protein zero and myelin basic protein, is reduced

248 t cause severe disease, such as those in the myelin protein zero gene (MPZ) and the peripheral myelin

249 More than 120 mutations in the Myelin Protein Zero gene (MPZ, P0) cause various forms o

250 defective Aire-mediated central tolerance to myelin protein zero initiates an autoimmune Th1 effector

251 ropathy in part because the misfolded mutant myelin protein zero is retained in the endoplasmic retic

252 duplication), 11 a connexin 32 mutation, 5 a myelin protein zero mutation, 5 a peripheral myelin prot

253 ent with a CMT2 clinical phenotype had three myelin protein zero mutations (I89N+V92M+I162M).

254 Id2 was found to augment activation of Mpz (myelin protein zero) expression.

255 The Mpz (myelin protein zero) gene codes for the principal compon

256 changes, we found increased transcripts for myelin protein zero, a gene that, when mutated, can caus

257 mice, but not in the mice with deficiency of myelin protein zero, a major structural protein of compa

258 heral nerves in both mice and humans targets myelin protein zero, an Ag for which expression is Aire-

259 tant alleles: two for connexin 32, three for myelin protein zero, and two for peripheral myelin prote

260 eral proteins: peripheral myelin protein 22, myelin protein zero, connexin 32, early growth response

261 mpz gene, encoding the ortholog of mammalian myelin protein zero, is expressed in oligodendrocytes of

262 , transcription factor AP-1, dystroglycan 1, myelin protein zero, mitogen-activated protein kinase 3,

263 on in MPZ causing a gain of glycosylation in myelin protein zero, the main protein of peripheral nerv

264 such as periaxin, myelin basic protein, and myelin protein zero, was decreased, genes associated wit

265 st homology to myelin protein zero (MPZ) and myelin protein zero-like 2 (MPZL2, also called epithelia

266 issense mutation in the predicted Ig protein Myelin Protein Zero-Like 3 (Mpzl3).

267 We therefore named this gene Mpzl3 (myelin protein zero-like 3).

268 ells and are autoreactive against peripheral myelin protein zero.

269 th disease type 1B is caused by mutations in myelin protein zero.

270 response to neuregulin1 and did not express myelin protein zero.

271 ssion of myelination-associated genes (e.g., myelin protein zero; Mpz), and failed to myelinate axons