ライフサイエンスコーパス: myelin protein

1 It represents approximately 7% of total myelin protein.

2 inating and differentiating cells to express myelin proteins.

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

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

5 to overcome neurite outgrowth inhibition by myelin proteins.

6 ubsequent adaptive inflammatory responses to myelin proteins.

7 ng of transfectants that expressed different myelin proteins.

8 characterization of the repertoire of human myelin proteins.

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

10 nct complements of transcription factors and myelin proteins.

11 ndrocytes, including numerous genes encoding myelin proteins.

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

13 iple layers of bimolecular lipid leaflet and myelin proteins.

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

15 ainst paralysis induced by immunization with myelin proteins.

16 nectin production, and prevents synthesis of myelin proteins.

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

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

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

20 RK and other myelin genes such as peripheral myelin protein 2 and oligodendrocyte myelin glycoprotein

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

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

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

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

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

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

27 the peripheral nerve myelin gene Peripheral Myelin Protein 22 (PMP22) causes multiple forms of inher

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

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

30 y show that the helical tetraspan peripheral myelin protein 22 (PMP22) exhibits a pronounced preferen

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

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

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

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

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

36 cation and point mutations in the peripheral myelin protein 22 (PMP22) gene.

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

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

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

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

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

42 Peripheral myelin protein 22 (PMP22) is an essential peripheral mye

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

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

45 The absence of functional peripheral myelin protein 22 (PMP22) is associated with shortened l

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

64 p411Gly EGR2 to activate a PMP22 (peripheral myelin protein 22) enhancer element compared to wild-typ

65 models overexpressing the PMP22 (peripheral myelin protein 22) protein and in dermal fibroblasts fro

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

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

68 a chromosomal segment surrounding Peripheral Myelin Protein 22, or PMP22 gene, which is classified as

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

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

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

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

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

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

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

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

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

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

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

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

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

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

83 d an important decrease in the expression of myelin proteins and a substantial reduction in the perce

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

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

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

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

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

89 ous tolDCs loaded with peptides from various myelin proteins and from AQP4.

90 a significant reduction in the synthesis of myelin proteins and in the percentage of myelinated axon

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

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

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

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

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

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

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

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

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

100 Although myelin proteins are considered potential autoantigenic t

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

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

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

104 rotein 22 (PMP22) is an essential peripheral myelin protein because its genetic abnormalities account

105 y, PERK inactivation reversed attenuation of myelin protein biosynthesis in oligodendrocytes and rest

106 ment, the UPR activation, and attenuation of myelin protein biosynthesis; and resulted in late-onset,

107 ination include those that encode structural myelin proteins but also many that encode proteins invol

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

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

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

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

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

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

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

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

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

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

118 Myelin protein content in the nucleus accumbens was redu

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

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

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

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

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

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

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

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

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

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

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

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

131 Myelin protein expression was restored in SMA Schwann ce

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

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

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

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

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

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

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

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

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

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

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

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

144 Myelin proteins had been thought to be sequestered behin

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

162 An autoimmune response against myelin protein is considered one of the key pathogenic p

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

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

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

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

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

168 blots and immunohistochemical analysis with myelin protein markers.

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

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

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

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

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

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

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

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

177 udy, we demonstrate the important role for a myelin protein, myelin and lymphocyte protein (MAL), in

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

193 Myelin protein P2 is a peripheral membrane protein of th

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

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

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

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

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

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

200 R and ERAD in oligodendrocytes in regulating myelin protein production and maintaining myelin structu

201 ain myelin thickness in adults by regulating myelin protein production.

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

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

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

205 oteolipid Protein 1 (PLP1), encoding a major myelin protein, resulting in profound developmental dela

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

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

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

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

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

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

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

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

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

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

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

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

218 dly increased expression of myelin genes and myelin proteins, suggesting a direct induction of genes

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

235 ness in the adult CNS through suppression of myelin protein translation by activating PERK.SIGNIFICAN

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

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

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

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

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

241 BP) and myelin-associated glycoprotein (MAG) myelin proteins were markedly increased in the cortices

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

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

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

245 Myelin proteins, which are produced in the endoplasmic r

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

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

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

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

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

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

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

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

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

255 n in peripheral myelin, and mutations in the Myelin Protein Zero (Mpz) gene produce wide-ranging here

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

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

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

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

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

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

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

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

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

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

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

267 Myelin Protein Zero (MPZ/P0) is the most abundant glycop

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

287 of key proteins such as nerve growth factor, myelin protein zero, and brain derived neurotrophic fact

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

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

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

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

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

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

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

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

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

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

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

299 ells and are autoreactive against peripheral myelin protein zero.

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