ライフサイエンスコーパス: oligodendrocyte

1 normal but did not rescue the proportion of oligodendrocytes.

2 ecific alterations in synaptic signaling and oligodendrocytes.

3 jor glial populations, namely astrocytes and oligodendrocytes.

4 cellular processes, which contact uninfected oligodendrocytes.

5 on, and for initiating the generation of new oligodendrocytes.

6 c neurons) but also with enteric neurons and oligodendrocytes.

7 modifying developmental myelin targeting by oligodendrocytes.

8 dysregulate transcriptional pause release in oligodendrocytes.

9 n ClC-2 was disrupted in both astrocytes and oligodendrocytes.

10 (PSP), tau also aggregates in astrocytes and oligodendrocytes.

11 induce the generation of new premyelinating oligodendrocytes.

12 ons to regional abundances of astrocytes and oligodendrocytes.

13 and localized to the lysosome compartment in oligodendrocytes.

14 differentiate into astrocytes, neurons, and oligodendrocytes.

15 n through modulation of lysosome function in oligodendrocytes.

16 ammation and attenuating the chronic loss of oligodendrocytes.

17 nhanced remyelination from new and surviving oligodendrocytes.

18 the process of cell-to-cell viral spread in oligodendrocytes.

19 hila neurons, mouse muscle cells, and rodent oligodendrocytes.

20 PLP1 gene, which is expressed in the CNS by oligodendrocytes.

21 red to maintain proper cathepsin D levels in oligodendrocytes.

22 ation via ferroptosis-mediated rapid loss of oligodendrocytes.

23 glia/macrophages to support remyelination by oligodendrocytes.

24 ecificity of myelin regeneration after acute oligodendrocyte ablation.

25 ebral atherosclerosis associated with higher oligodendrocyte abundance.

26 tion of pancreatic ER kinase (PERK) protects oligodendrocytes against inflammation in the experimenta

27 ion, including integrated actions across the oligodendrocyte and astroglial compartments that are at

28 lating that plasticity, and the evidence for oligodendrocyte and myelin dysfunction in neurodevelopme

29 lial cells, with strikingly fewer astrocyte, oligodendrocyte and neuron-related genes, the notable ex

30 dditionally, prdm8 mutant larvae have excess oligodendrocytes and a concomitant deficit of OPCs.

31 JCPyV predominately targets two cell types, oligodendrocytes and astrocytes.

32 anglionic eminence, which gives rise to both oligodendrocytes and CINs that express somatostatin and

33 e wrapping by Schwann cells, but its role in oligodendrocytes and CNS myelination remains unknown.

34 s for activation of NF-kappaB selectively in oligodendrocytes and demonstrated that NF-kappaB activat

35 for activation of NF-kappaB specifically in oligodendrocytes and found that enhanced NF-kappaB activ

36 and non-coding, were detected in astrocytes, oligodendrocytes and microglia.

37 Considering that normal GLUT1 expression in oligodendrocytes and myelin is needed to metabolically s

38 s significantly reduces the number of mature oligodendrocytes and myelin production throughout the re

39 Destruction of oligodendrocytes and myelin sheaths in cortical gray mat

40 re they terminally differentiate into mature oligodendrocytes and myelinate axons.

41 ial cells, pericytes, astrocytes, microglia, oligodendrocytes and neurons to model the effects of hyp

42 ajor component of mRNA transport granules in oligodendrocytes and neurons.

43 ar mechanism for the maturational failure of oligodendrocytes and offers a potential therapeutic targ

44 and external capsule, and decline of mature oligodendrocytes and oligodendrocyte precursor cells.

45 c genes but converge onto shared loci within oligodendrocytes and oligodendrocyte precursors.

46 sheaths and perhaps additional functions of oligodendrocytes and OPCs.

47 Also, mature oligodendrocytes and reactive astrocytes were only detec

48 ttenuation of myelin protein biosynthesis in oligodendrocytes and restored myelin thickness in the CN

49 found that microglia closely associate with oligodendrocytes and specifically phagocytose myelin she

50 an additional form of plasticity - affecting oligodendrocytes and the myelin sheaths they produce - t

51 n antibody-mediated dysfunction of NMDARs in oligodendrocytes and the white matter alterations report

52 icits along with dramatic decrease in mature oligodendrocytes and their progenitor cells.

53 to program hPSCs into neurons, fibroblasts, oligodendrocytes and vascular endothelial-like cells tha

54 ed by a decline in the number of myelinating oligodendrocytes and with a reduction in proliferating o

55 some metabolic processes (with enrichment in oligodendrocytes) and upweighted genes to protein locali

56 rate both forms of macroglia: astrocytes and oligodendrocytes, and can form neurospheres in culture.

57 ons, participating cells include astrocytes, oligodendrocytes, and microglia.

58 s (glutamatergic neurons, GABAergic neurons, oligodendrocytes, and microglia/astrocytes) from three d

59 d manipulate interactions between microglia, oligodendrocytes, and neurons during development.

60 ricytes, endothelial cells, microglia cells, oligodendrocytes, and neurons.

61 ted to pathological alpha-syn aggregation in oligodendrocytes, and the OEMVs found in peripheral bloo

62 ompanied by impaired NF-kappaB activation in oligodendrocytes, and were completely rescued by enhance

63 Oligodendrocyte- and neuron-specific genes were strongly

64 promote myelin compaction and development of oligodendrocytes, as well as in remyelination by Schwann

65 tion being a cluster of mostly downregulated oligodendrocyte-associated genes in the P7SCI + 7d gene-

66 k-out mice, oligodendrocyte monocultures and oligodendrocyte-astrocyte cocultures, we demonstrate blo

67 cation and identify Zfp36l1 as necessary for oligodendrocyte-astrocyte lineage transition and glioma

68 the experiment, while preserving clusters of oligodendrocytes, astrocytes, and endothelial cells and

69 Bmal1 deficiency reduced the chronic loss of oligodendrocytes at the injury epicenter 6 weeks post SC

70 found that enhanced NF-kappaB activation in oligodendrocytes attenuated EAE disease severity and ame

71 intracellular Ca(2+) in turn affects OPC and oligodendrocyte biology in the healthy nervous system an

72 d that TET3 is present in mature neurons and oligodendrocytes but is absent in astrocytes.

73 st, there is a selective reduction of mature oligodendrocytes, but not oligodendrocyte precursor cell

74 of Ca(2+) channels and receptors in OPCs and oligodendrocytes by neurotransmitters converges on regul

75 ndicates that localized changes in Ca(2+) in oligodendrocytes can regulate the formation and remodeli

76 ions among progenitors, neurons, astrocytes, oligodendrocytes, cancer cells, and non-central nervous

77 showed that Sel1L deficiency specifically in oligodendrocytes caused ERAD impairment, the UPR activat

78 In mice, Nf1 loss in adult oligodendrocytes causes myelin decompaction and increase

79 specifically alter the function of NMDARs in oligodendrocytes, causing a decrease of expression of GL

80 pendently of neuronal axons, and resulted in oligodendrocyte cell loss.

81 nhibitors in demyelinating diseases in which oligodendrocyte cell-death is one of the pathological fe

82 vealed in reduced phalloidin and deficits in oligodendrocyte cellular branching complexity at the pea

83 n of differentiated but not undifferentiated oligodendrocytes cellular markers.

84 reveal that N-Wasp plays a distinct role in oligodendrocytes compared with Schwann cells, highlighti

85 During development, oligodendrocytes contact and wrap neuronal axons with my

86 el of multiple system atrophy and in primary oligodendrocyte cultures, and the mechanism involved was

87 nstrated that NF-kappaB activation prevented oligodendrocyte death and myelin damage in the EAE model

88 These results suggest that oligodendrocyte defects account for aspects of brain dys

89 developed to isolate blood CNPase-positive, oligodendrocyte-derived enriched microvesicles (OEMVs),

90 lation plays an important regulatory role in oligodendrocyte development and CNS myelination.

91 To define the importance of iron storage in oligodendrocyte development and function, the ferritin h

92 aling and between RNA splicing and increased oligodendrocyte development and myelination.

93 involving key UPS components contributes to oligodendrocyte development and repair and reveal a new

94 ore, Fth iron storage is essential for early oligodendrocyte development as well as for OPC maturatio

95 Oligodendrocyte development is tightly controlled by ext

96 tnatal weeks is important for an appropriate oligodendrocyte development, and suggest that Fth iron s

97 Daam2 and their mutual antagonism regulates oligodendrocyte differentiation during development.

98 rthdating experiments indicated a precocious oligodendrocyte differentiation in the mPFC at P15, lead

99 rocyte were sufficient to convey support for oligodendrocyte differentiation while this support was l

100 ation, creating a permissive environment for oligodendrocyte differentiation.

101 ar processes including axon ensheathment and oligodendrocyte differentiation.

102 that HIFalpha dysregulation in OPCs but not oligodendrocytes disturbed normal developmental myelinat

103 skeletal targets and actin reorganization in oligodendrocytes during developmental myelination.

104 cytoprotective effects of PERK activation on oligodendrocytes during EAE are not mediated by activati

105 cking Fth synthesis in Sox10 or NG2-positive oligodendrocytes during the first or the third postnatal

106 ever, whether and how the UPS contributes to oligodendrocyte dysfunction and repair after white matte

107 Myelinating oligodendrocytes enable fast propagation of action poten

108 e biotin (MD1003) might enhance neuronal and oligodendrocyte energetics, resulting in improved cell f

109 coordination of neuron/astrocyte and neuron/oligodendrocyte entities was termed as neuron-glia integ

110 Oligodendrocytes establish thick myelination demanded fo

111 tau protein accumulates in astrocytes and/or oligodendrocytes, even though these glial cells produce

112 In normoxic mice and oligodendrocytes, exposure to a mitochondrial uncoupler

113 Specifically, all oligodendrocytes express NCoR1, but only a subset expres

114 Patients' CSF also reduced oligodendrocyte expression of glucose transporter GLUT1

115 rescued by enhanced NF-kappaB activation in oligodendrocytes (female mice).

116 but also in initiating the generation of new oligodendrocytes for myelin repair.

117 rk defines mechanisms by which HIF1a impairs oligodendrocyte formation and establishes that cell-type

118 te oligodendrocyte progenitor cell (OPC) and oligodendrocyte formation and function.

119 MEK/ERK inhibition also drove oligodendrocyte formation in hypoxic regions of human ol

120 godendrocytes that prevented later-generated oligodendrocytes from occupying the cortex.

121 on-canonical targets to impair generation of oligodendrocytes from OPCs.

122 eta2gamma1 conforms the bulk of GABA(A)Rs in oligodendrocytes from rat neonates.

123 Myelin can be restored by regenerating oligodendrocytes from resident progenitors; however, it

124 ay directly affect microglial, astrocyte and oligodendrocyte function, suggesting an integrated netwo

125 To define the importance of iron storage in oligodendrocyte function, we have deleted the ferritin h

126 godendrocyte precursor cell differentiation, oligodendrocyte generation and myelin sheath remodeling

127 We show here that GDE3 controls the pace of oligodendrocyte generation by negatively regulating olig

128 gnaling overcame the HIF1a-mediated block in oligodendrocyte generation by restoring Sox10 expression

129 o-expression network enriched for myelin and oligodendrocyte genes (OLIGs), whereas a multicellular g

130 Investigations of myelin oligodendrocyte glycoprotein (MOG) antibodies are usuall

131 linical features, disease course, and myelin oligodendrocyte glycoprotein (MOG) antibody (Ab) dynamic

132 induced by immunization of mice with myelin oligodendrocyte glycoprotein (MOG)(35-55) Ig-like transc

133 agonist ITE and a T cell epitope from myelin oligodendrocyte glycoprotein (MOG)(35-55) induced tolero

134 vels of proteolipid protein (PLP) and myelin oligodendrocyte glycoprotein (MOG), the membrane protein

135 positive, 3 double-Ab-seronegative, 4 myelin oligodendrocyte glycoprotein (MOG)-Ab-seropositive and 4

136 disorders with IgG antibodies against myelin-oligodendrocyte glycoprotein (MOG-IgG) have been increas

137 confined to induction with either the myelin oligodendrocyte glycoprotein epitope MOG(35-55) or the f

138 Anti-myelin oligodendrocyte glycoprotein immunoglobulin G (MOG-IgG)

139 Inducing EAE by immunization with a myelin oligodendrocyte glycoprotein peptide (MOG(35-55)) reveal

140 elinating and myelin basic protein(+)/myelin oligodendrocyte glycoprotein(+) mature oligodendrocytes

141 pathogenetic serum IgG antibodies to myelin oligodendrocyte glycoprotein, an antigen in the outer my

142 C57BL/6J mice activated in vivo with myelin oligodendrocyte glycoprotein, Staphylococcal enterotoxin

143 found that enhanced NF-kappaB activation in oligodendrocytes had a minimal effect on their viability

144 ligodendrogenesis without affecting existing oligodendrocytes impaired memory consolidation of water

145 radigms, with a role of metabolically active oligodendrocytes in cortical information processing.

146 the roles of autophagy in Schwann cells and oligodendrocytes in development, plasticity, and disease

147 detrimental effects of PERK inactivation in oligodendrocytes in EAE were accompanied by impaired NF-

148 however, the role of NF-kappaB activation in oligodendrocytes in MS and EAE remains elusive.

149 cytoprotective effects of PERK activation on oligodendrocytes in MS and EAE.SIGNIFICANCE STATEMENT Nu

150 ar factor kappaB (NF-kappaB) is activated in oligodendrocytes in multiple sclerosis (MS) and its anim

151 gation, though the process is centred around oligodendrocytes in multiple system atrophy.

152 maladies, and reveals an unexpected role of oligodendrocytes in Parkinson's disease.

153 d the role of the integrated UPR and ERAD in oligodendrocytes in regulating myelin protein production

154 of pancreatic ER kinase (PERK) activation on oligodendrocytes in the EAE model.

155 numbers of oligodendroglia or differentiated oligodendrocytes in the healthy or remyelinating CNS, co

156 oliferate and differentiate into myelinating oligodendrocytes in the medial prefrontal cortex.

157 ever, the effects of NF-kappaB activation on oligodendrocytes in these diseases remain elusive.

158 oligodendrocyte precursor cells into mature oligodendrocytes in vitro.

159 based therapeutic agents can be delivered to oligodendrocytes in vivo to modulate neurological functi

160 nct aspects of CNS myelination by individual oligodendrocytes in vivo.

161 MAL is expressed in oligodendrocytes, in Schwann cells, where it is essentia

162 Subsequently, oligodendrocytes increase cholesterol levels as a prereq

163 nstrated orthogonal programming by including oligodendrocyte-inducible hPSCs with unmodified hPSCs to

164 by aberrant and misguided elongation of the oligodendrocyte inner lip membrane.

165 Thus, decoding how OPCs and myelinating oligodendrocytes integrate and process Ca(2+) signals wi

166 orrelated variably with cell number density, oligodendrocyte interconnectivity, axonal orientation, a

167 e third postnatal week significantly reduces oligodendrocyte iron storage and maturation.

168 al, we show that sheath generation by mature oligodendrocytes is not only possible but also increases

169 that membrane-associated Nogo-A produced in oligodendrocytes is processed proteolytically by BACE1,

170 nitors, and also regulates the allocation of oligodendrocyte lineage cell fates.This article has an a

171 Moreover, the loss of Mettl14 in oligodendrocyte lineage cells causes aberrant splicing o

172 lar mechanisms that govern the maturation of oligodendrocyte lineage cells remain unclear.

173 nsive cell type at Day 1, but astrocytes and oligodendrocyte lineage cells subsequently became more r

174 Cells of the oligodendrocyte lineage express a wide range of Ca(2+) c

175 recent work characterizing plasticity in the oligodendrocyte lineage following sensory experience and

176 Oligodendrocyte lineage markers and birthdating experime

177 Here, we demonstrate that oligodendrocyte lineage progression is accompanied by dy

178 The oligodendrocyte lineage-associated glioblastoma subtype

179 rritin heavy chain (Fth) specifically in the oligodendrocyte lineage.

180 riggers iron-mediated lipid peroxidation and oligodendrocyte loss (via ferroptosis).

181 Oligodendrocyte loss in neurological disease leaves axon

182 a induces SARM1-dependent axon degeneration, oligodendrocyte loss, and subsequent retinal ganglion ce

183 disease severity and ameliorated EAE-induced oligodendrocyte loss, demyelination, and axon degenerati

184 dy imply that the integrated UPR and ERAD in oligodendrocytes maintain myelin thickness in adults by

185 strategies to deplete microglia resulted in oligodendrocytes maintaining excessive and ectopic myeli

186 trate that PI5P4Kalpha co-localizes with the oligodendrocyte marker, Olig2, whereas PI5P4Kbeta co-loc

187 ocyte precursor cells in culture resulted in oligodendrocyte maturation and expression of myelin diff

188 vitro Mettl14 ablation disrupts postmitotic oligodendrocyte maturation and has distinct effects on O

189 postnatal development significantly reduces oligodendrocyte maturation and myelination.

190 tream OPC differentiation but not downstream oligodendrocyte maturation and that HIFalpha dysregulati

191 Postnatal failure of oligodendrocyte maturation has been proposed as a cellul

192 these changes promote myelin restoration and oligodendrocyte maturation throughout remyelination.

193 response to IH challenge and fully preserved oligodendrocyte maturation, axonal myelination, and neur

194 ciated with development of diffuse WMI: poor oligodendrocyte maturation, diffuse axonal hypomyelinati

195 al elongation is a dominant pathway blocking oligodendrocyte maturation.

196 However, the molecular mechanisms for oligodendrocyte maturational failure remain unclear.

197 lutamatergic and GABAergic) and nonneuronal (oligodendrocytes, microglia, astrocytes, and endothelial

198 Mature oligodendrocytes (MOLs) show transcriptional heterogenei

199 Using a combination of PAR1 knock-out mice, oligodendrocyte monocultures and oligodendrocyte-astrocy

200 Oligodendrocyte myelination depends on actin cytoskeleto

201 tes causes myelin decompaction and increases oligodendrocyte nitric oxide (NO) levels.

202 To evaluate the activity of oligodendrocyte NMDARs and alpha-amino-3-hydroxy-5-methy

203 ter component, METTL14, results in decreased oligodendrocyte numbers and CNS hypomyelination, althoug

204 d not observe improvements in remyelination, oligodendrocyte numbers, and effects on microglial activ

205 tides in postnatal jimpy mice fully restored oligodendrocyte numbers, increased myelination, improved

206 60 has no effect on myelin production and/or oligodendrocyte numbers.

207 However, the mechanisms underlying oligodendrocyte (OL) cell loss and demyelination are not

208 rentially expressed genes (DEGs) highlighted oligodendrocyte (OL) dysregulation, which we confirmed i

209 ow that in response to demyelination, mature oligodendrocytes (OLG) bordering the lesion express Ndst

210 Oligodendrocytes (OLs) express functional GABA(A) recept

211 system, a myelin sheath that originates from oligodendrocytes or Schwann cells wraps around axons to

212 Whether oligodendrocyte pathology is sufficient to affect brain-

213 The generation of myelin-forming oligodendrocytes persists throughout life and is regulat

214 include membrane-associated proteins of the oligodendrocyte plasma membrane and astrocyte-derived, m

215 In addition, oligodendrocytes play diverse non-canonical roles includ

216 Astrocytes and oligodendrocytes play essential roles in regulating neur

217 we show that Nf1 gene inactivation in adult oligodendrocytes (Plp-Nf1 (fl/+) mice) results in a moto

218 sly undiscovered Serpina3n(+)C4b(+) reactive oligodendrocyte population in mice.

219 te numbers and CNS hypomyelination, although oligodendrocyte precursor cell (OPC) numbers are normal.

220 ndrocyte generation by negatively regulating oligodendrocyte precursor cell (OPC) proliferation.

221 ligodendrogenesis, it subsequently increases oligodendrocyte precursor cell differentiation, oligoden

222 cultures by co-culturing with astrocytes and oligodendrocyte precursor cells (complex culture).

223 ovide an additional source of human cortical oligodendrocyte precursor cells (OPCs) and define a line

224 igration of both rat Schwann cells (SCs) and oligodendrocyte precursor cells (OPCs) and explored the

225 We report that oligodendrocyte precursor cells (OPCs) contact sprouting

226 During differentiation, oligodendrocyte precursor cells (OPCs) extend a network

227 Addition of anacardic acid to cultured oligodendrocyte precursor cells (OPCs) rapidly increased

228 udy, we found that, in injured optic nerves, oligodendrocyte precursor cells (OPCs) undergo transient

229 n deep layer excitatory neurons and immature oligodendrocyte precursor cells (OPCs), and these contri

230 itors sequentially produce motor neurons and oligodendrocyte precursor cells (OPCs).

231 al targets and cellular process expansion by oligodendrocyte precursor cells as well as expression an

232 s indicated 4-AP stabilization of myelin and oligodendrocyte precursor cells associated with increase

233 hibiting myelination by deletion of Olig2 in oligodendrocyte precursor cells impairs spatial memory i

234 Gold nanocrystal treatment of oligodendrocyte precursor cells in culture resulted in o

235 cyte-derived TIMP-1 drove differentiation of oligodendrocyte precursor cells into mature oligodendroc

236 e, we demonstrate that fear learning induces oligodendrocyte precursor cells to proliferate and diffe

237 of origin for glioma, neural stem cells and oligodendrocyte precursor cells, exhibited a high glioma

238 y lethality, effects on myelination, loss of oligodendrocyte precursor cells, increased apoptosis in

239 changed the GABA-response characteristics in oligodendrocyte precursor cells, indicating their partic

240 g the muscarinic acetylcholine receptor 1 in oligodendrocyte precursor cells, or promoting oligodendr

241 eduction of mature oligodendrocytes, but not oligodendrocyte precursor cells, suggesting triglial dys

242 , and decline of mature oligodendrocytes and oligodendrocyte precursor cells.

243 onto shared loci within oligodendrocytes and oligodendrocyte precursors.

244 letal reorganization and MBP localization to oligodendrocyte processes.SIGNIFICANCE STATEMENT Myelina

245 Ca(2+) channels and receptors that regulate oligodendrocyte progenitor cell (OPC) and oligodendrocyt

246 nal LB supplementation promoted neuronal and oligodendrocyte progenitor cell development.

247 CN3 is a matricellular protein that promotes oligodendrocyte progenitor cell differentiation and myel

248 signaling increases neurogenesis and reduces oligodendrocyte progenitor cell proliferation (OPC) in t

249 nsequences of disrupting Fth iron storage in oligodendrocyte progenitor cells (OPCs) after demyelinat

250 ination of the central nervous system (CNS), oligodendrocyte progenitor cells (OPCs) proliferate and

251 rect effects on the myelinating potential of oligodendrocyte progenitor cells (OPCs), in addition to

252 ation, proliferation, and differentiation of oligodendrocyte progenitor cells (OPCs).

253 the autocrine Wnt/beta-catenin signaling in oligodendrocyte progenitor cells (OPCs).

254 CSPG4/NG2 is a hallmark protein of oligodendrocyte progenitor cells (OPCs).

255 ocytes and with a reduction in proliferating oligodendrocyte progenitor cells (OPCs).

256 Moreover, we showed that CNS oligodendrocyte progenitor cells are activated following

257 this mild inflammatory environment promotes oligodendrocyte progenitor cells maturation and myelin r

258 S immune milieu and concurrent activation of oligodendrocyte progenitor cells with subsequent remyeli

259 56 regulates cortical lamination, whereas in oligodendrocyte progenitor cells, GPR56 controls develop

260 tem inflammation as well as promoting neural/oligodendrocyte progenitor development in the offspring.

261 e mPFC at P15, leading to a depletion of the oligodendrocyte progenitor pool in MS adults.

262 NS cells expressing A2B5, an early marker in oligodendrocytes progenitor cell differentiation as well

263 Solicitation of endogenous oligodendrocytes progenitor cells, the precursor of olig

264 ccumulation in pluripotent-stem-cell-derived oligodendrocyte progenitors (OPCs), we demonstrate that

265 At the cellular level, astrocytes and oligodendrocyte progenitors displayed more differences i

266 60 has no effect on myelin production and/or oligodendrocyte quantities.

267 These findings suggest that impaired ERAD in oligodendrocytes reduces myelin thickness in the adult C

268 k differentiation through suppression of the oligodendrocyte regulator Sox10.

269 ferentiate into mature myelination-competent oligodendrocytes, reminiscent of what is observed in hum

270 Oligodendrocyte signatures suggested impaired axonal mye

271 weeks caused a premature differentiation of oligodendrocytes similar to the MS pups, while chemogene

272 th sexes and young male and female mice with oligodendrocyte-specific deletion of mechanistic target

273 ct cell type association between PD risk and oligodendrocyte-specific gene expression.

274 and restored myelin thickness in the CNS of oligodendrocyte-specific Sel1L-deficient mice (both male

275 on exacerbated myelin thinning in the CNS of oligodendrocyte-specific Sel1L-deficient mice (both male

276 Here we report that oligodendrocytes-specific deletion of N-Wasp in mice of

277 H-ABC, likely due to independent effects on oligodendrocytes, striatal neurons, and cerebellar granu

278 n neonatal mice and cultured differentiating oligodendrocytes, sublethal intermittent hypoxic (IH) st

279 e development of new treatments that enhance oligodendrocyte survival in MS patients by targeting the

280 profile and was recently reported to enhance oligodendrocyte survival, exerts effects on immune cells

281 Nf1 loss led to a persistence of immature oligodendrocytes that prevented later-generated oligoden

282 n is an enormous extended plasma membrane of oligodendrocytes that wraps and insulates axons.

283 f denuded axons and the ability of surviving oligodendrocytes to generate new myelin sheaths.

284 mouse CD4(+) T cells, subsequently acting on oligodendrocytes to induce anxiety-like behaviors.

285 ndrocytes progenitor cells, the precursor of oligodendrocytes, to remyelinate axons may abort the ons

286 turation and has distinct effects on OPC and oligodendrocyte transcriptomes.

287 uring the process of myelination in the CNS, oligodendrocytes undergo extensive morphological changes

288 cells in the mTOR cKO and in mTOR inhibited oligodendrocytes undergoing differentiation in vitro The

289 ession of the glucose transporter (GLUT1) in oligodendrocytes was assessed by immunocytochemistry.

290 yelination and axonal coverage by endogenous oligodendrocytes was extensive, as assessed using electr

291 While acute loss of neurons and oligodendrocytes was unaffected, Bmal1 deficiency reduce

292 eLa knock-out cell line and primary cultured oligodendrocytes, we determined that loss of TMEM106B le

293 nged dramatically after regeneration, as new oligodendrocytes were formed in different locations and

294 me OPCs differentiate rapidly as myelinating oligodendrocytes, whereas others remain into adulthood.

295 ked by the pathology in the myelin-producing oligodendrocytes, which are lytically destroyed by the v

296 treatment and differentiate into myelinating oligodendrocytes, which results in neo-oligodendrogenesi

297 were robustly reduced after preincubation of oligodendrocytes with patients' CSF or SSM5 but remained

298 yelin oligodendrocyte glycoprotein(+) mature oligodendrocytes with reciprocal downregulation of paire

299 nally distinct populations of astrocytes and oligodendrocytes within cerebral organoids.

300 utoimmune disease characterized by attack on oligodendrocytes within the central nervous system (CNS)