ライフサイエンスコーパス: oligodendrocyte

1 function and limited access to primary human oligodendrocytes.

2 elong generation of interneuron subtypes and oligodendrocytes.

3 ifferentiating into neurons, astrocytes, and oligodendrocytes.

4 nting to the involvement of myelin-producing oligodendrocytes.

5 or neurons, identified as mature gray matter oligodendrocytes.

6 e forms and glial tau in both astrocytes and oligodendrocytes.

7 ays in multiple cellular contexts, including oligodendrocytes.

8 ciated cultures of adult human brain-derived oligodendrocytes.

9 , or drive their direct differentiation into oligodendrocytes.

10 on by ERK1/2 in an Akt-independent manner in oligodendrocytes.

11 variable cellular effects in neurons and/or oligodendrocytes.

12 an immortalized human cell line derived from oligodendrocytes.

13 cytosis, and induce the death of neurons and oligodendrocytes.

14 evelopment and decreases the total number of oligodendrocytes.

15 the subsequent generation of astrocytes and oligodendrocytes.

16 ction protein expressed by Schwann cells and oligodendrocytes.

17 cells from differentiating into myelinating oligodendrocytes.

18 These findings link phagocytosis of injured oligodendrocytes, a pathological hallmark of MS lesions

19 activation acts cell autonomously to protect oligodendrocytes against inflammation in animal models o

20 e also showed that NF-kappaB inactivation in oligodendrocytes aggravated IFN-gamma-induced remyelinat

21 after fluorescence-activated cell sorting of oligodendrocyte and neuronal nuclei.

22 the estrous cycle are related to myelin and oligodendrocytes and 12 of the 63 DEGs in the hypothalam

23 per-suppressor of NF-kappaB, specifically in oligodendrocytes and demonstrated that IkappaBalphaDelta

24 hes reveal stage-specific miR-219 targets in oligodendrocytes and further uncover a novel network for

25 portant decline in the number of myelinating oligodendrocytes and in the rate of OPC proliferation.

26 -AG hydrolysis augments the number of mature oligodendrocytes and increases MBP, leading to remyelina

27 l nervous system cells including neurons and oligodendrocytes and is a critical receptor in axonal gu

28 ing of this metabolic supportive function of oligodendrocytes and its potential impact in human neuro

29 and synapse loss, disease-related changes to oligodendrocytes and myelin are also suspected of playin

30 rstanding of how neuronal activity regulates oligodendrocytes and myelinated axons in vivo, with a fo

31 Finally, oligodendrocytes and myelinated axons were analyzed usin

32 signals in this social context primarily to oligodendrocytes and neurons, respectively, and we show

33 itatory and inhibitory neurons as well as in oligodendrocytes and oligodendrocyte precursor cells.

34 Myelin in the CNS is generated by oligodendrocytes and recent evidence has shown that many

35 and an association between schizophrenia and oligodendrocytes and replicating fetal cortical cells.

36 BalphaDeltaN blocked NF-kappaB activation in oligodendrocytes and resulted in exacerbated oligodendro

37 s of large amounts of lipids and proteins by oligodendrocytes and Schwann cells.

38 clein-positive structures were also found in oligodendrocytes and the neuropil.

39 or inactivation of NF-kappaB specifically in oligodendrocytes and then used this model to determine t

40 abnormal patterning and decreased numbers of oligodendrocytes, and increased cell death.

41 f oligodendrocyte precursor cells (OPCs) and oligodendrocytes, and increased levels of neurotrophic f

42 nd 12 of the 63 DEGs in the hypothalamus are oligodendrocyte- and myelin-specific genes.

43 ction and protects against caspase-dependent oligodendrocyte apoptosis during CNS remyelination.

44 -type mice with demyelinating injury reduced oligodendrocyte apoptosis, thereby increasing oligodendr

45 propagation, more recent data indicate that oligodendrocytes are essential for providing metabolic s

46 Oligodendrocytes are glial cells that populate the entir

47 During development, oligodendrocytes are initially specified, after which ol

48 suggest that we have established a powerful oligodendrocyte-based model system for studies of JCV-de

49 Thus, this oligodendrocyte-based model system will be useful for a

50 en astroglial lipid synthesis was inhibited, oligodendrocytes began incorporating circulating lipids

51 the entire cell body and distal processes of oligodendrocytes, but there was no accumulation of micro

52 ll cultures and exerted robust protection on oligodendrocytes by preventing cell death in both naive

53 infection of particular brain cells, termed oligodendrocytes, by the JC virus.

54 By live-imaging oligodendrocyte Ca(2+) activity in vivo, we find that hi

55 In the adult brain, both neurons and oligodendrocytes can be generated from neural stem cells

56 ame gene in astrocytes, or in astrocytes and oligodendrocytes, caused a persistent hypomyelination, a

57 mechanisms underlying subsequent adult human oligodendrocyte cell death.

58 Here, we report that the G144 oligodendrocyte cell line supports both infection by JC

59 cellular defects involving both neuronal and oligodendrocyte cell types in vitro.

60 To determine if mutant ATXN3 acts on oligodendrocytes cell-autonomously, we manipulated the r

61 re conducted using adult human brain-derived oligodendrocytes challenged by metabolic stress conditio

62 Remyelination failure by oligodendrocytes contributes to the functional impairmen

63 lineage, and mice lacking HMGNs show reduced oligodendrocyte count and decreased spinal cord myelinat

64 strocytes (Cx43-Cx43) and between astrocytes-oligodendrocytes (Cx43-Cx47).

65 SCI leads to oligodendrocyte death and demyelination, and clinical tr

66 oligodendrocytes and resulted in exacerbated oligodendrocyte death and hypomyelination in young, deve

67 s aggravated IFN-gamma-induced remyelinating oligodendrocyte death and remyelination failure in the c

68 peutic targets for diseases characterized by oligodendrocyte death, including multiple sclerosis.

69 r, activation of AMPKalpha partially rescues oligodendrocyte defects caused by DHFR-inhibition both i

70 However, remyelination, restoration of oligodendrocyte densities, and motor recovery after the

71 ligodendrocyte apoptosis, thereby increasing oligodendrocyte density and myelin basic protein stainin

72 After demyelination, oligodendrocytes derived from these newly-formed progeni

73 A expression, function, and mechanism during oligodendrocyte development and after injury.

74 secretion that non-cell autonomously stunts oligodendrocyte development and decreases the total numb

75 cent evidence has shown that many aspects of oligodendrocyte development and myelination can be modul

76 the expression of OLIG1&2, thereby affecting oligodendrocyte development and myelination, and mouse b

77 n profiles of lncRNAs at different stages of oligodendrocyte development and uncover a cohort of stag

78 metabolism, however folate/DHFR activity in oligodendrocyte development has not been fully understoo

79 eport that regulatory T cells (Treg) promote oligodendrocyte differentiation and (re)myelination.

80 Myrf is a key transcription factor for oligodendrocyte differentiation and central nervous syst

81 wild-type oligodendrocyte progenitor cells, oligodendrocyte differentiation and de novo myelination

82 technology, we show that Shp2 is involved in oligodendrocyte differentiation and early myelination, b

83 led changes in several genes associated with oligodendrocyte differentiation and maturation following

84 FICANCE STATEMENT Ion channels implicated in oligodendrocyte differentiation and maturation may induc

85 Here, we demonstrate that LINGO-1 regulates oligodendrocyte differentiation and maturation through t

86 we demonstrate that NCAM and ST8SIA2 promote oligodendrocyte differentiation and myelin repair as wel

87 phosphatase Shp2 is an important mediator of oligodendrocyte differentiation and myelination, both du

88 ) is an essential regulator of developmental oligodendrocyte differentiation and myelination, oligode

89 igate the genomic effects of SMF exposure on oligodendrocyte differentiation and neurotrophic factors

90 developmental processes with a main role in oligodendrocyte differentiation and regulation of myelin

91 whether voltage Ca(2+) entry is involved in oligodendrocyte differentiation and remyelination, we us

92 mechanism for understanding how it supports oligodendrocyte differentiation and remyelination.

93 otein 1 (LINGO-1) is a negative regulator of oligodendrocyte differentiation and that anti-LINGO-1 pr

94 cetylase sirtuin-2 (SIRT2) play key roles in oligodendrocyte differentiation by acting as dominant fa

95 Furthermore, we show that Shp2 regulates oligodendrocyte differentiation following demyelination

96 Overexpression of lncOL1 promotes precocious oligodendrocyte differentiation in the developing brain,

97 The mechanism by which LINGO-1 regulates oligodendrocyte differentiation is unknown.

98 gene set enriched for decreased myelination, oligodendrocyte differentiation, and expression.

99 In contrast, ST8SIA4 delays oligodendrocyte differentiation, explaining its adverse

100 ggests lower expression of genes involved in oligodendrocyte differentiation, regulation of glutamate

101 ted substantially impaired remyelination and oligodendrocyte differentiation, which was rescued by ad

102 e progenitor cells, suggesting impairment of oligodendrocyte differentiation.

103 luence neurogenesis, oligodendrogenesis, and oligodendrocyte differentiation.

104 nd displayed a defect in their potential for oligodendrocyte differentiation.

105 polysialylation of the cell surface promotes oligodendrocyte differentiation.

106 myelin thickness in the CNS, independent of oligodendrocyte differentiation.

107 ur findings reveal a complex role for TSC in oligodendrocytes during remyelination in which the timin

108 th myelinated axon tracts and upregulated in oligodendrocytes during RGC axon regeneration.

109 slower and produce less myelin than control oligodendrocytes during the recovery period after CPZ in

110 highlight a previously unrecognized role for oligodendrocyte dysfunction in SCA3 disease pathogenesis

111 ced damage to hippocampal myelin sheaths and oligodendrocytes, enhanced expression of the synaptic pr

112 paminergic neurons (Engrailed 1) and for the oligodendrocyte fate acquisition (Olig2).

113 Shp2 regulates the timely differentiation of oligodendrocytes following lysolecithin-induced demyelin

114 ccumulation of alpha-synuclein aggregates in oligodendrocytes, forming glial cytoplasmic inclusions.

115 potent stem cells (hiPSCs) and hiPSC-derived oligodendrocytes from 12 individuals with mutations span

116 ligodendrocytes or promote production of new oligodendrocytes from oligodendrocyte progenitor cells.

117 on of CNS myelin involves differentiation of oligodendrocytes from oligodendrocyte progenitor cells.

118 n adenosine triphosphate (ATP) buffering, in oligodendrocyte function.

119 terestingly, the smaller pool of spinal cord oligodendrocytes generates myelin that is of normal thic

120 type-specific changes in DNA methylation of oligodendrocyte genes and a global impairment of the mye

121 or two strongly down-regulated genes, myelin oligodendrocyte glycoprotein (Mog) and ermin (Ermn), and

122 Autoantibodies against myelin oligodendrocyte glycoprotein (MOG) are associated with a

123 proteolysis-sensitive immunodominant myelin oligodendrocyte glycoprotein (MOG) epitope (residues 40-

124 eficient in miR-146a and specific for myelin oligodendrocyte glycoprotein (MOG), an autoantigen in th

125 ents and also assessed their value in myelin oligodendrocyte glycoprotein (MOG)-ab positive and ab-ne

126 t to EAE induced by immunization with myelin oligodendrocyte glycoprotein (MOG)35-55 The mechanism of

127 out (KO) mice developed a more severe myelin oligodendrocyte glycoprotein (MOG)35-55-induced experime

128 tibodies recognizing the autoantigen, myelin oligodendrocyte glycoprotein and tumour target, HER2.

129 itopes such as has been suggested for myelin oligodendrocyte glycoprotein epitope 35-55 (MOG35-55) an

130 were given subcutaneous injections of myelin oligodendrocyte glycoprotein fragment1-125 emulsified in

131 We evaluated the seroprevalence of myelin oligodendrocyte glycoprotein immunoglobulin G1 (MOG-IgG)

132 and crossed these with mice bearing a myelin oligodendrocyte glycoprotein-specific TCR transgene.

133 rity by limiting central tolerance to myelin oligodendrocyte glycoprotein.

134 ronal aggregation yet is primarily linked to oligodendrocytes, highlighting early white matter dysfun

135 pinal and spinal motor neurons as well as in oligodendrocytes in brain regions that are affected in A

136 lted in exacerbated apoptosis of regenerated oligodendrocytes in central nervous system (CNS) lesions

137 ssibly restore myelin elaborated by existent oligodendrocytes in early and evolving MS lesions, and s

138 the precise role of NF-kappaB activation in oligodendrocytes in models of MS.

139 ever, the effects of NF-kappaB activation on oligodendrocytes in MS and EAE remain unknown.

140 rotective effects of NF-kappaB activation on oligodendrocytes in MS and EAE.SIGNIFICANCE STATEMENT Mu

141 derstand the role of NF-kappaB activation in oligodendrocytes in MS have been unsuccessful.

142 cytes contribute to the death of neurons and oligodendrocytes in neurodegenerative disorders, and pro

143 demonstrated that KSHV infected neurons and oligodendrocytes in parenchymal brain tissues.

144 haps compensatory, role of Sox10 and BRG1 in oligodendrocytes in regulating the motivation for heroin

145 in rats, a subpopulation of pre-myelinating oligodendrocytes in the auditory brainstem receive excit

146 Oligodendrocytes in the central nervous system produce m

147 rylated at serine residue 312 in neurons and oligodendrocytes in the putamen of patients with multipl

148 e 312 was more apparent in inclusion bearing oligodendrocytes in the putamen.

149 onal activity raises [Ca(2+)]i in developing oligodendrocytes in vivo and that myelin sheath elongati

150 ell types (neurons, glia, endothelial cells, oligodendrocytes) in the stimulated area.

151 ver, we found that NF-kappaB inactivation in oligodendrocytes increased the susceptibility of mice to

152 f human stem cell-derived and primary murine oligodendrocytes indicated that the opposing roles of ST

153 n failure to properly distribute mbp mRNA in oligodendrocytes, indicating a paradoxical role for the

154 During myelination, individual oligodendrocytes initially over-produce short myelin she

155 From birth onward, oligodendrocytes initiate wrapping of neuronal axons wit

156 ing the pathogenic response of astrocytes to oligodendrocyte injury.

157 We conclude that lipid synthesis by oligodendrocytes is heavily supplemented by astrocytes i

158 derstanding the regulation of myelination by oligodendrocytes is therefore critical for developing th

159 n of Tsc1 from OPCs, but not differentiating oligodendrocytes, is beneficial to remyelination.

160 r define the development of the "dying-back" oligodendrocyte lesion in situ and to model the developm

161 how that alpha-synuclein fibril uptake in an oligodendrocyte-like cell line is equally dependent on h

162 ogenitor cell (NPC) differentiation into the oligodendrocyte lineage (O4(+) cells) by BDE-99 involves

163 sed mitochondrial ATP production directly in oligodendrocyte lineage cell cultures and exerted robust

164 ed DWMI and show that while the ISR protects oligodendrocyte lineage cells from hypoxia in vitro, gen

165 e (ISR) is activated by hypoxia and protects oligodendrocyte lineage cells in other disease models.

166 ation seen with Tsc1 or Tsc2 deletion in the oligodendrocyte lineage during CNS development and point

167 o transcription factors that are crucial for oligodendrocyte lineage specification and nerve myelinat

168 reduced ability to differentiate towards the oligodendrocyte lineage, and mice lacking HMGNs show red

169 ion of BDE-99 on h/mNPC development into the oligodendrocyte lineage.

170 ia differently depending on the stage of the oligodendrocyte lineage.

171 Chronic oligodendrocyte loss, which occurs in the demyelinating

172 Sox10), and mature oligodendrocyte markers (CNP, MBP) were quantified.

173 t appeared after 6 months, while more mature oligodendrocyte markers were not present until 1 year af

174 provides evidence that NKX6-2 is involved in oligodendrocyte maturation and might act within the same

175 hanism by which neuronal signaling regulates oligodendrocyte maturation and myelination in TSC.

176 , miR-219 overexpression promotes precocious oligodendrocyte maturation and regeneration processes in

177 Here we show that folate enhances oligodendrocyte maturation both in vitro and in vivo, wh

178 We characterize oligodendrocyte maturation both in vitro and in vivo.

179 Our results indicate that VGCCs can modulate oligodendrocyte maturation in the demyelinated brain and

180 at neuronal TSC1/2 orchestrates a program of oligodendrocyte maturation through the regulated secreti

181 of polycomb repressive complex 2, to promote oligodendrocyte maturation, in part, through Suz12-media

182 -treated microglia promoted OPC survival and oligodendrocyte maturation.

183 in part through epigenetic reprogramming of oligodendrocytes, may lastingly disrupt cortical myelina

184 E STATEMENT We report that creatine enhances oligodendrocyte mitochondrial function and protects agai

185 oligodendrocyte progenitor development, and oligodendrocyte morphology and capacity for myelination.

186 lin quantity and polymerization, with normal oligodendrocyte morphology and myelin gene expression.

187 morphology but were associated with altered oligodendrocyte morphology, myelin gene expression, and

188 During central nervous system development, oligodendrocytes must be formed in proportion to the num

189 , possibly from axons, activate FGFR2 in the oligodendrocyte/myelin compartment to increase ERK1/2 ac

190 uing possibility that FGF receptor 2, in the oligodendrocyte/myelin compartment, may be one such sign

191 A lack of sufficient oligodendrocyte myelination contributes to remyelination

192 rs of cellular functions, but their roles in oligodendrocyte myelination remain undefined.

193 ar hypomyelination associated with increased oligodendrocyte numbers and arrays of microtubules in ol

194 myelination, there were no changes in OPC or oligodendrocyte numbers in either model.

195 of the spinal cord associated with increased oligodendrocyte numbers with accumulation of microtubule

196 verning myelination, and acts on myelinating oligodendrocyte (OL) cells across the human lifespan.

197 yte transcription factor 1 (Olig1), promotes oligodendrocyte (OL) development and is essential during

198 f THAP1 in the CNS retards maturation of the oligodendrocyte (OL) lineage, delaying myelination and c

199 Oligodendrocyte (OL) maturation and axon-glial communica

200 bal inducible (Lrp1(flox/flox);CAG-CreER) or oligodendrocyte (OL)-lineage specific ablation (Lrp1(flo

201 Rapid and efficient protocols to generate oligodendrocytes (OL) from human induced pluripotent ste

202 Myelin elaborated by oligodendrocytes (OLs) in the central nervous system (CN

203 nhibits OPC differentiation into myelinating oligodendrocytes (OLs) while promoting an astrocytic fat

204 systems that promote myelinating activity of oligodendrocytes or promote production of new oligodendr

205 in the CNS is a specialised extension of the oligodendrocyte plasma membrane and clemastine fumarate

206 ein (BMP) signaling, such as Noggin, promote oligodendrocyte precursor cell (OPC) production after hy

207 y, we identified novel molecules involved in oligodendrocyte precursor cell differentiation and valid

208 Specifically, exogenous CCL19 abolished oligodendrocyte precursor cell differentiation observed

209 We have identified an oligodendrocyte precursor cell line, termed G144, that s

210 tate-methyltransferase (Gamt) did not affect oligodendrocyte precursor cell recruitment, but resulted

211 in reminiscent of neural stem cells (NSC) or oligodendrocyte precursor cells (OPC).

212 type 1 to type 2 status, elevated numbers of oligodendrocyte precursor cells (OPCs) and oligodendrocy

213 t hypoxia activates the ISR in primary mouse oligodendrocyte precursor cells (OPCs) in vitro and that

214 rocytes are initially specified, after which oligodendrocyte precursor cells (OPCs) migrate and proli

215 Sox8 is known to be expressed in oligodendrocyte precursor cells (OPCs) together with oth

216 Oligodendrocyte precursor cells (OPCs; PDGFRalpha+) prod

217 ne fumarate can stimulate differentiation of oligodendrocyte precursor cells in vitro, in animal mode

218 NG2 cells, also known as oligodendrocyte precursor cells or polydendrocytes, whic

219 ived mediators influenced differentiation of oligodendrocyte precursor cells through a crosstalk with

220 NLGN3 is cleaved from both neurons and oligodendrocyte precursor cells via the ADAM10 sheddase.

221 y neurons as well as in oligodendrocytes and oligodendrocyte precursor cells.

222 , supplemented cholesterol directly supports oligodendrocyte precursor proliferation and differentiat

223 Human oligodendrocytes precursor cells (OPCs) were stimulated

224 that spontaneous myelin repair by endogenous oligodendrocyte precursors is much more robust than prev

225 differentiation of NCAM- or ST8SIA2-negative oligodendrocyte precursors suggested an underlying cell-

226 differentiation defects of miR-219-deficient oligodendrocyte precursors.

227 It has been proposed to regulate aspects of oligodendrocyte process extension and thereby myelinatio

228 In vitro studies indicated that oligodendrocyte process retraction, which was linked to

229 n by acting at several critical steps during oligodendrocyte progenitor cell (OPC) development.

230 d increases both adult mouse and adult human oligodendrocyte progenitor cell (OPC) differentiation, i

231 ibute to remyelination failure by perturbing oligodendrocyte progenitor cell (OPC) maturation.

232 Treg directly promoted oligodendrocyte progenitor cell differentiation and myel

233 hogenetic protein (BMP) signaling pathway in oligodendrocyte progenitor cells (OPCs) and suppresses r

234 ular mechanisms that drive the maturation of oligodendrocyte progenitor cells (OPCs) during the remye

235 l myelinating glial cells, centrally derived oligodendrocyte progenitor cells (OPCs) ectopically exit

236 Differentiation and maturation of oligodendrocyte progenitor cells (OPCs) involve the asse

237 cal changes, while in developing neurons and oligodendrocyte progenitor cells (OPCs) it induces cellu

238 n which Tsc1 is deleted by Cre expression in oligodendrocyte progenitor cells (OPCs) or in premyelina

239 Many chronically demyelinated lesions have oligodendrocyte progenitor cells (OPCs) within their bor

240 In oligodendrocyte progenitor cells (OPCs), Lrp1 is require

241 rve conduction, and the ectopic migration of oligodendrocyte progenitor cells (OPCs), the resident my

242 rotein fibronectin perturb the maturation of oligodendrocyte progenitor cells (OPCs), thereby impedin

243 liferation, migration and differentiation of oligodendrocyte progenitor cells (OPCs).

244 ig1-Cre-expressing cells reduces the pool of oligodendrocyte progenitor cells (OPCs).

245 emyelination by impairing differentiation of oligodendrocyte progenitor cells (OPCs).

246 myelin and myelin repair by differentiating oligodendrocyte progenitor cells (OPCs).

247 iated neuroinflammation, and an expansion of oligodendrocyte progenitor cells (OPCs).

248 brinogen inhibits nerve repair by preventing oligodendrocyte progenitor cells from differentiating in

249 ly tune axonal diameter, promote re-entry of oligodendrocyte progenitor cells into the cell cycle, or

250 arative capabilities, and transplantation of oligodendrocyte progenitor cells, have generated substan

251 ed to the expansion of genetically wild-type oligodendrocyte progenitor cells, oligodendrocyte differ

252 sis, remyelination can fail despite abundant oligodendrocyte progenitor cells, suggesting impairment

253 mote production of new oligodendrocytes from oligodendrocyte progenitor cells.

254 tire CNS after they have differentiated from oligodendrocyte progenitor cells.

255 ves differentiation of oligodendrocytes from oligodendrocyte progenitor cells.

256 efects in PLP1 mRNA expression and splicing, oligodendrocyte progenitor development, and oligodendroc

257 ides a favorable environment for SVZ-derived oligodendrocyte progenitor generation.

258 NG2(+) glial cells (also called oligodendrocyte progenitors or polydendrocytes) also pro

259 Moreover, EGFR(+) oligodendrocyte progenitors, but not neuroblasts, expres

260 Unlike oligodendrocyte progenitors, SPNs displayed pronounced r

261 he extracellular microenvironment regulating oligodendrocyte properties and discuss stem cell tools t

262 BDE-99 reduced hMBP expression due to oligodendrocyte reduction, but concentrations that did n

263 se resident cells are a major contributor to oligodendrocyte regeneration.

264 Expression of human ABCD1 in oligodendrocytes rescued apoptosis in the abcd1 mutant.

265 precursor cells (OPCs; PDGFRalpha+) produced oligodendrocytes responsible for de novo ensheathment of

266 pment and uncover a cohort of stage-specific oligodendrocyte-restricted lncRNAs, including a conserve

267 Lineage-specific programming of oligodendrocytes results from sensing environmental cues

268 tion from proteolipid protein (PLP)-positive oligodendrocytes slowed remyelination.

269 odendrocyte differentiation and myelination, oligodendrocyte-specific deletion of tuberous sclerosis

270 o, which is accompanied with upregulation of oligodendrocyte-specific DHFR expression.

271 Interestingly, we showed that oligodendrocyte-specific expression of IkappaBalphaDelta

272 The oligodendrocyte-specific inactivation of sterol regulato

273 nce first in motor neurons and then in these oligodendrocytes suggest that they may be mediators of t

274 methotrexate (MTX) causes severe defects in oligodendrocyte survival and differentiation, which coul

275 s a metabolic regulator AMPKalpha to promote oligodendrocyte survival and differentiation.

276 of folate/DHFR/AMPKalpha axis in regulating oligodendrocyte survival and myelination during CNS deve

277 fore, pharmacological compounds that promote oligodendrocyte survival could be beneficial for neuropr

278 to lesions, suggesting that creatine affects oligodendrocyte survival independently of inflammation.

279 es in the presence of morphologically intact oligodendrocytes; these included degeneration of the inn

280 nt decrease in the number of OPCs and mature oligodendrocytes throughout postnatal development in Oli

281 pair goes beyond the intrinsic incapacity of oligodendrocytes to (re)generate myelin and that failed

282 Exclusive exposure of rat oligodendrocytes to GD1a, but not other gangliosides, ov

283 pe and its downstream signaling molecules in oligodendrocytes to obtain better insights into the regu

284 RNA granules from primary cultured mammalian oligodendrocytes to show that they indeed associate with

285 The basic helix-loop-helix protein, oligodendrocyte transcription factor 1 (Olig1), promotes

286 Changes in oligodendrocyte transcripts are driven cell-autonomously

287 Two robustly elevated oligodendrocyte transcripts, Acy3 and Tnfrsf13c, were co

288 Oligodendrocytes transfer energy metabolites to neurons

289 appaBalphaDeltaN expression had no effect on oligodendrocytes under normal conditions (both sexes).

290 e a novel function for creatine in promoting oligodendrocyte viability during CNS remyelination.SIGNI

291 rocyte numbers and arrays of microtubules in oligodendrocytes was demonstrated in the human patient s

292 d myelination capacity of the SMF stimulated oligodendrocytes was validated in a dorsal root ganglion

293 progenitor cells (OPCs) or in premyelinating oligodendrocytes, we reveal that deletion of Tsc1 affect

294 ddition, increased numbers of Olig2(+)APC(+) oligodendrocytes were detected.

295 ed glial cultures (astrocytes, microglia and oligodendrocytes) were exposed to the mitochondrial comp

296 trolling myelin formation and development in oligodendrocytes which is crucial for the powerful brain

297 Oligodendrocytes, which are responsible for white matter

298 In contrast to astrocytes and oligodendrocytes, which arise from multiple progenitor p

299 iNSCs differentiated into neurons and oligodendrocytes with indication of long term integratio

300 PML results when oligodendrocytes within immunocompromised individuals ar