ライフサイエンスコーパス: OPC

1 OPCs also produced the majority of myelinating Schwann c

2 OPCs are conventionally considered a homogeneous populat

3 OPCs from chemotherapy-naive mice similarly exhibit incr

4 lar interaction in MS suggests that aberrant OPC perivascular migration not only impairs their lesion

5 t FA synthesis is essential to sustain adult OPC-derived OLs and efficient remyelination.

6 , and suggest that Fth iron storage in adult OPCs is also essential for an effective remyelination of

7 over, we depleted FASN specifically in adult OPCs to examine its relevance for remyelination.

8 ontributed to neurodegeneration by affecting OPC viability and/or development.

9 tion of intracellular Ca(2+) in turn affects OPC and oligodendrocyte biology in the healthy nervous s

10 Aged OPCs become unresponsive to pro-differentiation signals,

11 Aged OPCs treated with metformin regain responsiveness to pro

12 of young brains, we find that isolated aged OPCs cultured on these scaffolds are molecularly and fun

13 nd restore the regenerative capacity of aged OPCs, improving remyelination in aged animals following

14 selective synthesis of the preclinical agent OPC 51803.

15 rrides mechanical signals in vivo and allows OPCs to maintain activity in the ageing CNS.

16 ndroglioma by promoting proliferation and an OPC-like identity via Ets overactivity.

17 der stem cell conditions as compared with an OPC-like cell.

18 required for increased neural stem cell and OPC proliferation in the adult mouse SVZ following demye

19 eroxisome biogenesis, lipid homeostasis, and OPC differentiation during white matter development and

20 creased lesion size, sustained microglia and OPC reactivity.

21 riptional repressor, during motor neuron and OPC formation.

22 receptors that regulate Ca(2+) signaling and OPC development and myelination.

23 of myelin membrane formation, in vitro, and OPC differentiation in fibronectin aggregate containing

24 additional functions of oligodendrocytes and OPCs.

25 the same direction of effect in both SCs and OPCs stimulated with EFs, while the remaining DEGs respo

26 replacement practice, end points included as OPC, follow-up terms for specific OPC, patient populatio

27 emphasize the ability of glial cells such as OPCs to positively respond to moderate intensity SMF sti

28 a cohort of 66 patients with HPV-associated OPC and 22 healthy individuals.

29 cellular immunotherapies for HPV-associated OPC patients.

30 omavirus (HPV)-related oropharyngeal cancer (OPC) generally present with more advanced disease but ha

31 ble fractions (AFs) in oropharyngeal cancer (OPC) have not been evaluated in depth.

32 the management of p16+ oropharyngeal cancer (OPC).

33 uccess in HPV-positive oropharyngeal cancer (OPC).

34 remains an unmet need in oropharynx cancer (OPC).

35 Oropharyngeal candidiasis (OPC) is an opportunistic infection of the oral mucosa ca

36 ous IL-17F deficiency in mice does not cause OPC susceptibility, whereas mice lacking IL-17A are mode

37 ely affects oligodendroglial precursor cell (OPC) differentiation and remyelination via its envelope

38 ent agent of oligodendrocyte precursor cell (OPC) differentiation and remyelination.

39 on, although oligodendrocyte precursor cell (OPC) numbers are normal.

40 gin, promote oligodendrocyte precursor cell (OPC) production after hypoxic-ischemic (HI) injury, the

41 y regulating oligodendrocyte precursor cell (OPC) proliferation.

42 Oligodendrocyte precursor cell (OPC)-specific TrkB deletion in chemotherapy-naive mice r

43 at regulate oligodendrocyte progenitor cell (OPC) and oligodendrocyte formation and function.

44 teps during oligodendrocyte progenitor cell (OPC) development.

45 adult human oligodendrocyte progenitor cell (OPC) differentiation, in addition to its immune regulato

46 n exclusive oligodendrocyte progenitor cell (OPC) fate during differentiation in vitro and in vivo.

47 to promote oligodendrocyte progenitor cell (OPC) maturation, whereas NPCs from age-matched control c

48 perturbing oligodendrocyte progenitor cell (OPC) maturation.

49 ls (NSC) or oligodendrocyte precursor cells (OPC).

50 e and human oligodendrocyte precursor cells (OPCs) and coculture systems, we find that BZA enhances d

51 an cortical oligodendrocyte precursor cells (OPCs) and define a lineage trajectory.

52 s (SCs) and oligodendrocyte precursor cells (OPCs) and explored the molecular mechanism using RNA-seq

53 numbers of oligodendrocyte precursor cells (OPCs) and oligodendrocytes, and increased levels of neur

54 ntiation of oligodendrocyte precursor cells (OPCs) and remyelination in a cross talk between neuronal

55 Oligodendrocyte precursor cells (OPCs) are abundant in the adult central nervous system,

56 report that oligodendrocyte precursor cells (OPCs) contact sprouting endothelial tip cells in mouse,

57 rentiation, oligodendrocyte precursor cells (OPCs) extend a network of processes that make contact wi

58 ustering of oligodendrocyte precursor cells (OPCs) in certain active MS lesions, representing an inab

59 imary mouse oligodendrocyte precursor cells (OPCs) in vitro and that genetically inhibiting the ISR i

60 after which oligodendrocyte precursor cells (OPCs) migrate and proliferate before differentiating int

61 to cultured oligodendrocyte precursor cells (OPCs) rapidly increased expression of myelin genes and m

62 f recruited oligodendrocyte precursor cells (OPCs) to complete remyelination and to sustain axonal su

63 xpressed in oligodendrocyte precursor cells (OPCs) together with other SoxE factors and we show here

64 tic nerves, oligodendrocyte precursor cells (OPCs) undergo transient proliferation but fail to differ

65 Human oligodendrocytes precursor cells (OPCs) were stimulated with moderate intensity SMF (0.3 T

66 nd immature oligodendrocyte precursor cells (OPCs), and these contributed almost half (47%) of all ch

67 napses with oligodendrocyte precursor cells (OPCs), but the circuit context of these neuron to OPC sy

68 by resident oligodendrocyte precursor cells (OPCs), might partially compensate myelin loss in the ear

69 the pool of oligodendrocyte precursor cells (OPCs).

70 neurons and oligodendrocyte precursor cells (OPCs).

71 Oligodendrocyte precursor cells (OPCs; PDGFRalpha+) produced oligodendrocytes responsible

72 storage in oligodendrocyte progenitor cells (OPCs) after demyelination.

73 pathway in oligodendrocyte progenitor cells (OPCs) and suppresses remyelination.

74 OL progenitor cells (OPCs) are not specified into distinct MOL populations du

75 ind strongly to osteogenic progenitor cells (OPCs) but also stimulate osteogenic cell Akt signaling i

76 uration of oligodendrocyte progenitor cells (OPCs) during the remyelination process is essential to d

77 ly derived oligodendrocyte progenitor cells (OPCs) ectopically exit the spinal cord and myelinate per

78 nmental manipulation of OL progenitor cells (OPCs) has profound effects on the establishment of funct

79 FA synthase (FASN) from OL progenitor cells (OPCs) in transgenic mice.

80 uration of oligodendrocyte progenitor cells (OPCs) involve the assembly and disassembly of actin micr

81 cytes from oligodendrocyte progenitor cells (OPCs) is associated with irreversible neurodegeneration

82 eurons and oligodendrocyte progenitor cells (OPCs) it induces cellular death.

83 ression in oligodendrocyte progenitor cells (OPCs) or in premyelinating oligodendrocytes, we reveal t

84 tem (CNS), oligodendrocyte progenitor cells (OPCs) proliferate and migrate to their final destination

85 s adjacent oligodendrocyte progenitor cells (OPCs) to divide and migrate to the lesion, but stroke OP

86 sions have oligodendrocyte progenitor cells (OPCs) within their borders.

87 s known as oligodendrocyte progenitor cells (OPCs)(2).

88 ulation of oligodendrocyte progenitor cells (OPCs), as well as their proliferation and three-dimensio

89 expressing oligodendrocyte progenitor cells (OPCs), but not astrocytes, microglia, or oligodendrocyte

90 tential of oligodendrocyte progenitor cells (OPCs), in addition to OPC-indirect effects involving enh

91 In oligodendrocyte progenitor cells (OPCs), Lrp1 is required for cholesterol homeostasis and

92 ng primary oligodendrocyte progenitor cells (OPCs), microglia-depleted mice, and conditional OPC-spec

93 gration of oligodendrocyte progenitor cells (OPCs), the resident myelinating glial cell of the CNS, i

94 uration of oligodendrocyte progenitor cells (OPCs), thereby impeding remyelination, in the demyelinat

95 -deficient oligodendrocyte progenitor cells (OPCs), they fail to differentiate into mature oligodendr

96 is that of oligodendrocyte progenitor cells (OPCs), we investigated here whether their infection by t

97 Oligodendrocyte progenitor cells (OPCs), which differentiate into myelinating oligodendroc

98 tiation of oligodendrocyte progenitor cells (OPCs).

99 rentiating oligodendrocyte progenitor cells (OPCs).

100 pansion of oligodendrocyte progenitor cells (OPCs).

101 tiation of oligodendrocyte progenitor cells (OPCs).

102 he pool of oligodendrocyte progenitor cells (OPCs).

103 tiation of oligodendrocyte progenitor cells (OPCs).

104 gnaling in oligodendrocyte progenitor cells (OPCs).

105 liferating oligodendrocyte progenitor cells (OPCs).

106 protein of oligodendrocyte progenitor cells (OPCs).

107 s), microglia-depleted mice, and conditional OPC-specific peroxisome proliferator-activated receptor

108 The optical phase conjugation (OPC) through photonic nanostructures in coherent optics

109 er understanding of the factors that control OPC maturation in order to stimulate this pool of progen

110 correlated with overall postoperative costs (OPCs) in all OSS groups (rs = 0.444-0.810 vs 0.445-0.820

111 anada), and (2) an optical plankton counter (OPC) and net collections to identify and enumerate copep

112 Direct exposure of cultured OPCs to aggregating Abeta triggered cell senescence.

113 ic mice, we show that increased or decreased OPC density results in cognate changes in white matter v

114 Lrp1-deficient OPC/OLs show a strong increase in the sterol-regulatory

115 We also tested the capacity of Fth-deficient OPCs to remyelinate the adult brain in the cuprizone mod

116 We report that delamanid (OPC-67683), an approved drug for multi-drug resistant tu

117 The regulatory mechanisms of stage-dependent OPC differentiation uncovered here suggest a translatabl

118 iPSC-derived OPCs from CSPG4(A131T) mutation carriers exhibited abnor

119 ically inhibiting the ISR in differentiating OPCs increases their susceptibility to in vitro hypoxia.

120 RNAseq indicates two distinct OPC transcriptomes associated with the proliferative and

121 ssion of cell activity marker (c-fos), early OPC (Olig1, Olig2.

122 er is compromised in the presence of ectopic OPCs.

123 mostly unaffected in the presence of ectopic OPCs.

124 mbined, cholesterol and pioglitazone enhance OPC differentiation into mature OLs.

125 re critical to facilitate efforts to enhance OPC differentiation in neurological disorders that disru

126 cal demyelination, we find that BZA enhances OPC differentiation and remyelination.

127 on therapeutic approaches aimed at enhancing OPC differentiation.

128 th a greater recruitment of IL-33-expressing OPCs in mice which received anacardic acid when compared

129 y oligodendrocyte development as well as for OPC maturation in the demyelinated adult brain.

130 ation and is an essential Ca(2+) channel for OPC maturation during the remyelination of the adult bra

131 enhances actin dynamics and is essential for OPC morphogenesis and differentiation.

132 ese OPC apply, and (statistical) methods for OPC development.

133 calcium channels (L-VGCCs) are required for OPC development during remyelination, we generated an in

134 pectedly, HPV-specific T cell responses from OPC patients were not constrained to the E6 and E7 antig

135 o impair generation of oligodendrocytes from OPCs.

136 provide evidence that deletion of Tsc1 from OPCs, but not differentiating oligodendrocytes, is benef

137 Thus, decoding how OPCs and myelinating oligodendrocytes integrate and proc

138 HPV attributable oropharyngeal cancer (HPV-OPC) incidence is increasing in many high-income countri

139 hs potentially conferring higher risk of HPV-OPC among these men.

140 h oral HPV persistence, the precursor of HPV-OPC, is unknown.

141 the progression of oral HPV infection to HPV-OPC.

142 demonstration of its activity on adult human OPCs, leads us to propose dual PDE7-GSK3 inhibition, and

143 We further show that human OPCs undergo consecutive symmetric divisions to exponent

144 genetic and functional evidence to implicate OPC dysfunction as a candidate pathophysiological mechan

145 and the molecular systems that are active in OPC responses in white matter stroke, OPCs were virally

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

147 Hypoxia induced increases in OPC numbers, vessel density and endothelial cell express

148 of transcripts encoding proteins involved in OPC function, replicative senescence, and inflammation.

149 linico-pathological predictors of outcome in OPC.

150 tigen to cytotoxic CD8 T cells, resulting in OPC death.

151 -17 stimulation induces NOTCH1 activation in OPCs, contributing to Th17-mediated demyelinating diseas

152 tiffness is a crucial regulator of ageing in OPCs, and provide insights into how the function of adul

153 These electrophysiological changes in OPCs correlate with the differentiation potential of OPC

154 er sex, we establish that Cav1.2 deletion in OPCs leads to less efficient remyelination of the adult

155 nderlie the differentiational differences in OPCs between regions and, likewise, differentiation fail

156 aturation and that HIFalpha dysregulation in OPCs but not oligodendrocytes disturbed normal developme

157 ter MTX depends on intact TrkB expression in OPCs.

158 HIF1a activated a unique set of genes in OPCs through interaction with the OPC-specific transcrip

159 ncreases the intracellular calcium influx in OPCs as well as the gene expression of L-type channel su

160 suggest that voltage-gated Ca(2+) influx in OPCs is critical for remyelination.

161 ctivin A receptor type I (ACVR1) knockout in OPCs.

162 tivation of Ca(2+) channels and receptors in OPCs and oligodendrocytes by neurotransmitters converges

163 ial proliferative and reparative response in OPCs, but this is blocked by a local cellular niche wher

164 Aberrant Wnt tone in OPCs mediates their dysfunctional vascular detachment an

165 ed a conditional knockout mouse for VGCCs in OPCs.

166 white matter OPCs, increased but incomplete OPC differentiation, and a persistent deficit in myelina

167 he composition and bioactivity of individual OPCs and more generally highlight the potential of tradi

168 ur findings suggest a role for Abeta-induced OPC cell senescence in neuroinflammation and cognitive d

169 We demonstrate that Noggin-induced OPC production requires Olig1 function.

170 In functional assays, Matrilin-2 induces OPC differentiation, and Inhibin A inhibits OPC Matrilin

171 investigate how neuroinflammation influences OPCs, we perform in vivo fate-tracing in an inflammatory

172 OPC differentiation, and Inhibin A inhibits OPC Matrilin-2 expression and inhibits OPC differentiati

173 s phosphorylation of Smad 1/5/8 and inhibits OPC differentiation into myelinating oligodendrocytes (O

174 ibits OPC Matrilin-2 expression and inhibits OPC differentiation.

175 GDE3 inhibits OPC proliferation by stimulating ciliary neurotrophic fa

176 Hyaluronan (HA) inhibits OPC maturation and complexes with the heavy chain (HC) o

177 a Cre reporter, we establish that Cav1.2(KO) OPCs display a reduced maturational rate through the ent

178 Specifically, Cav1.2(KO) OPCs mature slower and produce less myelin than control

179 ion, in a mouse line in which the Cav1.2(KO) OPCs were identified by a Cre reporter, we establish tha

180 yte precursor production of Matrilin-2 limit OPC differentiation, tissue repair, and recovery in this

181 g is activated in the later stage of limited OPC differentiation.

182 Treatment of Lrp1(-/-) OPCs with cholesterol or activation of peroxisome prolif

183 we find a similar depletion of white matter OPCs, increased but incomplete OPC differentiation, and

184 feration and, at a late stage, by modulating OPC maturation.

185 uggest that Prdm8 regulates the motor neuron-OPC switch by controlling the level of Shh activity in p

186 he subventricular zone (SVZ) to generate new OPCs in the lesion site has been debated.

187 considered one of the primary sources of new OPCs in the adult forebrain.

188 Tsc1 deletion from NG2(+) OPCs accelerated remyelination.

189 Differences in HPV-AFs or ASRs of OPC cannot be explained by differences in the prevalence

190 HPV-AFs or age-standardized rates (ASRs) of OPC, genital HPV in healthy women, or tobacco use.

191 be taken into account in the construction of OPC include the maturity of THV technology, variability

192 velopment, excluding a major contribution of OPC intrinsic mechanisms determining MOL heterogeneity.

193 ounteract fibronectin-mediated inhibition of OPC maturation.

194 Conditional knockout of OPC Wntless resulted in diminished white matter vascular

195 sive ion channel PIEZO1 as a key mediator of OPC mechanical signalling.

196 These findings indicate properties of OPC derivation, proliferation, and dispersion important

197 linating oligodendrocytes and in the rate of OPC proliferation.

198 ey regulator of CNTF-dependent regulation of OPC proliferation through release of CNTFRalpha.

199 otein 1 (LINGO-1) is a negative regulator of OPC differentiation.

200 gorithm, were assessed in 4 public series of OPC (n = 235).

201 ion of microglia inhibit different stages of OPC differentiation.

202 aptically-restricted rabies virus tracing of OPC afferents, we identified extensive afferent synaptic

203 gesting that inhibiting immune activation of OPCs may facilitate remyelination.

204 Transcriptome analysis of OPCs revealed that senescent NPCs induced expression of

205 ligodendrocytes and a concomitant deficit of OPCs.

206 alpha is required for the differentiation of OPCs and we describe for the first time how oral treatme

207 ofile, proliferation, and differentiation of OPCs by altering the expression of regulatory cytoplasmi

208 ces the proliferation and differentiation of OPCs in the developing CNS.

209 we find that BZA enhances differentiation of OPCs into functional oligodendrocytes.

210 ent to cause age-related loss of function of OPCs.

211 ter, which results in arrested maturation of OPCs and myelination failure.

212 IFNgamma also reduces the absolute number of OPCs and alters remaining OPCs by inducing the immunopro

213 was a significant decrease in the number of OPCs and mature oligodendrocytes throughout postnatal de

214 iferative and limited-regeneration phases of OPCs after stroke.

215 This smaller pool of OPCs results from altered cell cycle and reduced cell pr

216 relate with the differentiation potential of OPCs; thus, they may underlie the differentiational diff

217 Surprisingly, in the presence of OPCs, perineurial glia exited the CNS normally.

218 e proliferation and differentiation rates of OPCs are increased.

219 er tracts in Olig1-null mice lacked Olig2(+) OPCs, and instead proliferating neuronal precursors and

220 ocyte maturation and has distinct effects on OPC and oligodendrocyte transcriptomes.

221 for SERMs to mediate their potent effects on OPC differentiation and remyelination in vivo and highli

222 hibiting effect of aggregated fibronectin on OPC maturation by activating a PKA-dependent signaling p

223 hibiting effect of aggregated fibronectin on OPC maturation, both in vitro and in vivo, by activating

224 GD1a exerts its effect on OPCs by inducing their proliferation and, at a late stag

225 ssociated with EF-guided migration of SCs or OPCs alone.

226 f treatment intensity for patients with p16+ OPC can reduce long-term toxicity without compromising s

227 For patients with p16+ OPC, current treatment approaches are well established.

228 Axin2 in white matter, suggesting paracrine OPC-endothelial signaling.

229 Perivascular OPCs can themselves disrupt the BBB, interfering with as

230 modality for many patients with HPV-positive OPC.

231 C isoform Cav1.2 was deleted in NG2-positive OPCs (Cav1.2(KO)).

232 have found that Fth deletion in NG2-positive OPCs significantly delays the remyelination process in t

233 Fth deletion in NG2-positive OPCs significantly reduces the number of mature oligoden

234 oRG-derived Pre-OPCs provide an additional source of human cortical olig

235 Here, we identify EGFR-expressing "Pre-OPCs" that originate from outer radial glial cells (oRGs

236 ans IL-17R signaling is essential to prevent OPC in mice and humans, but the individual roles of its

237 Here, we used primary OPCs in culture isolated from neonatal rat cortices of b

238 urification of oligomeric proanthocyanidins (OPCs) derived from grape seed extract yielded pure OPC d

239 and mobilization of endogenous progenitors (OPC) which participate in myelin repair.

240 em-cell-derived oligodendrocyte progenitors (OPCs), we demonstrate that HIF1a activates non-canonical

241 igodendrocyte progenitor cell proliferation (OPC) in the developing SVZ, thereby altering cellular ou

242 synthesis are activated during proliferative OPC phases after stroke; inflammatory and growth factor

243 scovered that anti-LINGO-1 antibody-promoted OPC differentiation was accompanied by upregulation of c

244 ion, whereas overexpression of cGSN promoted OPC differentiation in vitro and remyelination in vivo F

245 dium from FSD-C10-treated microglia promoted OPC survival and oligodendrocyte maturation.

246 very after white matter stroke, and promotes OPC differentiation and ultrastructural evidence of remy

247 Furthermore, RAPID gels protect OPCs from mechanical membrane disruption and acute loss

248 studies suggest that while the ISR protects OPCs from hypoxia in vitro, it does not appear to play a

249 derived from grape seed extract yielded pure OPC dimer, trimer, tetramer, and their gallates (pOPCs).

250 Treating rat OPCs with cGSN siRNA reduced OPC differentiation, wherea

251 Treating rat OPCs with cGSN siRNA reduced OPC differentiation, whereas overexpression of cGSN prom

252 signaling did not affect HIFalpha-regulated OPC differentiation and myelination.

253 ng molecular mechanism in HIFalpha-regulated OPC differentiation.

254 Mechanistically, Seh1 regulates OPCs differentiation by assembling Olig2 and Brd7 into a

255 reciated HIFalpha-Sox9 pathway in regulating OPC differentiation.SIGNIFICANCE STATEMENT Promoting dis

256 absolute number of OPCs and alters remaining OPCs by inducing the immunoproteasome and MHC class I.

257 lecular tool to boost maturation of resident OPCs to overcome remyelination failure and halt disease

258 he differentiation potential of adult rodent OPCs decreases with age.

259 transfection of healthy non-carrier sibling OPCs confirmed a pathogenic effect on cell survival of b

260 Some OPCs differentiate rapidly as myelinating oligodendrocyt

261 ncluded as OPC, follow-up terms for specific OPC, patient populations to which these OPC apply, and (

262 divide and migrate to the lesion, but stroke OPCs have only a limited differentiation into mature oli

263 ive in OPC responses in white matter stroke, OPCs were virally labeled and laser-captured in the regi

264 hy correlate with an increased number of SVZ OPCs, suggesting ET-1's role as a regulator of glial pro

265 These findings indicate that OPC-endothelial cell interactions regulate neonatal whit

266 Here we report that OPC differentiation is inhibited by both effector T cell

267 Mechanistically, we showed that OPC-intrinsic GPR17 signaling and sustained activation o

268 areas and thalamic nuclei, illustrating that OPCs have strikingly comprehensive synaptic access to br

269 e-cell electrophysiological recordings, that OPCs start out as a homogeneous population but become fu

270 The OPC data revealed two prey layers comprised almost exclu

271 With higher CDC grades, the OPC tended to increase an upward trend.

272 Prediction of upstream regulators of the OPC stroke transcriptome identifies several candidate mo

273 Here we show that the OPC microenvironment stiffens with age, and that this me

274 Additionally, we find that the OPC-enriched gene, PCDH15, mediates daughter cell repuls

275 e that the EGFP signal co-localizes with the OPC markers throughout the brain.

276 f genes in OPCs through interaction with the OPC-specific transcription factor OLIG2.

277 Therefore, OPCs may be co-opted by the immune system in MS to perpe

278 ific OPC, patient populations to which these OPC apply, and (statistical) methods for OPC development

279 ulate osteogenic cell Akt signaling in those OPCs.

280 cyte progenitor cells (OPCs), in addition to OPC-indirect effects involving enhanced astrocyte expres

281 tional vascular detachment and also leads to OPC secretion of Wif1, which interferes with Wnt ligand

282 from a premature switch from motor neuron to OPC production.

283 gnaling, coincident with the motor neuron to OPC switch.

284 , but the circuit context of these neuron to OPC synapses remains incompletely understood.

285 Unlike Il17f(-/-) mice that are resistant to OPC, Il17f(S65L/S65L) mice showed increased oral fungal

286 stently, Defb3(-/-) mice were susceptible to OPC.

287 Also, when added to OPCs, anacardic acid resulted in the induction of IL-33.

288 "tri-functional" compound that: (i) binds to OPCs, (ii) targets bone, and (iii) induces "pro-survival

289 tified extensive afferent synaptic inputs to OPCs residing in secondary motor cortex, corpus callosum

290 itors switch from producing motor neurons to OPCs with distinct fates is poorly understood.

291 or 5-year survival than RPA with traditional OPC N categories.

292 -way communication with the standard Unicorn OPC process control protocol.

293 er survival than patients with HPV-unrelated OPC.

294 lination by transiently controlling upstream OPC differentiation but not downstream oligodendrocyte m

295 In vitro, OPCs exposed to IFNgamma cross-present antigen to cytoto

296 pithelial default state is IPC-like, whereas OPC identity is derived.

297 Using zebrafish mutants in which OPCs migrate out of the spinal cord and myelinate periph

298 duration of surgery were all associated with OPC (P < 0.001).

299 ronment, the CCI presented associations with OPC.

300 s (OECs) and in tongue tissue from mice with OPC.