ライフサイエンスコーパス: Olig2

1 nd for the oligodendrocyte fate acquisition (Olig2).

2 of the oligodendroglial lineage determinant Olig2.

3 ker NeuN, as well as, oligodendrocyte marker olig2.

4 molecular interactions between CDK2/CDK4 and Olig2.

5 basic helix-loop-helix transcription factor, Olig2.

6 ed by altering a single transcription factor Olig2.

7 ogenitors: Ascl1 (Mash1), Ngn2 (Neurog2) and Olig2.

8 markers of this lineage like PDGFRalpha and Olig2.

9 omeodomain protein Dbx1 and the bHLH protein Olig2.

10 antagonized in oligodendrocyte precursors by Olig2.

11 n with the OPC-specific transcription factor OLIG2.

12 l activity marker (c-fos), early OPC (Olig1, Olig2.

13 l" features in glioblastoma upon ablation of Olig2.

14 rgic ENs labeled by the transcription factor olig2.

15 n neural tube patterning: Nkx2.2, Nkx6.1 and Olig2.

16 ctions by functional analysis of the bHLH TF OLIG2.

17 intranuclear compartmentalization of murine Olig2.

18 nducible form of Cre under the regulation of Olig2, a basic helix-loop-helix transcription factor hig

19 90% of embryonic and adult NG2 cells express Olig2, a basic helix-loop-helix transcription factor req

20 partially co-localizing at binding sites of OLIG2, a key activator of motor neuron differentiation.

21 In the Olig2-ablated cortex and spinal cord, the formation of a

22 d oligodendrocytes migrate dorsally into the Olig2-ablated territory but cannot fully compensate for

23 Depletion of mitotic Olig2(+) progenitors or Olig2 ablation impeded tumor initiation.

24 ell-type-specific mutagenesis indicates that Olig2 ablation in GFAP+ astrocytes and their precursors

25 In addition, cortical Olig2 ablation results in a decrease in proliferation of

26 We further demonstrate that the ectopic Olig2 accounts for the reduced Pax6 and Tbr2 expression,

27 Functionally, deletion of Olig2 alone results in a preferential reduction of PCs i

28 is and operating in genetic interaction with Olig2, an essential transcriptional regulator in oligode

29 regulates OPCs differentiation by assembling Olig2 and Brd7 into a transcription complex at nuclear p

30 wild-type subventricular zone cells, Mash1, Olig2 and Dlx2 loci have high levels of histone 3 trimet

31 Like DISC1 and NRG1, OLIG2 and ERBB4 are promising candidate susceptibility g

32 d ventrally located progenitors that express Olig2 and Gsx1, respectively.

33 nce of cross-repressive interactions between Olig2 and Irx3 transcription factors.

34 r of cross-repressive transcription factors, Olig2 and Irx3.

35 Overexpression of Ascl1, Olig2 and Nkx2-2 alone stimulated the specification of O

36 nduction and maintenance of co-expression of Olig2 and Nkx2-2 in OLPs, and thyroid hormone-responsive

37 further showed that Ascl1 collaborates with Olig2 and Nkx2-2 in promoting differentiation of OLPs in

38 vidence that the transcription factors Pax6, Olig2 and Nkx2.2 (Nkx2-2), which define the positional i

39 r another 10 d, these progenitors convert to OLIG2 and NKX2.2-expressing pre-OPCs.

40 by repressing SHH-dependent co-expression of OLIG2 and NKX2.2.

41 first study reporting an association between OLIG2 and OCD, specifically when TD comorbidity is absen

42 In the cerebellum, deletion of both Olig2 and Olig1 results in impaired genesis of Purkinje

43 It was hypothesized a priori that OLIG2 and OLIG1 were associated with OCD regardless of t

44 from PCPs to PIPs is negatively regulated by Olig2 and positively by Gsx1, and contributes to underst

45 ural tube specification genes such as Olig1, Olig2 and Prdm12 are excluded dorsally.

46 rget of oligodendrogenesis-promoting factors Olig2 and Smarca4/Brg1 and is required for proper onset

47 oligodendrocytes, increased transcription of Olig2 and Sox10 genes, augmented myelination, and restor

48 types of OCD have distinct associations with OLIG2 and the functionally related OLIG1 gene.

49 basic helix-loop-helix transcription factor Olig2 and up-regulated the p21(WAF1/CIP1) tumor suppress

50 on of the three transcription factors Sox10, Olig2 and Zfp536 was sufficient to reprogram mouse and r

51 a rapidly dividing outer region of SOX2(+), OLIG2(+), and TLX(+) cells surrounding a hypoxic core of

52 ranscription factors (SOX2, OCT4, NANOG, and OLIG2), and FACT occupied the promoters of these genes.

53 lecithin-induced demyelination by increasing Olig2+ and CC1+ cells in response to injury.

54 d growth factor receptor alpha (PDGFRalpha), Olig2+, and P0+ cells following contusion SCI in mice.

55 try demonstrated positive staining for GFAP, Olig2, and a high Ki-67 proliferative index.

56 f free radical injury, an OL-specific marker Olig2, and histologic evaluation of hyaluronan (HA), an

57 inatorial expression and function of Dlx1&2, Olig2, and Mash1 transcription factors in the ventral te

58 DGFralpha) and transcription factors (Olig1, Olig2, and Sox10).

59 sary to induce Nkx2.2, but have no effect on Olig2, and thereby contribute to the establishment of th

60 in AD mouse models, Abeta plaque-associated Olig2- and NG2-expressing oligodendrocyte progenitor cel

61 In addition, increased numbers of Olig2(+)APC(+) oligodendrocytes were detected.

62 es demonstrate that these diverse actions of Olig2 are gated by phosphorylation at two distinct motif

63 In Arx mutant mice, ventral genes, including Olig2, are ectopically expressed dorsally.

64 scription factors in this network, Olig1 and Olig2, are expressed exclusively by oligodendrocytes aft

65 To examine OLIG2 as a candidate gene for OCD susceptibility and to

66 Loss of HMGNs affects the expression of OLIG2 as well as that of OLIG1, two transcription factor

67 Unphosphorylated Olig2, as seen in mature white matter, is localized main

68 ciated, oligodendrocyte transcription factor OLIG2 at 14-18 weeks gestational age (GA) (period of neu

69 tin organization around Nkx2.2-, Nkx6.1- and Olig2-bound regions, together with co-analysis of engage

70 ite matter, CD82 is coexpressed with CC1 and olig2 but not with NG2 or GFAP.

71 all parenchymal progenitors at P4 are Sox2(+)Olig2(+), but by P8 a Sox2(-) subpopulation emerges, sug

72 express the transcription factors Olig1 and Olig2, called pMN progenitors, produce motor neurons and

73 Inhibition of CDK2/CDK4 activity disrupted Olig2-CDK2/CDK4 interactions and attenuated Olig2 protei

74 The data indicate that olig2(+) cells are ENs whose activity is modulated with

75 la melanogaster ventral nerve cord, with the Olig2(+) cells behaving as ganglion mother cells.

76 s hypothesis, we have prospectively isolated Olig2(+) cells from murine embryonic day (E)9.5 and E13.

77 stly expressed in proliferating progenitors, Olig2(+) cells in the cerebellar VZ are in the process o

78 r total NeuN(+) cells in the hippocampus, or olig2(+) cells in the corpus callosum.

79 both the proliferating and overall number of Olig2(+) cells in the injured cortex.

80 ciated and total pools of mRNA isolated from Olig2(+) cells indicated that the in vivo gene expressio

81 When olig2(+) cells were tracked during the peak period of mo

82 This shift occurs in Olig2(+) cells within hours and in multiple genetic back

83 tal number of oligodendrocyte lineage cells (Olig2(+) cells) was increased, suggesting that Cdk5 loss

84 P(+) cells, while enhancer 1056 is active in Olig2(+) cells.

85 ammation that regulates the proliferation of Olig2(+) cells.

86 ating the proliferation of Olig2-expressing (Olig2(+)) cells after brain injury.

87 yte lineage transcription factor 2-positive (OLIG2(+)) cells begin to express the transcription facto

88 g at 3 dpe revealed the presence of Mash1(+) Olig2(-) cells in the migratory route accompanied by ect

89 ells transfected with 2 spectrally different OLIG2 clones.

90 ells in constitutive and tamoxifen-inducible Olig2 conditional knockout mice in which Olig2 was delet

91 Moreover, using Olig2(cre) to conditionally inactivate Gsx2 throughout t

92 79R GOF transgenic mouse in combination with Olig2(cre/+) mice to target embryonic ventral telencepha

93 eleting the gene in neural progenitors using Olig2-Cre and Wnt1-Cre mice, respectively.

94 f the medial ganglionic eminence (MGE) using Olig2-Cre mice causes moderate or severe defects in the

95 ing proteins in oligodendrocytes (OLs) using Olig2-Cre results in mice displaying rapid tremors at po

96 al inactivation of Pten in oligodendrocytes, Olig2-cre, Pten(fl/fl) mice.

97 ngs with a battery of inducible Cre drivers (Olig2-Cre-ER(T2), GFAP-Cre-ER(T2), FoxJ1-Cre-ER(T2) and

98 Olig2 deletion causes a tumor phenotypic shift from an o

99 Olig2 deletion further sensitizes glioma cells to EGFR i

100 demonstrate that Dlx1&2 negatively regulate Olig2-dependant OPC formation and that Mash1 promotes OP

101 and myelination by promoting assembly of an Olig2-dependent transcription complex and define a nucle

102 rlier identified as potential suppressors of OLIG2 dimerization and found to inhibit tumor growth in

103 mechanism of action, we undertook a study of OLIG2 dimerization using fluorescence cross-correlation

104 stream of Shh signaling, in which Nkx2.2 and Olig2 direct repression of alternative neural progenitor

105 nd expression profiling analyses reveal that Olig2 directly activates cell-proliferation machinery to

106 reas conditional Hoxa2 overexpression in the Olig2(+) domain inhibited oligodendrogenesis throughout

107 astoma tumorigenesis and relapse, suggesting OLIG2-driven oncogenic networks as potential therapeutic

108 ogenitors transiently express the pMN marker Olig2 during spinal cord development.

109 sing time-lapse microscopy demonstrated that olig2-EGFP(+) OPCs exhibit enhanced cell migration withi

110 lized to neuronal progenitors expressing the olig2:egfp transgene rather than the Muller glia.

111 OLIG2 (encoding oligodendrocyte lineage transcription fa

112 In the absence of swimming, olig2(+) ENs had basal firing rates near 8 spikes/s, and

113 odevelopmental TFs (POU3F2, SOX2, SALL2, and OLIG2) essential for GBM propagation.

114 ticipates in regulating the proliferation of Olig2-expressing (Olig2(+)) cells after brain injury.

115 Here we identify mitotic Olig2-expressing cells as tumor-propagating cells in pro

116 cted transgenic reporter lines indicate that Olig2-expressing cells in the astroglial but not the oli

117 gehog (SHH) medulloblastomas, and identified OLIG2-expressing glial progenitors as transit-amplifying

118 The NE cells are then specified to OLIG2-expressing motoneuron progenitors in the presence

119 example, motor neurons are generated from an olig2-expressing population of pMN-like ependymoradial g

120 opment of oligodendrocytes and neurones from olig2-expressing precursor cells.

121 these neuroepithelial cells are specified to OLIG2-expressing progenitors in the presence of retinoic

122 r sequential specification of ventral spinal OLIG2-expressing progenitors, pre-oligodendrocyte precur

123 th different responses were observed with an Olig2-expressing subset relatively more sensitive to tre

124 controls oligodendrocyte-specification gene Olig2 expression and functions as a molecular switch for

125 ficient and necessary for the suppression of Olig2 expression and proper control of MN versus V2 inte

126 stream target of proneural genes, suppresses Olig2 expression and therefore controls ventral spinal c

127 al Mash1 (also known as Ascl1) and gliogenic Olig2 expression are preserved, but Dlx2, a key downstre

128 We show that the ectopic Olig2 expression can be repressed by blocking SHH signal

129 Increased OLIG2 expression in DS cells directly upregulates intern

130 as well as to the K23 enhancer, which drives Olig2 expression in the pMN domain.

131 We have found that Olig2 expression is spontaneously downregulated in NG2 c

132 Thus, altered OLIG2 expression may underlie neurodevelopmental abnorma

133 inactivation promotes Erk-dependent, ectopic Olig2 expression specifically in transit-amplifying prog

134 f progenitors, the progressive initiation of olig2 expression, and oligodendrocyte formation.

135 oliferation, reduces Tbr2 levels and induces Olig2 expression, indicative of premature gliogenesis.

136 in the so-called pMN domain characterized by Olig2 expression.

137 es oligodendrocyte development by repressing Olig2 expression.

138 rs descended to the pMN domain and initiated olig2 expression.

139 Wild-type OLIG2 forms stable homodimers, whereas mutant (unphospho

140 spinal cord, or independent requirements for Olig2 function in somatic motor neuron and OPC developme

141 s express the Olig2 transcription factor and Olig2 function is necessary for formation of spinal moto

142 ntrolled mutagenesis revealed that postnatal Olig2 function is required for astrocyte differentiation

143 Olig2 function is required for proliferation of neural p

144 Mouse embryos deficient for Olig2 function lack somatic motor neurons and OPCs, but

145 In the absence of olig2 function, r5 and r6 precursors remain in the cell

146 Studies in mice suggest that Olig2 gene dosage alters cerebral cortical interneuron d

147 The OLIG2 gene is also highly expressed in brain regions imp

148 x1 interacts with the regulatory elements of Olig2 gene locus in vivo and it is critical for proper O

149 rectly binds to the proximal promoter of the Olig2 gene locus, as well as to the K23 enhancer, which

150 uggest that Prox1 suppresses the activity of Olig2 gene promoter and K23 enhancer.

151 nterneurons in NPCs via direct repression of Olig2 gene regulatory elements.

152 e upstream molecular mechanisms that control Olig2 gene transcription are not well understood.

153 We have generated OLIG2-GFP hPSC reporter lines that reliably mark MNs and

154 Here we use an Olig2-GFP human embryonic stem cell (hESC) reporter to d

155 st that GBM characterized by high-expressing Olig2 GIC may exhibit greater sensitivity to NVP-HSP990

156 NVP-HSP990 attenuated cell proliferation in Olig2-high GIC lines.

157 Similarly, increased density of Olig2-immunoreactive cells in PFC WM was significantly a

158 strocyte formation, we conditionally ablated Olig2 in a spatiotemporally controlled manner.

159 To assess the function of Olig2 in astrocyte formation, we conditionally ablated O

160 at least in part attributable to the loss of Olig2 in developing astrocytes and their precursors.

161 reveal both common and independent roles for olig2 in development of somatic motor neurons and oligod

162 Despite the critical role of Olig2 in nervous system development and cancer progressi

163 cell proliferation, is directly repressed by OLIG2 in neural progenitors and gliomas.

164 To further examine the role of Olig2 in NG2 cell fate determination, we used genetic fa

165 Deletion of Olig2 in NG2 cells in perinatal mice also resulted in as

166 Constitutive deletion of Olig2 in NG2 cells in the neocortex and corpus callosum

167 Inhibiting myelination by deletion of Olig2 in oligodendrocyte precursor cells impairs spatial

168 Here we demonstrate that the repression of Olig2 in p2 domain is controlled by mir-17-3p microRNA-m

169 basic helix-loop-helix transcription factor Olig2 in the developing dorsal telencephalon.

170 Although the role of Olig2 in the lineage is well established, the role of Ol

171 this backdrop, the bHLH transcription factor Olig2 in the oligodendrocyte lineage is unorthodox, show

172 Thus, our studies uncover a crucial role for Olig2 in white matter astrocyte development and reveal d

173 of the CNS-restricted transcription factor, OLIG2, in human glioma stem and progenitor cells reminis

174 ing, implicating a role for SHH signaling in Olig2 induction.

175 We further show that OLIG2 inhibition or over-expression regulates potassium

176 entiation, and that the transcription factor OLIG2 is a central node in the affected pathway.

177 Olig2 is a direct target of EZH2, and repression of this

178 We also showed that Olig2 is a functional marker associated with cell prolif

179 Olig2 is a key transcription factor in these networks by

180 show here that the proliferative function of Olig2 is controlled by developmentally regulated phospho

181 Sustained expression of Olig2 is counterintuitive because all known functions of

182 Thus, our studies suggest that Olig2 is critical for postinjury gliosis.

183 The bHLH transcription factor Olig2 is essential for motoneuron and oligodendrocyte fo

184 Olig2 is essential for the selection of motor neuron and

185 Olig2 is expressed in an opposite gradient within pTH-C

186 Further analyses demonstrate that Olig2 is expressed in both cerebellar VZ progenitors and

187 The bHLH transcription factor Olig2 is expressed in cycling neural progenitor cells bu

188 ic eminence of the embryonic forebrain where Olig2 is mostly expressed in proliferating progenitors,

189 triple serine motif in the amino terminus of Olig2 is phosphorylated in cycling neural progenitors bu

190 Phosphorylated Olig2 is preferentially localized to a transcriptionally

191 basic helix-loop-helix transcription factor Olig2 is required for oligodendrocyte specification and

192 During cortical development, Olig2 is transiently expressed in immature developing as

193 t, we demonstrate that after cortical injury Olig2 is upregulated in reactive astrocytes coincident w

194 godendrocyte lineage transcription factor 2 (OLIG2) is an essential regulator in the development of c

195 shRNA-mediated knockdown of OLIG2 largely reverses abnormal gene expression in early

196 addition of a transgene containing the human OLIG2 locus.

197 In the phosphorylated state, Olig2 maintains antineural (i.e., promitotic) functions

198 Targeting Olig2 may circumvent resistance to EGFR-targeted drugs.

199 neuron progenitors and largely excluded from Olig2+ MN progenitors (pMN).

200 Genomic profiling revealed that OLIG2 modulates chromatin landscapes and activates oncog

201 suggest that microRNA-mediated repression of Olig2 mRNA plays a critical role during the patterning o

202 by mir-17-3p microRNA-mediated silencing of Olig2 mRNA.

203 local white matter and preferentially became Olig2+, Myelin Associated Glycoprotein-positive, Myelin

204 tantially from astroglia differentiated from Olig2-negative hESC-derived neural progenitor cells (NPC

205 and a small subset of OPCs arise from common olig2(+) neuroepithelial precursors in rhombomeres r5 an

206 nge of Wnt signaling, which is necessary for olig2(+) neuron development.

207 By contrast, olig2(+) neurons did not develop in embryos deficient fo

208 rded in current clamp and voltage clamp from olig2(+) neurons in immobilized larval zebrafish (before

209 s of the cerebellum to regulate formation of olig2(+) neurons.

210 roduced a two-fold increase in the number of olig2(+) neurons.

211 In addition to OLIG2(+) NG2(+) I(Na)(+) OPCs and OLIG2(+) NG2(neg) I(Na

212 ddition to OLIG2(+) NG2(+) I(Na)(+) OPCs and OLIG2(+) NG2(neg) I(Na)(neg) OLs, we identified cells wi

213 tial activation of the transcription factors OLIG2, NKX2.2 and SOX10 is required for sequential speci

214 on induced a dorsoventral enlargement of the Olig2/Nkx2.2-expressing oligodendrocyte progenitor domai

215 ction of three transcription factors (SOX10, OLIG2, NKX6.2) in iPSC-derived neural progenitor cells i

216 ral progenitors, Dcx(+) newborn neurons, and Olig2(+) oligodendrocyte populations.

217 Total Olig2+ oligodendrocyte lineage cells first decreased bet

218 cl1 and Hes5 (Notch signaling mediators) and Olig2 (oligodendrogenesis mediator).

219 motoneurons and myelinating glia depends on Olig2, one of the five Olig family bHLH transcription fa

220 hite matter tracts in Olig1-null mice lacked Olig2(+) OPCs, and instead proliferating neuronal precur

221 e no alterations in expression of Iba1 or in Olig2 or CNPase.

222 s, but the combinatorial action of Ascl1 and Olig2 or Nkx2-2 was required for further promoting their

223 cells remained PDGF receptor alpha positive, olig2(+), or NG2(+) or became CC1(+) nonmyelinating olig

224 Thus, Olig2-orchestrated receptor signaling drives mitotic gro

225 Finally, neural progenitors from Olig2 over-expressing transgenic mice exhibit these same

226 These findings suggest that OLIG2 over-expression inhibits neural progenitor prolife

227 Finally, over-expression of vertebrate Olig2 partially rescues the walking defects of oli-defic

228 We asked how transcription factor OLIG2 participates in this MN-OLP fate switch.

229 nterneuron progenitors are transitioned from Olig2(+) PC progenitors.

230 The marker profile of infected cells, NG2+, olig2+, PDGFR-alpha+, nestin+, GFAP-, and CC1-, indicate

231 cells (hESCs), we generated highly enriched OLIG2(+)/PDGFRalpha(+)/NKX2.2(+)/SOX10(+) human OPCs, wh

232 loid leukemia (AML): NOR1, CDH13, p15, NPM2, OLIG2, PGR, HIN1, and SLC26A4.

233 The oligodendrocyte transcription factor Olig2 plays a crucial role in the neurogenesis of both s

234 riven lesions are clonal, H3K27me3 depleted, Olig2 positive, highly proliferative, and diffusely spre

235 godendrocyte lineage transcription factor 2 (Olig2)-positive cells that resemble OPCs.

236 We further detected a significant loss of OLIG2-positive cells in the corpus callosum of Tmem106b-

237 te development by promoting specification of olig2-positive cells in the hindbrain and other brain re

238 n of disc1 or nrg1 caused near total loss of olig2-positive cerebellar neurones, but caused no appare

239 normal murine OPCs and highly proliferative Olig2-positive glioma cells identified all the transcrip

240 e various cell types found within the brain, Olig2-positive tumor cells are most similar to OPCs.

241 o not similarly develop from shared pools of olig2(+) precursors.

242 tional insights into the temporal control of Olig2 progenitor cell fate change by the identification

243 tal development also expanded this NG2+Mash1+Olig2+ progenitor population and promoted SVZ-to-lesion

244 ciency of OPC induction is reduced, only few Olig2 progenitors are recruited to generate OPCs, meanwh

245 sults indicate that glial lineage-associated OLIG2(+) progenitors are tumor-initiating cells during m

246 Although OLIG2(+) progenitors become quiescent stem-like cells in

247 X6(+)) neural stem cells, which give rise to OLIG2(+) progenitors by day 12.

248 C) reporter to demonstrate that hESC-derived Olig2(+) progenitors generate a subtype of previously un

249 monstrate the importance of postnatal Sox2(+)Olig2(+) progenitors in pontine growth and oligodendroge

250 Depletion of mitotic Olig2(+) progenitors or Olig2 ablation impeded tumor ini

251 o known as NG2) Ascl1+ (also known as Mash1) Olig2+ progenitors and functional remyelination were acc

252 dendrogenesis and remyelination by NG2+Mash1+Olig2+ progenitors.

253 x-loop-helix transcription factors Olig1 and Olig2 promote myelination, whereas bone morphogenetic pr

254 Pax6 and Nkx6.1, but not DsRed driven by the olig2 promoter in these cells.

255 y attributed to compensatory upregulation of Olig2 protein expression in the spinal cord after Olig1

256 we perform an independent study to show that Olig2 protein is transiently expressed in the cerebellar

257 Olig2-CDK2/CDK4 interactions and attenuated Olig2 protein stability.

258 The OLIG2 proteins showed change in diffusion time under com

259 Our findings identify an Olig2-regulated lineage-restricted pathway critical for

260 ility of TF motifs NR1H4 and OLIG (OLIGI and OLIG2), respectively.

261 Intriguingly, deletion of Olig2 resulted in tumors that grow, albeit at a decelera

262 In combination with other markers, olig2 reveals a dorsoventral organization of cerebellar

263 The later, postnatal Olig2(+) RPCs also made terminal divisions, which were b

264 The embryonic Olig2(+) RPCs underwent terminal divisions, producing sm

265 sphorylation at two distinct motifs and that Olig2's proliferative function acts in opposition to the

266 omodimers, whereas mutant (unphosphorylated) OLIG2(S147A) prefers to form heterodimers with Neurogeni

267 ockdown of four transcription factors (SOX2, OLIG2, SALL2, and POU3F2) that drive the proneural BTIC

268 Olig2(+) /Sox-10(+) cells appeared inside the lining of

269 After the latter development, the number of Olig2(+) /Sox-10(+) cells decreased to 0.21 +/- 0.07 (P3

270 At P21, Olig2(+) /Sox-10(+) cells inside the CC lining started t

271 we noticed the presence of small numbers of Olig2(+) /Sox-10(+) cells inside the lining of the centr

272 Olig2(+) /Sox-10(+) cells usually did not proliferate in

273 developing mouse spinal cord, expression of Olig2, Sox10 and Nkx2.2 is sequentially up-regulated in

274 ulated relative to normal hESC GPCs; NKX2.2, OLIG2, SOX10, MYRF, and their downstream targets were al

275 In 11 cases, OPC numbers (Olig2 strong; NogoA negative) were also decreased; in ei

276 godendrocyte lineage transcription factor 2 (Olig2), suggesting that oligodendrocyte differentiation

277 atal pons expressed the transcription factor Olig2, suggesting an oligodendrocyte lineage.

278 pressed the oligodendrocyte precursor marker Olig2, suggesting caution when using DCX as a marker for

279 How are the biological functions of Olig2 suppressed in terminally differentiated oligodendr

280 Re-expression of MAL and OLIG2 to physiological levels dramatically reduced the g

281 pMN cells express the Olig2 transcription factor and Olig2 function is necessa

282 in restored the levels of phospho-Smad1/5/8, Olig2 transcription factor, oligodendrocyte maturation,

283 locus in vivo and it is critical for proper Olig2 transcription regulation.

284 g ribosome affinity purification (TRAP) from Olig2-TRAP transgenic mice.

285 ges comprising the radiation response of the Olig2(+) tumor bulk cells, we used translating ribosome

286 We discovered that Olig1 and Olig2, two genes that are triplicated in Down syndrome a

287 hiPSCs) derived from DS patients overproduce OLIG2(+) ventral forebrain neural progenitors.

288 ble Olig2 conditional knockout mice in which Olig2 was deleted specifically in NG2 cells.

289 Serine 147 in the helix-loop-helix domain of OLIG2 was phosphorylated during MN production and dephos

290 proportion of proliferating cells that were Olig2(+) was similar through the first 7 months of life

291 In all lesions (n = 20), the number of OLs (Olig2 weak/NogoA positive) was reduced compared to contr

292 3 single nucleotide polymorphism markers on OLIG2 were associated with the OCD without TD phenotype:

293 Two genes studied in detail, MAL and OLIG2, were silenced during transformation, initially th

294 o-localizes with the oligodendrocyte marker, Olig2, whereas PI5P4Kbeta co-localizes with the neuronal

295 ulating two Shh-Gli target genes, Nkx2.2 and Olig2, which are initially induced in a common pool of p

296 Here we show that expression of olig2, which encodes a bHLH transcription factor, marks

297 ted promitogenic functions of phosphorylated Olig2, which reflect, at least in part, an oppositional

298 ion of the intrinsic oligodendrogenic factor Olig2 while inducing expression of the interneuron fate

299 tion assays show that phosphorylation brings Olig2 within 30 nm of p53 within the open chromatin comp

300 fects on animal survival, while knockdown of Olig2 within Id1(low) cells has a significant survival b