ライフサイエンスコーパス: Olig2

1 nd for the oligodendrocyte fate acquisition (Olig2).

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

3 molecular interactions between CDK2/CDK4 and Olig2.

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

5 ed by altering a single transcription factor Olig2.

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

7 l" features in glioblastoma upon ablation of 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 ells in pMN express the transcription factor Olig2.

12 bservations on the bHLH transcription factor Olig2.

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

14 ctions by functional analysis of the bHLH TF OLIG2.

15 intranuclear compartmentalization of murine Olig2.

16 of the oligodendroglial lineage determinant Olig2.

17 l activity marker (c-fos), early OPC (Olig1, 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 In Olig2-ablated cortices, myelination is arrested at the p

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

67 Our findings indicate complex regulation of Olig2 by stage- and lineage-specific regulatory elements

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

84 Olig2+ cells were found to be infected, and many of thes

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

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

87 79R GOF transgenic mouse in combination with Olig2(cre/+) mice to target embryonic ventral telencepha

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

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

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

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

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

93 Olig2 deletion causes a tumor phenotypic shift from an o

94 Olig2 deletion further sensitizes glioma cells to EGFR i

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

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

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

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

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

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

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

102 elopment but not normal pattern formation in Olig2(-/-) embryos.

103 OLIG2 (encoding oligodendrocyte lineage transcription fa

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

123 es oligodendrocyte development by repressing Olig2 expression.

124 stream of Olig2, Sox10 activity can modulate Olig2 expression.

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

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

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

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

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

130 Olig2 function is required for proliferation of neural p

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

132 Thus, spatially restricted ablation of Olig2 function unmasks a contribution of dorsal progenit

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

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

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

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

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

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

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

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

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

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

143 ression during the development of pMN cells: Olig2(high) maintains the pMN state, thereby holding cel

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

159 or Shh signaling, the initial expression of Olig2 in the pMN domain is completely abolished.

160 generated transgenic mice that overexpressed OLIG2 in the thymus.

161 ons between SCL and the transcription factor Olig2 in the ventral neural tube.

162 s Nkx6-regulated expression of the bHLH gene Olig2 in this domain.

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

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

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

166 Olig2 is a bHLH-class transcription factor in pMN cells,

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

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

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

170 Olig2 is a key transcription factor in these networks by

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

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

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

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

175 Olig2 is essential for the selection of motor neuron and

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

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

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

179 r suggest that transcriptional regulation of Olig2 is involved in segregation of pMN neuroblasts.

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

181 o investigate whether enforced expression of OLIG2 is oncogenic, we generated transgenic mice that ov

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

183 Phosphorylated Olig2 is preferentially localized to a transcriptionally

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

185 It was found that over-expression of Olig2 is sufficient to induce Sox10, Nkx2.2 and precocio

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

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

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

189 49 primary tumors from SCL/LMO1, OLIG2/LMO1, OLIG2, LMO1, NUP98/HOXD13, and p27(-/-)/SMAD3(+/-) mice

190 lation is important for the proliferation of OLIG2-LMO1 leukemic cells.

191 owth of leukemic cell lines established from OLIG2/LMO1 transgenic mice was suppressed by a gamma-sec

192 s and 29 of 49 primary tumors from SCL/LMO1, OLIG2/LMO1, OLIG2, LMO1, NUP98/HOXD13, and p27(-/-)/SMAD

193 ted a large BAC clone encompassing the human OLIG2 locus that rescues motor neuron and oligodendrocyt

194 addition of a transgene containing the human OLIG2 locus.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

209 Our data support a model in which the Olig2/Ngn2 ratio in progenitor cells serves as a gate fo

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

211 We found that cells expressing Olig2, Nkx2.2, and NG2 were enriched among virus-infecte

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

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

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

215 Total Olig2+ oligodendrocyte lineage cells first decreased bet

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

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

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

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

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

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

222 Thus, Olig2-orchestrated receptor signaling drives mitotic gro

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

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

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

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

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

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

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

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

231 basic helix-loop-helix transcription factor Olig2, placing them in the oligodendrocyte lineage.

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

233 spinal cord, the bHLH transcription factor, Olig2, plays critical roles in pattern formation and the

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

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

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

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

240 Olig2-positive, polysialylated neural cell adhesion mole

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

242 Previous studies have shown that Olig2 primes pMN cells to become motor neurons by trigge

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

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

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

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

247 The observation that most Olig2(+) progenitors do not maintain neurogenic potentia

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

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

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

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

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

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

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

257 How are the multiple functions of Olig2 regulated?

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

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

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

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

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

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

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

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

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

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

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

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

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

271 indicated that Sox10 functions downstream of Olig2, Sox10 activity can modulate Olig2 expression.

272 ontrol of oligodendrocyte differentiation by Olig2, Sox10 and Nkx2.2 is a dosage-dependent developmen

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

274 he function and hierarchical relationship of Olig2, Sox10 and Nkx2.2 transcription factors in the con

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 cooperate with the bHLH transcription factor Olig2 to promote precocious and ectopic oligodendrocyte

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

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

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

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

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

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

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

289 lls and radial glia expressed Olig1, whereas Olig2 was localized predominantly in mature OLs and a su

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

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

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

293 3 single nucleotide polymorphism markers on OLIG2 were associated with the OCD without TD phenotype:

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

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