ライフサイエンスコーパス: ZEB2

1 0) and zinc finger E-box binding homeobox 2 (ZEB2).

2 alysis revealed Id2 to be a direct target of Zeb2.

3 bronectin as well as EMT regulators ZEB1 and ZEB2.

4 by downregulating its target genes, ZEB1 and ZEB2.

5 ox6 as a potential downstream target gene of Zeb2.

6 on of miR-205 and its target genes, ZEB1 and ZEB2.

7 expression of miR-200a target genes ZEB1 and ZEB2.

8 anscriptional repressors, including ZEB1 and ZEB2.

9 nce cDC1 development, such as Nfil3, Id2 and Zeb2.

10 C-modulating miRNAs is inhibited by Zeb1 and Zeb2.

11 r E-box-binding homeobox factor 1 (ZEB1) and ZEB2.

12 with ZV in repressing Zp via binding ZEB1 or ZEB2.

13 ta1-induced EMT via inhibition of ZNF532 and ZEB2.

14 consistent with increased expression of ZEB1/ZEB2.

15 ses EMT by repressing expression of ZEB1 and ZEB2.

16 in turn, led to increased expression of ZEB1/ZEB2.

17 of miR-221 upregulates GAX and downregulates ZEB2.

18 ts ability to downregulate the expression of ZEB2.

19 type, partially through suppressing ZEB1 and ZEB2.

20 regulation of Ednrb expression by SOX10 and ZEB2.

21 in treatment through suppression of Slug and ZEB2.

22 nd NFIL3 compete for binding to sites in the Zeb2 -165 kb enhancer and support or repress Zeb2 expres

23 e presence of C/EBPbeta binding sites in the Zeb2 -165 kb enhancer, as this effect is lost in Delta1+

24 All macrophages in Zeb2( -165) mice were exclusively of embryonic origin.

25 Germline deletion of this 400-bp region (Zeb2( -165)mice) specifically prevented Zeb2 expression

26 ics of cell morphogenesis factors, including ZEB2, a known epithelial-mesenchymal transition regulato

27 next expressed miR-221 in ECs and identified ZEB2, a modulator of the epithelial-mesenchymal transiti

28 in smooth muscle long-distance enhancers for ZEB2, a transcription factor extensively studied in the

29 of the mice had retroviral integrations near Zeb2, a transcriptional corepressor leading to overexpre

30 Zeb2 activation appears to be a key step in the EMT proc

31 cute lymphoblastic leukemia, suggesting that Zeb2 activation promotes the transformation of CALM-AF10

32 apitulating miR-221 expression or inhibiting ZEB2 activation.

33 interaction with HDAC1/2-NuRD and abolishes Zeb2 activity for SC differentiation.

34 ression, mediated by the zinc-finger protein Zeb2 (also known as Sip1), is essential for differentiat

35 We found that Zeb2 (also named Sip1, Zfhx1b), a zinc finger transcript

36 uman/mouse VISTA enhancer (62 kb upstream of Zeb2) also up-regulated the Zeb2 promoter, providing evi

37 e that zinc-finger E-box-binding homeobox 2 (Zeb2, also called Sip1) transcription factor is a critic

38 ation are both perturbed, demonstrating that Zeb2, although undetectable in adult Schwann cells, has

39 through its impaired ability to inhibit ZEB1/ZEB2 and acquired concomitant ability to repress new tar

40 lly, we identified the E-cadherin regulators ZEB2 and BMI1 as likely miR-708 targets.

41 o-mesenchymal transition (EMT) markers ZEB1, ZEB2 and CDH2 (which encodes N-cadherin).

42 lase KDM1A as a novel interaction partner of ZEB2 and demonstrated that mouse and human T-ALLs with i

43 Mice with combined mutations in Zeb2 and Edn3 (double mutants) had more severe enteric a

44 w gene fusions and focal deletions of MBNL1, ZEB2 and ELF1, were disproportionately prevalent in youn

45 p of PPP1R1A-regulated gene set with that of ZEB2 and EWS, which regulates metastasis and neuronal di

46 sion of IL-1beta, Ccl2, Cxcl5, Snail1, Zeb1, Zeb2 and Foxf1.

47 wth, accompanied by upregulation of SLUG and ZEB2 and increased invasive properties.

48 transcriptional regulators such as Snail and ZEB2 and is sufficient to drive the transition to epithe

49 Here, we studied the role of Zeb2 and its domains in neurogenesis and neural differen

50 ated through the opposite regulation of ZEB1/ZEB2 and miR-200b and miR-200c.

51 We speculate that the actions of GH on ZEB2 and P- and E-cadherin expression play a role in the

52 ssion of miR-200 decreased the expression of Zeb2 and Pkd1 in HNF-1beta mutant cells.

53 The expression of miR-200 targets, Zeb2 and Pkd1, was increased in HNF-1beta knock-out kidn

54 rations, consistent with the hypothesis that Zeb2 and Ras pathway activation promotes B-lineage leuke

55 d RNA polymerase II localization and reduced Zeb2 and Snail1 binding to epithelial gene promoters.

56 ZEB2 and T-bet cooperate to switch on a terminal CTL dif

57 t miR-192 downregulates expression of Bcl-2, Zeb2 and VEGFA in vitro and in vivo, which is responsibl

58 Smad2 and Smad5 form a complex with Zeb2 and Ywhab/14-3-3beta and Ywhag/14-3-3gamma form a c

59 te-stage NK-cell maturation including T-BET, ZEB2, and BLIMP-1 without affecting viability or prolife

60 These targets include SIAH1, SETD2, ZEB2, and especially FOXN3, which we demonstrated for th

61 expression of E- and P-cadherins, targets of ZEB2, and inhibited E-cadherin promoter activity.

62 the DNA-binding transcription factors Zeb1, Zeb2, and Klf4.

63 ssion profiling assay, we identified Twist1, Zeb2, and PDGFRalpha and beta as Foxq1 downstream target

64 s, suggesting cooperativity among CALM-AF10, Zeb2, and Ras pathway mutations.

65 was necessary to promote coordinated Tbx21, Zeb2, and S1pr5 downregulation.

66 was necessary to promote coordinated Tbx21, Zeb2, and S1pr5 downregulation.

67 Dicer-KO CDs, its direct target genes Zeb1, Zeb2, and Snail2 are upregulated, and miRNA-depleted CDs

68 zinc finger E-box binding homeobox protein, ZEB2, and the down-regulation of miR-200b and miR-200c.

69 a receptor TGFBR2 and the EMT inducers ZEB1, ZEB2, and the snail transcriptional repressor SNAI2, eac

70 e HIF-1alpha expression and attenuated Zeb1, Zeb2, and Twist expression.

71 jor EMT regulatory genes (Snai1, Slug, Zeb1, Zeb2, and Twist1) involved in EMT.

72 binding (ZEB) transcription factors ZEB1 and ZEB2, and undergo EMT on TGF-beta stimulation.

73 o negatively regulate the expression of ZEB1/ZEB2, and we found that the expression of miR-200s was l

74 ociated gene expression of Snail1, Zeb1, and Zeb2; and down-regulated E-cadherin.

75 Zeb2 antagonizes inhibitory effectors including Notch an

76 This indicated that 2 copies of Zeb2 are required for EDN3 to prevent neuronal different

77 ade could also operate in human as T-bet and Zeb2 are similarly regulated in mouse and human NK cells

78 finger E-box-binding (ZEB) proteins ZEB1 and ZEB2 are transcription factors essential in TGF-beta-med

79 ZEB1 and ZEB2 are zinc-finger E homeobox-binding transcription fa

80 data, we identified the transcription factor ZEB2 as a novel AML dependency.

81 l-mesenchymal transition (EMT) and establish ZEB2 as a novel regulator of AML proliferation and diffe

82 nc finger E-box-binding transcription factor ZEB2 as a recurrent genetic lesion in immature/ETP-ALL.

83 in vitro validation, we identified CAD gene ZEB2 as a target through which these lncRNAs exert their

84 This study reveals ZEB2 as an oncogene in the biology of immature/ETP-ALL a

85 We identified Slug and ZEB2 as direct functional targets of miR-218.

86 e miR-200 family and their targets, ZEB1 and ZEB2, as unique P(4)/PR-mediated regulators of uterine q

87 human UBC cells through the TGFbeta1-ZEB2NAT-ZEB2 axis.

88 Our results extend the role of ZEB2 beyond regulating epithelial-mesenchymal transition

89 Mutation of ZEB2 binding sites on the E-cadherin promoter abolished

90 matin immunoprecipitation, we identified two ZEB2 binding sites that modulate the ability of ZEB2 to

91 of key EMT and CSC genes, including TWIST1, ZEB2, BMI1, and POU5F1.

92 EDN3, Zeb2(+/+) EPCs continued expression of ZEB2 but did not undergo any neuronal differentiation.

93 s have detailed microRNA-mediated control of Zeb2, but little is known about the genomic context of t

94 Knockdown of ZEB2, but not ZEB1, led to EBV lytic reactivation.

95 transcriptionally regulated by NF-kappaB and ZEB2, but not ZEB1.

96 ation, establishing that timely induction of Zeb2 by T-bet is an essential event during NK cell diffe

97 Both ZEB1 and ZEB2 can bind Zp via the ZV element.

98 Thus, we conclude that either ZEB1 or ZEB2 can play a central role in the maintenance of EBV l

99 Here we show that the transcription factor Zeb2 cell-autonomously represses Smad signalling to limi

100 creased neuronal differentiation compared to Zeb2(+/+) cells.

101 Zeb2 chromatin immunoprecipitation analysis revealed Id2

102 reased expression of c-Met, fibronectin, and Zeb2 compared with Huh7 and Hep3B cells, which have an e

103 The transcription factor Zeb2 controls fate specification and subsequent differen

104 Therefore, Zeb2 controls SC maturation by recruiting HDAC1/2-NuRD c

105 sults indicate that the transcription factor Zeb2 controls the expression of molecules thereby regula

106 nd by T-bet, and this binding was altered by ZEB2 deficiency.

107 Zeb2-deficient Schwann cells continuously express repres

108 Zeb2 deletion arrests SCs at an undifferentiated state d

109 mice with a Zeb2 loss-of-function mutation (Zeb2(Delta)) and mice carrying a spontaneous recessive m

110 However, microglia develop normally in Zeb2(Delta-165kb) mice, indicating that primitive hemato

111 Zeb2(Delta/+) EPCs had increased neuronal differentiatio

112 Overexpression of EDNRB in Zeb2(Delta/+) EPCs restored inhibition of neuronal diffe

113 Incubation of Zeb2(Delta/+) EPCs with EDN3, on the other hand, resulte

114 EPCs) or were heterozygous for the mutation (Zeb2(Delta/+) EPCs) were exposed to EDN3; we analyzed th

115 In parallel, Edn3(ls) mice were crossed with Zeb2(Delta/+)mice; intestinal tissues were collected fro

116 ZEB2 depletion impaired the proliferation of both human

117 The transcription factors SOX10 and ZEB2 directly activated the EDNRB promoter.

118 , mice in which CD11c(+) cells overexpressed Zeb2 displayed a reduction in cDC1s.

119 subtype of human leukemia and possibly other ZEB2-driven malignancies.

120 Moreover, Zeb2-driven mouse leukaemia exhibit some features of the

121 aggressive subtype of human T-ALL using our Zeb2-driven mouse model.

122 in the repression of E-cadherin by ZEB1 and ZEB2 during EMT, thereby enhancing migration and invasio

123 fied endogenous NFIL3 binding in the -165 kb Zeb2 enhancer(8) at three sites that also bind the CCAAT

124 Putative miR-200-regulated genes included Zeb2, enriched 3.5-fold in the pull down.

125 When exposed to EDN3, Zeb2(+/+) EPCs continued expression of ZEB2 but did not

126 al differentiation, similar to incubation of Zeb2(+/+) EPCs with EDN3.

127 embryos that expressed only wild-type Zeb2 (Zeb2(+/+) EPCs) or were heterozygous for the mutation (Z

128 the epithelial state by suppressing the Zeb1/Zeb2 epithelial gene transcriptional repressors.

129 zinc finger transcription factors, ZEB1 and ZEB2, execute EMT programs in embryonic development and

130 in influx assay, shRNA-mediated knockdown of ZEB2 expression abrogated this effect.

131 Attenuation of ZEB2 expression activates the PI3K/AKT pathway, enhances

132 cells consistently showed increased ZEB1 and ZEB2 expression and decreased E-cadherin expression.

133 by LKB1 loss in lung ADC, which upregulates ZEB2 expression and represses DNp63 transcription in a d

134 n with small interfering RNA (siRNA) reduced Zeb2 expression and resulted in decreased FcepsilonRI-me

135 PTEN ceRNA, and demonstrates that abrogated ZEB2 expression cooperates with BRAF(V600E) to promote m

136 This suggests that low Zeb2 expression differentially regulates signaling pathw

137 ion (Zeb2( -165)mice) specifically prevented Zeb2 expression in hematopoietic stem cell (HSC)-derived

138 ation of all three NFIL3-C/EBP sites ablated Zeb2 expression in myeloid, but not lymphoid progenitors

139 Gain of Zeb2 expression in pulmonary-residing melanoma cells pro

140 n mouse model, we demonstrate that sustained Zeb2 expression initiates T-cell leukaemia.

141 ma cells undergo a conversion in state where ZEB2 expression is replaced by ZEB1 expression associate

142 This was caused by both a dependence of Zeb2 expression on T-bet and a probable cooperation of t

143 GH-dependent increase in ZEB2 expression results in loss of P- and E-cadherins in

144 ct from its ability to downregulate Zeb1 and Zeb2 expression, because silencing them only marginally

145 Zeb2 -165 kb enhancer and support or repress Zeb2 expression, respectively.

146 two microRNAs known to downregulate ZEB1 and ZEB2 expression.

147 migration and invasion by promoting ZEB1 and ZEB2 expression.

148 fects p53-regulated EMT by altering ZEB1 and ZEB2 expression.

149 egulated miR-192 family members also repress ZEB2 expression.

150 mal transition (EMT) by suppressing Zeb1 and Zeb2 expression.

151 cing of the miR-200 family microRNAs affects ZEB2 expression.

152 thelial mesenchymal transition: VIM, TGFss1, ZEB2, FOXC1, CXCR4, were striking compared to cell lines

153 rin in the chick, but both Snail factors and Zeb2 fulfil a similar role in chick and mouse in directl

154 ZEB2 function exerts opposing behaviors in melanoma by p

155 T-bet overexpression could not fully bypass ZEB2 function.

156 The signal localizes to intron 2 of the ZEB2 gene (zinc finger E box-binding homeobox 2).

157 The zinc-finger, E-box-binding homeobox-2 (Zeb2) gene encodes a SMAD-interacting transcription fact

158 , JUP, MED15, MED9, PTPRE SREBF1, TOP2A, and ZEB2, genes that interact with established CHD proteins

159 Zeb2 genetic inactivation impaired the differentiation p

160 Ablation of Zeb2 hampered outgrowth of primary melanomas in vivo, wh

161 In humans, SIP1 (ZEB2) haploinsufficiency leads to Mowat-Wilson syndrome,

162 ABCs are reduced in ZEB2 haploinsufficient individuals and in mice lacking Z

163 including Twist1, Snail1, Snail2, ZEB1, and ZEB2, have been shown to induce epithelial mesenchymal t

164 pression is required for the transition from Zeb2(hi) and Id2(lo) CDPs to Zeb2(lo) and Id2(hi) CDPs,

165 siRNA knockdown of ZEB1 and ZEB2 impaired As-transformed p53lowHBEC migration and in

166 insufficient individuals and in mice lacking Zeb2 in B cells.

167 Mice conditionally lacking Zeb2 in CD11c(+) cells had a cell-intrinsic reduction in

168 d that Nfil3 acts upstream of Id2, Batf3 and Zeb2 in cDC1 development but did not reveal its mechanis

169 expectedly, nuclear expression of the EMT-TF ZEB2 in human primary melanoma has been shown to correla

170 ell function was preserved, but mice lacking Zeb2 in NK cells were more susceptible to B16 melanoma l

171 We conclude that GH increases expression of ZEB2 in part by increasing expression of a ZEB2 natural

172 Mice lacking Zeb2 in Schwann cells develop a severe peripheral neurop

173 Transgenic expression of Zeb2 in Tbx21(-/-) NK cells partially restored a normal

174 Haploinsufficiency of Zeb2 in this developmental context reflects inheritance

175 R-200 family and down-regulation of ZEB1 and ZEB2 in two different mouse models of preterm labor.

176 resses E-cadherin expression by upregulating Zeb2, in part, through a microRNA-mediated mechanism and

177 B resulted in the loss of TWIST1, SNAI2, and ZEB2 induction, and a failure of cells to invade and met

178 r findings suggest that genetic variation in ZEB2 influences the risk of RCC.

179 Excitingly, we observed that ZEB1 and ZEB2 inhibit expression of the contraction-associated ge

180 A total of 91% (10 of 11) of mice with Zeb2 insertions developed B-lineage acute lymphoblastic

181 More than half of the mice with Zeb2 integrations also had Nf1 integrations, suggesting

182 entified, all of which occurred in mice with Zeb2 integrations, consistent with the hypothesis that Z

183 reverted when the transcriptional repressor Zeb2 is ablated.

184 n mouse model, we recently demonstrated that ZEB2 is an oncogenic driver of immature T-cell acute lym

185 When Zeb2 is deleted in adult mice, Schwann cells readily ded

186 d gain-of-function approaches indicated that Zeb2 is essential for controlling apoptosis and neuronal

187 Zeb2 is known to control epithelial to mesenchymal trans

188 We report here that ZEB2 is required for outgrowth for primary melanomas and

189 structs and an inhibitor, we determined that ZEB2 is upregulated by serum and downregulates GAX, whil

190 box binding homeobox transcription factor-2 (ZEB2) is correlated with poor prognosis and patient outc

191 factor Zinc finger E-box-binding homeobox 2 (ZEB2) is increased in stressed cardiomyocytes and induce

192 ein complex through direct disruption of the ZEB2-KDM1A interaction or pharmacological inhibition of

193 miR-200 expression and Zeb2 knockdown are known to inhibit cell invasion in in

194 However, Zeb2 knockdown does not fully recapitulate miR-200c over

195 Conditional Zeb2 knockouts and separate acute loss- and gain-of-func

196 n of miR-192 and p53, via the miR-192 target Zeb2, leading to augmentation of downstream events relat

197 ion by downregulating expression of ZEB1 and ZEB2, leading to production of infectious virus.

198 Experimental knockdown of Zeb2 leads to an increase in BMP-Smad-dependent axon gro

199 Zeb2 levels are downregulated in the embryonic rodent mi

200 d that mouse and human T-ALLs with increased ZEB2 levels critically depend on KDM1A activity for surv

201 ere observed between miR-218 levels and Slug/ZEB2 levels in cancer tissue samples.

202 stablished that the GH-dependent increase in ZEB2 levels is associated with increased transcription o

203 transition from Zeb2(hi) and Id2(lo) CDPs to Zeb2(lo) and Id2(hi) CDPs, which represent the earliest

204 We performed studies in mice with a Zeb2 loss-of-function mutation (Zeb2(Delta)) and mice ca

205 E-cadherin) and mesenchymal (vimentin, ZEB1, ZEB2) markers and decreased aggressiveness as judged by

206 , YAP is inactivated, which in turn relieves ZEB2-mediated default repression of DNp63 and triggers s

207 rmore, the loss of Mel-18 promoted ZEB1- and ZEB2-mediated downregulation of E-cadherin transcription

208 ar plasticity transcription factors ZEB1 and ZEB2 modulate in opposing directions the adaptive antiox

209 We show that ZEB2 modulates PTEN protein levels in a microRNA-depende

210 putative microRNA decoys for PTEN, validates ZEB2 mRNA as a bona fide PTEN ceRNA, and demonstrates th

211 sis showed significant reduction in ZEB1 and ZEB2 mRNA expression.

212 concentrations, T-bet induced expression of Zeb2 mRNA, which then triggered CTLs to adopt terminally

213 ctivity in peripheral neuropathies caused by ZEB2 mutations.

214 associated with increased transcription of a ZEB2 natural antisense transcript required for efficient

215 f ZEB2 in part by increasing expression of a ZEB2 natural antisense transcript.

216 idbrain dopaminergic neurons, in conditional Zeb2 (Nestin-Cre based) knockout mice.

217 ions at 19 common insertion sites, including Zeb2, Nf1, Mn1, Evi1, Ift57, Mpl, Plag1, Kras, Erg, Vav1

218 Moreover, the immature phenotype of Zeb2(-/-) NK cells closely resembled that of Tbx21(-/-)

219 in EBV-positive cells containing both ZEBs, ZEB2, not ZEB1, was the primary ZEB family member bound

220 ke Claudin 23, and to EMT inducer genes like Zeb2, Notch2 and Gli2.

221 via their effects on expression of ZEB1 and ZEB2 of the switch between latent and lytic infection by

222 Mutations in TCF4, MEF2C, UBE3A, ZEB2 or ATRX cause phenotypically overlapping, syndromic

223 A mutant miR-221 fails to downregulate ZEB2 or upregulate GAX.

224 on or antagonism of its target genes (Bcl-2, Zeb2 or VEGFA) may have considerable therapeutic potenti

225 Thus, the coordinated actions of T-bet and ZEB2 outline a novel genetic pathway that forces commitm

226 tion (post-MI), while cardiomyocyte-specific ZEB2 overexpression improves cardiomyocyte survival and

227 eb2 protein-binding domains, suggesting that Zeb2 partners co-determine neuronal output from the mous

228 transcription by the EMT inducers Snail1 and Zeb2 plays a fundamental role in defining embryonic terr

229 The transcription factor Sip1 (Zeb2) plays multiple roles during CNS development from e

230 KZF3 (AIOLOS), TBX21 (T-bet), NFIL3 (E4BP4), ZEB2, PRDM1 (BLIMP1), and RORA mRNA levels are higher in

231 The transcription factors ZEB1 and ZEB2 promote EMT.

232 e, derived from the deleted region, enhanced Zeb2 promoter activity in transcription assays.

233 2 kb upstream of Zeb2) also up-regulated the Zeb2 promoter, providing evidence of a string of conserv

234 E2F1 on vimentin, fibronectin, and ZEB1 and ZEB2 promoters.

235 Therefore, targeting the ZEB2 protein complex through direct disruption of the ZE

236 at the border of the SMAD-binding domain of ZEB2 protein induces ribosomal pausing and compromises p

237 sion of cancer cells, as well as reduced the ZEB2 protein level.

238 ively correlated with ZEB2NAT transcript and ZEB2 protein levels in human bladder cancer specimens.

239 n, we describe a novel mechanism that limits ZEB2 protein synthesis.

240 itionally, we demonstrate distinct roles for Zeb2 protein-binding domains, suggesting that Zeb2 partn

241 Thus, we conclude that Zeb2 regulates commitment to both the cDC2 and pDC linea

242 ibe a novel transgenic rodent model in which Zeb2 regulatory sequence has been disrupted, resulting i

243 gh expression of CX3CR1, HAVCR2 (TIM-3), and ZEB2 represents terminally differentiated status with th

244 r by P-cadherin We also show that Snail2 and Zeb2 repress P-cadherin transcription in the primitive s

245 Genetic ablation of ZEB2 reprograms TAM function and identity on the chromat

246 Reciprocally, ectopic expression of Zeb2 resulted in a higher frequency of mature NK cells i

247 Targeted deletion of Zeb2 resulted in impaired NK cell maturation, survival,

248 Cardiomyocyte-specific deletion of ZEB2 results in impaired cardiac contractility and infar

249 of lung cancer in part by modulation of Slug/ZEB2 signaling, and provide a potential therapeutic stra

250 y showed that the cellular proteins ZEB1 and ZEB2/SIP1 both play key roles in regulating the latent-l

251 actors, TWIST1, SNAI1/Snail1, SNAI2/Slug and ZEB2/Sip1, and are highly invasive.

252 , another zinc finger E-box-binding protein, ZEB2/SIP1, is the key player.

253 The Zeb2 siRNA-treated mast cells had altered cell cycle pro

254 iptional repressors ZEB1 (TCF8/deltaEF1) and ZEB2 (SMAD-interacting protein 1 [SIP1]/ZFXH1B).

255 senchymal transition (EMT) markers vimentin, Zeb2, Snail, and Twist.

256 of some transcription repressors, like Zeb1, Zeb2, Snail, and Twist.

257 f EMT-associated transcription factors ZEB1, ZEB2, Snail, Slug, and Twist.

258 s expression of the known EMT inducers ZEB1, ZEB2, Snail1, and transforming growth factor beta2 (TGFB

259 How Zeb2 subdomains support cell differentiation in various

260 n occurs upon Nfil3 induction and consequent Zeb2 suppression.

261 genome-wide transcriptome analysis reveals a Zeb2 target gene encoding the Notch effector Hey2 as a p

262 maturation such as Sox2 and Ednrb emerge as Zeb2 target genes, supporting its function as an 'inhibi

263 of other EMT-inducing TFs, with Twist, Zeb1, Zeb2, TGF-beta1, and FOXC2 being commonly induced.

264 expression of the E-Box repressors ZEB1 and ZEB2, thereby opposing TGF-beta-mediated downregulation

265 f the mesenchymal genes, as well as ZEB1 and ZEB2, through the mediation of the E2F1 transcription fa

266 2 binding sites that modulate the ability of ZEB2 to downregulate GAX promoter activity.

267 -cadherin by transcriptional upregulation of ZEB2 to stimulate cell invasion.

268 tified zinc finger E-box-binding homeobox 2 (ZEB2) to be up-regulated in a GH dose- and time-dependen

269 Zeb2 (which encodes the transcription factor Zeb2) to hinder effector differentiation.

270 the TF zinc finger E box-binding homeobox 2 (Zeb2) to play a crucial role in regulating DC developmen

271 EN ceRNAs and further characterized one, the ZEB2 transcript.

272 pt required for efficient translation of the ZEB2 transcript.

273 corepressor leading to overexpression of the Zeb2-transcript.

274 oRNAs repress both the EMT-inducing ZEB1 and ZEB2 transcription factors.

275 med subsets with increased IFN-y production, ZEB2-transcription factor-dependent cytotoxicity, and ca

276 n located 165 kilobases (kb) upstream of the Zeb2 transcriptional start site (TSS) that binds the E p

277 Mechanistically, we showed that ZEB2 transcriptionally represses genes that regulate mye

278 Here, using the microbiota-dependent ZEB2-transgenic mouse model of invasive CRC(7), we demon

279 Strikingly, a genetic Zeb2 variant associated with Mowat-Wilson syndrome disru

280 Conversely, Zeb2 was critical for generating effector cells.

281 Zeb2 was expressed from the pre-pDC and pre-cDC stage on

282 Expression of EMT genes TWIST and ZEB2 was increased in sensitive xenografts, suggesting a

283 Inverse correlation between miR-192 and Zeb2 was observed in glomeruli of human subjects with ea

284 we found that the transcription factor (TF) Zeb2 was the most highly induced TF during NK cell matur

285 Importantly, we found that T-bet and ZEB2 were required for S1pr5 induction and that local TG

286 Importantly, we found that T-bet and ZEB2 were required for S1pr5 induction and that local TG

287 factors known to activate EMT, both ZEB1 and ZEB2 were upregulated following mTOR repression.

288 miR-200b-3p targets, ZNF532, and ZEB2 were validated as direct targets using luciferase a

289 enes associated with myeloid identity (Spi1, Zeb2) were upregulated, whereas those associated with ti

290 nce memory development and as a repressor of Zeb2 (which encodes the transcription factor Zeb2) to hi

291 ger E-box binding homeobox proteins ZEB1 and ZEB2, which act as transcriptional repressors.

292 gulate E-cadherin by directly targeting ZEB1/ZEB2, which are transcriptional repressors of E-cadherin

293 ression through direct targeting of ZEB1 and ZEB2, which encode transcriptional repressors of E-cadhe

294 regulating the cellular transcription factor Zeb2, which represses the transcription of BZLF1.

295 e of their downstream targets, SIP1 (ZFHX1B, ZEB2), whose protein product suppresses E-cadherin expre

296 ed with a 12 kb deletion, 1.2 Mb upstream of Zeb2, within a 4.1 Mb gene desert.

297 an be mediated by activation of the ZEB1 and ZEB2 (ZEB) transcription factors, which repress miR-200

298 ngs suggest that reversible switching of the ZEB2/ZEB1 ratio enhances melanoma metastatic disseminati

299 d from embryos that expressed only wild-type Zeb2 (Zeb2(+/+) EPCs) or were heterozygous for the mutat

300 Herein we demonstrate that the Zfhx1b (Sip1, Zeb2) zinc finger homeobox gene is required in the MGE,