ライフサイエンスコーパス: TWIST1

1 ous TWIST1) and SW480 (expressing transgenic TWIST1).

2 latory DNA trans-factors (e.g. HIF1alpha and TWIST1).

3 -associated transcription factors, Snail and Twist1.

4 iR-1-1, which directly targets expression of TWIST1.

5 pendent on NF-kappaB-dependent regulation of Twist1.

6 zation of the oncogenic transcription factor Twist1.

7 binds to Twist1 and inhibits degradation of Twist1.

8 nd functions of STAT3 target genes including Twist1.

9 dimerize with class II bHLH proteins such as TWIST1.

10 s of miR-205 expression such as TGFbeta-1 or TWIST1.

11 of FGFRs 1-3, and inactivating mutations of TWIST1.

12 se-1 (MMP-1) as a novel downstream target of TWIST1.

13 pregulation of the transcriptional repressor Twist1.

14 asis via phoshorylation and stabilization of Twist1.

15 n 14 (FBXL14)-mediated polyubiquitination of Twist1.

16 directly interact to activate expression of Twist1.

17 ent miR-424 levels positively associate with TWIST1/2 and EMT-like gene signatures, and miR-424 is in

18 MNT loss (66%); up-regulation of DNM3 (75%), TWIST1 (69%), EPHA4 (66%), and PLS3 (66%); and down-regu

19 Additionally, we have identified Twist1, a basic helix-loop-helix transcription factor an

20 sion by a direct inhibitory interaction with Twist1, a basic helix-loop-helix transcription factor kn

21 termine the role of the transcription factor TWIST1, a master regulator of EMT, on cisplatin resistan

22 We show that TCF12 and TWIST1 act synergistically in a transactivation assay an

23 insight into how beta-catenin signaling via Twist1 actively suppresses the formation of cartilage an

24 We have determined that TWIST1 acts, in a dose-dependent manner, as a mediator b

25 nt to induce transcriptional upregulation of Twist1 along with EMT in mammary epithelial cells.

26 654-beta-catenin and attenuated lung Snail1, Twist1, alpha-smooth muscle actin, and type I collagen a

27 Although Twist1 also plays a role in embryonic vascular developme

28 Twist1 also silences Foxa1 promoter by inhibiting AP-1 r

29 Mechanistically, both Twist1 and BMI1 were critical for Stat5a/b induction of

30 TWIST1 and C3 colocalized at the invasive tumor edges, a

31 We investigated the association between TWIST1 and C3 in malignant tumors and in murine embryos.

32 ory CWR22Rv1 PCa cells significantly reduces Twist1 and CD44 expression, cell migration and sphere fo

33 rm REST knockdown enhanced the expression of Twist1 and CD44, cell migration and sphere formation.

34 lls via direct transcriptional repression of Twist1 and CD44.

35 ulatory and functional relationships between Twist1 and Foxa1 in breast cancer progression are unknow

36 cancer-associated genes including cyclind1, twist1 and hgf, as well as downregulation of tumor suppr

37 B functioned as a translational activator of TWIST1 and HIF1alpha.

38 During embryonic development, TWIST1 and HOXA9 are coexpressed in mouse prostate and t

39 Here we report that TWIST1 and HOXA9 coexpression are reactivated in mouse a

40 p62 binds to Twist1 and inhibits degradation of Twist1.

41 The tumors with high Twist1 and low Foxa1 expressions are associated with poo

42 rectly to the promoter regions of Snail2 and Twist1 and repressed gene transcription, as determined b

43 actor 1 (OCT1) (POU2F1) binding sites of the TWIST1 and SLUG promoters to repress expression of these

44 In human breast tumors, the expression of Twist1 and Snail2 is highly correlated.

45 and further suggest that the balance between Twist1 and Sox9 may determine the earliest steps of chon

46 otes breast cancer metastasis by stabilizing TWIST1 and subsequently enhancing EMT.

47 Moreover, Twist1 and Twist2 contributed to enhance expression and

48 Furthermore, with chronic NOD2 stimulation, Twist1 and Twist2 contributed to the decreased expressio

49 Therefore, after chronic NOD2 stimulation Twist1 and Twist2 coordinate the regulation of both tran

50 Although Twist1 and Twist2 did not coregulate each other's expres

51 synergized with additional PRRs to increase Twist1 and Twist2 expression and Twist-dependent pathway

52 Consistently, Twist1 and Twist2 expression was increased after chronic

53 The role for the transcriptional repressors Twist1 and Twist2 in regulating PRR-induced cytokine out

54 We found that Twist1 and Twist2 were required for optimal cytokine dow

55 Humans have two paralogous genes, TWIST1 and TWIST2, and mutations in each gene have been

56 TWIST1 overexpression led to coenrichment of TWIST1 and WDR5 as well as increased H3K4me3 chromatin a

57 of the EMT-regulatory transcription factors TWIST1 and ZEB1 attenuated mesothelial clearance in ovar

58 sociated transcription factors SNAI1, SNAI2, TWIST1 and ZEB1, which bind to E-box sites in the EpCAM

59 able CoLo741 cells (which express endogenous TWIST1) and SW480 (expressing transgenic TWIST1).

60 combination of altered expression of STAT4, TWIST1, and DNM3 or PLS3 could distinguish, respectively

61 lture and was also enriched along with BMI1, TWIST1, and DVL1 in mammospheric and ALDH1+ populations.

62 ion in vivo and the functional role of PLS3, TWIST1, and GATA6 in SS are being investigated.

63 d expression of pERK, pAkt, fibronectin, and Twist1, and lowered expression of E-cadherin, thereby fa

64 ously unrecognized interplay between ERK1/2, TWIST1, and MMP-1 that is likely significant in the prog

65 PAX5, SNAI3, MYO1H, TWIST1, and PAX7 are associated with craniofacial skelet

66 of neural crest specifiers Snail1/2, Foxd3, Twist1, and Tfap2b.

67 erexpression of transcription factors SNAI1, TWIST1, and ZEB1, which regulate the epithelial-to-mesen

68 These results suggest TWIST1- and EMT-driven increase in Akt activation, and t

69 ck et al. (2015) now show that low levels of Twist1 are essential for tumor initiation, maintenance,

70 nscription factors Snail2 (Slug), Snail1 and Twist1 are expressed in this region.

71 atiotemporal expression showed that Irf6 and Twist1 are found in different cell types.

72 cancer tissues, and the levels of TRIM28 and TWIST1 are positively correlated with the aggressiveness

73 It is known that Snail2 and Twist1 are required for both mesoderm formation and neur

74 Interferon Regulatory Factor 6 (IRF6) and TWIST1 are transcription factors necessary for craniofac

75 Moreover, methylated Twist1 (Arg-34), as such, could also emerge as a potenti

76 We identify the transcription factor Twist1 as a component of a STAT3-induced feedback loop t

77 Previously, we identified Twist1 as a critical downstream mediator of Wnt in repre

78 Our results identified TWIST1 as a transcription factor that regulates C3 expre

79 EMT and arginine 34 (Arg-34) methylation of Twist1 as a unique "methyl arginine mark" for active E-c

80 These findings implicate TWIST1 as an important factor regulating OA related gene

81 These findings identify Twist1 as an inhibitor of Sox9 and further suggest that

82 q1 or indirectly regulated through the Foxq1/Twist1 axis.

83 During EMT, we documented that Twist1 binding to beta-catenin enhanced the transcriptio

84 Mechanistically, Twist1 binds to Foxa1 proximal promoter and recruits the

85 sic helix-loop-helix transcription factor 1 (TWIST1) binds to the C3 promoter and enhances its expres

86 544) repress a signaling network comprising TWIST1, BMI1, ZEB1/2, and miR-200 family miRNAs and sile

87 Finally, Twist1 bound robustly to the 3'UTR of Sox9, the central

88 , IB promotes degradation of the EMT inducer Twist1 by enhancing F-box and leucine-rich repeat protei

89 l, double heterozygous embryos (Irf6 (+/-) ; Twist1 (+/-) ) can have severe mandibular hypoplasia tha

90 Similarly, mutations in TWIST1 cause craniosynostosis, mandibular hypoplasia and

91 Through this mechanism, Twist1 cleavage is triggered to regulate a beta-catenin-

92 Considering that variants in IRF6 and TWIST1 contribute to human craniofacial defects, this ge

93 we show that the negative regulatory factor Twist1 decreases expression of T-bet, Runx3, and IL-12Rb

94 Twist1 decreases Runx3 and T-bet binding at the Ifng loc

95 expression in skull progenitors, conditional Twist1 deletion partially phenocopied the absence of bet

96 phenocopied the absence of beta-catenin, and Twist1 deletion partially restored bone formation in the

97 Mice with a T cell-specific deletion of Twist1 demonstrate increased Th17 and T follicular helpe

98 TWIST1 dependent upregulation of Mmp3 expression was sup

99 T198D (p27CK-DD) activates STAT3 to induce a TWIST1-dependent EMT in human mammary epithelial cells a

100 rtemin (ARTN) has been reported to promote a TWIST1-dependent epithelial to mesenchymal transition of

101 ion, invasion, and tumorigenic activity in a TWIST1-dependent manner in vitro and in vivo.

102 omotes tumor cell growth and metastasis in a Twist1-dependent manner.

103 says demonstrated that TRIM28 interacts with TWIST1 directly and this interaction is presumed to prot

104 tat5a/b regulation of EMT marker expression (Twist1, E-cadherin, N-cadherin, vimentin, and fibronecti

105 Here we report that a TRIM28-TWIST1-EMT axis exists in breast cancer cells and TRIM28

106 o found that transgenic expression of either Twist1 (encoding twist family bHLH transcription factor

107 gly, the mammary epithelial cells expressing Twist1 exhibit much higher degrees of EMT and invasivene

108 itment also was essential for the ability of Twist1-expressing cells to elicit a strong angiogenic re

109 gerated mesenchymal phenotype with prominent Twist1-expressing TICs.

110 Conversely, suppressing Twist1 expression abrogated p65-induced cell migration,

111 However, mechanisms underlying TWIST1 expression and whether aberrant TWIST1 levels pro

112 Surprisingly, Twist1 expression did not increase the secretion of the

113 As Twist1 expression has been associated with poor survival

114 from the neural crest cell lineage, enhanced TWIST1 expression has been linked to worse clinical prog

115 Twist1 expression in MCF7 cells silenced Foxa1 expressio

116 beta-catenin directly activated Twist1 expression in skull progenitors, conditional Twis

117 Increased TWIST1 expression is a feature of OA-affected cartilage.

118 st cancer (LBC) with good prognosis, whereas Twist1 expression is associated with basal-like breast c

119 Twist1 expression is associated with dysregulation of T

120 Furthermore, Twist1 expression is negatively correlated with Foxa1 in

121 Furthermore, TWIST1 expression is required and sufficient to promote

122 TWIST1 expression led to increased tumour engraftment in

123 RNA sequencing analysis revealed that TWIST1 expression resulted in upregulation of GAS6 and L

124 ugh which the tumor microenvironment elicits Twist1 expression to promote cancer metastasis.

125 TWIST1 expression was increased in human OA knee cartila

126 ong a panel of EMT-promoting genes analyzed, TWIST1 expression was strongly activated in response to

127 WIST1 promoter, TWIST1 promoter activity and TWIST1 expression, reverts EMT and impairs metastasis, w

128 gh its transactivating ability in increasing TWIST1 expression.

129 rived cell lines that differed only in their TWIST1 expression.

130 effect is mediated through the inhibition of TWIST1 expression.

131 showed molecular (increased VIM, SNAIL1, and TWIST1 expression; decreased E-CAD expression) and morph

132 TWIST1 formed a complex with WDR5 and the lncRNA Hottip/

133 and this interaction is presumed to protect TWIST1 from degradation.

134 Suppression of TWIST1 function in the right coelomic cavity caused a se

135 interacting transcription factors MEF2C and TWIST1, genes not previously associated with PTB, both o

136 involved in upregulation of PLS3, GATA6, and TWIST1, genes that are undetected in normal lymphocytes.

137 ry PPARgamma agonist, restored expression of TWIST1, GPS2, and SMRT in adipose tissue.

138 In a mouse model of TWIST1 haploinsufficiency, cell mixing between the neura

139 Thus, Twist1 has a critical role in limiting both cell-mediate

140 Twist1 has a well-established role in inducing Epithelia

141 c basis for the antichondrogenic activity of Twist1 has not heretofore been established.

142 Human and mouse T cells lacking Twist1 have an increased ability to differentiate into T

143 for loss-of-function mutations in Tcf12 and Twist1 have severe coronal synostosis.

144 Hence, the dosage of TCF12-TWIST1 heterodimers is critical for normal coronal sutur

145 Notably, although the majority of eDCCs were Twist1(hi)E-cad(lo) and dormant, they eventually initiat

146 sub-population of Her2(+)p-p38(lo)p-Atf2(lo)Twist1(hi)E-cad(lo) early cancer cells that is invasive

147 ignature (nuclear beta-catenin(High)/nuclear Twist1(High)/E-cadherin(Low)/Sox15(Low)/CD133(High)) may

148 Our findings highlight a TWIST1-HOXA9 embryonic prostate developmental program th

149 ed immunohistochemistry to measure levels of TWIST1 in 201 colorectal tumor samples.

150 th enhanced expression of activated EGFR and TWIST1 in a cohort of human prostate cancer specimens an

151 We found that loss of Twist1 in COL1A2(+) cells led to increased fibrosis char

152 In conclusion, loss of Twist1 in collagen-producing cells led to increased bleo

153 We measured the expression of TWIST1 in human colorectal cancer (CRC) cell lines and e

154 We found that expression of Twist1 in human mammary epithelial cells potently promot

155 reports a role for the transcription factor Twist1 in inducing mesenchymal migration by relieving th

156 In vitro, we found that the loss of Twist1 in IPF lung fibroblasts increased expression of C

157 Depletion of TWIST1 in MMSET-overexpressing RWPE-1 cells blocked cell

158 Here, we report a novel function for Twist1 in modifying the tumor microenvironment to promot

159 e objective was to investigate the levels of TWIST1 in normal and OA cartilage and examine its role i

160 We compared the expression of SPZ1 and TWIST1 in specimens of hepatocarcinoma cells (HCCs) and

161 Attenuation of endogenous Twist1 in vivo blocked macrophage recruitment and angiog

162 In chondrocyte precursor cells, Twist1, in a Twist-box-dependent manner, inhibits Sox9-d

163 TWIST1, in part via GAS6 and L1CAM, led to higher expres

164 e located in the basic DNA binding domain of TWIST1, in two subjects with frontonasal dysplasia and a

165 ls, which were rescued by re-introduction of Twist1, indicating that Twist1 mediates Stat5a/b-induced

166 Twist1 induced dramatic transcriptional changes in extra

167 TWIST1 induced matrix metalloproteinase 3 (MMP3) express

168 , expression of the EMT transcription factor Twist1 induced rapid dissemination of cytokeratin-positi

169 Pharmacologic inhibition of HOXA9 prevented TWIST1-induced aggressive prostate cancer cellular pheno

170 d Twist1-repressed LBC markers and decreased Twist1-induced BLBC markers.

171 pha and cytokeratin 8 expression and reduced Twist1-induced integrin alpha5, integrin beta1 and MMP9

172 Restored Foxa1 expression did not change the Twist1-induced mesenchymal cellular morphology and the e

173 ion and metastasis, but less responsible for Twist1-induced mesenchymal morphogenesis and expression

174 Foxa1 expression is largely responsible for Twist1-induced migration, invasion and metastasis, but l

175 and E-cadherin knockdown strongly inhibited Twist1-induced single cell dissemination.

176 WDR5 and Hottip/HOTTIP was also required for TWIST1-induced upregulation of HOXA9 and aggressive cell

177 The transcription factor Twist1 induces epithelial-mesenchymal transition and ext

178 T3 activation and EMT through STAT3-mediated TWIST1 induction.

179 cific down-regulation of either HIF1alpha or TWIST1 inhibited the ability of CPEB2B to induce the acq

180 to demonstrate that the mesenchymal protein Twist1 inhibits p53, providing a novel target for reacti

181 his phenotypic overlap, we asked if Irf6 and Twist1 interact genetically during craniofacial formatio

182 gulatory genes (Snai1, Slug, Zeb1, Zeb2, and Twist1) involved in EMT.

183 ing epigenetic mechanisms of 5hmC induced by TWIST1 is a critical molecule to understanding OA pathog

184 Our findings demonstrate that Twist1 is a key downstream effector of p62 in regulation

185 TWIST1 is a transcription factor critical for developmen

186 TWIST1 is asymmetrically expressed on the right side in

187 Surprisingly, Twist1 is dispensable in endothelial cells but required

188 The E-box transcription factor TWIST1 is essential to epithelial-mesenchymal transition

189 , and stemness properties, establishing that Twist1 is required for NF-kappaB to induce these aggress

190 ion of the EMT-inducing transcription factor Twist1 is sufficient to promote carcinoma cells to under

191 Moreover, in our animal model, BRMS1(KD)/Twist1(KD) double knockdown cells were less efficient in

192 xia-induced transcription factors, Snail and Twist1, leading to decreased transactivation of EMT-asso

193 lying TWIST1 expression and whether aberrant TWIST1 levels promote steps in melanoma progression rema

194 nalysis demonstrated that MMSET binds to the TWIST1 locus and leads to an increase in H3K36me2, sugge

195 The phenotype in embryos subjected to TWIST1 loss- or gain-of-function suggests an important c

196 high expression of the transcription factor Twist1 may explain this prosurvival phenotype in vitro.

197 Twist1 may shape the IPF phenotype and regulate inflamma

198 temness of HNSCC cells through inhibition of Twist1-mediated let-7i downregulation and Rac1 activatio

199 Because TWIST1 mediates epithelial-mesenchymal transition (EMT),

200 y re-introduction of Twist1, indicating that Twist1 mediates Stat5a/b-induced EMT in PC cells.

201 udy, we report that the transcription factor Twist1 mediates TGF-beta-induced CLU expression.

202 Levels of TWIST1 messenger RNA (mRNA) were measured in blood sampl

203 ns, and increases in Tlr4, Nanog, Stat3, and Twist1 messenger RNAs.

204 Therefore, targeting PRMT1-mediated Twist1 methylation might represent a novel strategy for

205 initiator of chondrogenesis, suggesting that Twist1 might directly repress cartilage formation throug

206 Exposure to TNF-alpha rapidly induced Twist1 mRNA and protein expression in normal breast epit

207 Patients with CRC have higher levels of TWIST1 mRNA than healthy individuals.

208 TWIST1 mRNA was not translated in CRC cells with microsa

209 Levels of TWIST1 mRNA were significantly higher in blood samples f

210 Here, we report that elevated TWIST1 mRNA/protein expression is dependent on extracell

211 d with the same cells expressing the Ser 68A-Twist1 mutant.

212 Although about one hundred different TWIST1 mutations have been reported in patients with the

213 rmations in humans with craniosynostosis and TWIST1 mutations that are recapitulated in mouse models.

214 V malformations, similar to humans harboring TWIST1 mutations.

215 No trisomy was observed in TWIST1-negative stromal cells (0 of 1249 cells; P < .001

216 We found that Twist1-null cells expressed high levels of the T cell ch

217 enuated the exaggerated fibrosis observed in Twist1-null mice.

218 The effect of TWIST1 on expression of TET family (TET1, 2 and 3) was m

219 IL-12Rbeta2, compensates for the effects of Twist1 on IFN-gamma production, and Twist1 regulation of

220 Forced expression of TWIST1 on the left side induced ectopic expression domai

221 ve previously shown that the activity of the TWIST1 oncogene is antagonized by TRIM29 and now show th

222 uced renal fibrosis, conditional deletion of Twist1 or Snai1 in proximal TECs resulted in inhibition

223 e that miR-424 is upregulated early during a TWIST1 or SNAI1-induced EMT, and that it causes cells to

224 TWIST1 overexpression and DNM3OS amplification provides

225 hylation is associated with PLS3, GATA6, and TWIST1 overexpression in SS CD4+ T cells and that methyl

226 TWIST1 overexpression led to coenrichment of TWIST1 and

227 PC3 was associated with TWIST1 (P = 0.000076).

228 More importantly, overexpression of STAT3 or Twist1 partially reversed apigenin-impaired cell migrati

229 y, the MAOA-dependent HIF1alpha/VEGF-A/FOXO1/TWIST1 pathway was activated in high-grade PCa specimens

230 e stroma of human colorectal tumors contains TWIST1-positive cancer cells with mesenchymal phenotypes

231 The presence of TWIST1-positive cells in the stroma of human colorectal

232 stroma of human colorectal tumor samples for TWIST1-positive cells with a mesenchymal phenotype and n

233 ectal tumor samples, each of which contained TWIST1-positive cells with matching chromosomal gains in

234 Syngenic TWIST1-positive colon carcinoma cells (CT26) that invade

235 erapy may offer a rational strategy to treat Twist1-positive metastatic cancers.

236 ectively, suggesting that TRIM28 upregulates TWIST1 post-transcriptionally.

237 ally, negatively regulated by Snail2 but not Twist1, preferentially expressed in the neuroectoderm, a

238 c genetic deletion in mice demonstrated that TWIST1 promoted atherosclerosis by inducing inflammation

239 expression in these cells largely inhibited Twist1-promoted migration, invasion and metastasis.

240 educes STAT3 binding to the TWIST1 promoter, TWIST1 promoter activity and TWIST1 expression, reverts

241 is demonstrates that loss of BRMS1 increases Twist1 promoter occupancy of RelA/p65 K310-a key histone

242 d a functional NF-kappaB-binding site in the Twist1 promoter, and overexpression of p65 was sufficien

243 activated cells reduces STAT3 binding to the TWIST1 promoter, TWIST1 promoter activity and TWIST1 exp

244 ST1 signaling, allowing FOXO1 binding at the TWIST1 promoter.

245 1, a newly dscribed molecule, transactivates TWIST1 promoters, and that this SPZ1-TWIST axis mediates

246 We show that TWIST1 protein levels are especially high in melanoma ce

247 phorylation levels positively correlate with Twist1 protein levels in human embryonic kidney 293 and

248 and activator of transcription (pSTAT3), and TWIST1 proteins, and increases in Tlr4, Nanog, Stat3, an

249 Together, our findings show that how Twist1 recruits stromal macrophages through CCL2 inducti

250 s in the distal promoter region of CLU gene, Twist1 regulated basal and TGF-beta-induced CLU transcri

251 al cellular morphology and the expression of Twist1-regulated E-cadherin, beta-catenin, vimentin and

252 tudy demonstrates a novel mechanism by which TWIST1 regulates chromatin and gene expression by cooper

253 the CSC-like cell phenotype was mediated by TWIST1 regulation of BCL-2 expression.

254 fects of Twist1 on IFN-gamma production, and Twist1 regulation of Ifng depends on complex formation w

255 d mouse model, restored Foxa1 also increased Twist1-repressed LBC markers and decreased Twist1-induce

256 elial-mesenchymal transition (EMT) regulator Twist1 represses microRNA let-7i expression, leading to

257 ates the protein, but not the mRNA levels of TWIST1, respectively, suggesting that TRIM28 upregulates

258 Knockdown of Twist1 results in reversal of BRMS1(KD)-mediated EMT phe

259 These results demonstrate that Twist1's silencing effect on Foxa1 expression is largely

260 ctivation of neuropilin-1 promoted AKT/FOXO1/TWIST1 signaling, allowing FOXO1 binding at the TWIST1 p

261 vimentin and Slug, but it partially rescued Twist1-silenced ERalpha and cytokeratin 8 expression and

262 trogen receptor (ERalpha)-positive LBC cells Twist1 silences Foxa1 expression, which has an essential

263 mesenchymal transition (EMT) genes including TWIST1, SLUG, and SNAIL.

264 of EMT master-switch transcription factors, TWIST1, SNAI1/Snail1, SNAI2/Slug and ZEB2/Sip1, and are

265 ibition of NF-kappaB resulted in the loss of TWIST1, SNAI2, and ZEB2 induction, and a failure of cell

266 actor networks, including beta-catenin, MYB, TWIST1, SOX7, GATA3 and GATA6.

267 tion and suggest that targeting p62-mediated Twist1 stabilization is a promising therapeutic strategy

268 at TRIM28 enhances metastasis by stabilizing TWIST1, suggesting that targeting TRIM28 could be an eff

269 required for TNF-alpha-induced expression of Twist1, suggesting the involvement of canonical NF-kappa

270 Knockdown of Twist1 suppressed Jak2-Stat5a/b-induced EMT properties o

271 -like features, because genetic knockdown of Twist1 suppressed Stat5a/b-induced BMI1 expression and s

272 Here, we show that Twist1 suppresses cartilage development by directly inhi

273 E-cadherin/Sox15 complex to the beta-catenin/Twist1/TCF4 complex, the latter of which then binds to C

274 regulatory cascade containing PPARgamma and TWIST1 that controlled the expression of GPS2 and SMRT i

275 9 is necessary to block the up-regulation of TWIST1 that occurs in response to hypoxic stress.

276 of miR-1 and sustain oncogenic activation of TWIST1, thereby leading to accelerated bone metastasis.

277 Twist1, through its carboxyl-terminal Twist-box, binds t

278 Importantly, in distant sites, turning off Twist1 to allow reversion of EMT is essential for dissem

279 2 rescued the ability of tumor cells lacking Twist1 to attract macrophages and promote angiogenesis.

280 STAT3 induces TWIST1 to drive a p27-dependent epithelial-mesenchymal t

281 termed VGF induces the transcription factor TWIST1 to facilitate TKI resistance, EMT, and cancer dis

282 amily (TET1, 2 and 3) was measured in stable TWIST1 transfected TC28 cells, and TET1 expression was u

283 Further, our data suggest TWIST1 (twist family basic helix-loop-helix transcriptio

284 study, we identified the oncogenic protein, TWIST1 (Twist), which is overexpressed in high-grade bre

285 novel mechanism of catabolic reaction where TWIST1 up-regulates MMP3 expression by enriching 5hmC le

286 We suggest that targeting NF-kappaB-mediated Twist1 upregulation may offer an effective a therapeutic

287 senchymal transition markers Snail2 (SNAI2), Twist1, vimentin (VIM), and MMP2 and the reexpression of

288 ocked cell invasion and EMT, indicating that TWIST1 was a critical target of MMSET, responsible for t

289 IPF patients revealed that low expression of Twist1 was characterized by enrichment of T cell pathway

290 In adult porcine and murine arteries, TWIST1 was expressed preferentially at low shear stress

291 rotid arteries and cultured EC revealed that TWIST1 was induced by low shear stress via a GATA4-depen

292 TWIST1 was required to maintain the mesenchymal phenotyp

293 cells, up-regulation of transcription factor Twist1 was shown to promote an EMT.

294 The expression and function of TWIST1 was studied in EC in both developing vasculature

295 tion factors, such as Lhx4, Foxa1, Tbx5, and Twist1, was also observed.

296 ed STAT3 target genes MMP-2, MMP-9, VEGF and Twist1, which are involved in cell migration and invasio

297 imately 21% of cases, including mutations of TWIST1, which encodes a class II basic helix-loop-helix

298 kdown of TRIM28 reduces the protein level of TWIST1 with concurrent upregulation of E-cadherin and do

299 an expression profiling assay, we identified Twist1, Zeb2, and PDGFRalpha and beta as Foxq1 downstrea

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