ライフサイエンスコーパス: TWIST1

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

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

3 f mesenchymal marker genes SNAI1, SNAI2, and TWIST1.

4 y overexpression of the transcription factor Twist1.

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

6 directly interact to activate expression of Twist1.

7 -associated transcription factors, Snail and Twist1.

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

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

10 zation of the oncogenic transcription factor Twist1.

11 binds to Twist1 and inhibits degradation of Twist1.

12 nd functions of STAT3 target genes including Twist1.

13 dimerize with class II bHLH proteins such as TWIST1.

14 nt on activation of the transcription factor Twist1.

15 riven PDAC through its ability to antagonize Twist1.

16 n from renal fibrosis afforded by macrophage Twist1.

17 , invasion, and expression of the EMT factor TWIST1.

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

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

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

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

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

23 SPZ1 and TWIST1 expression, but not that of TWIST1 alone, enhanced vascular endothelial growth facto

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

25 istically, we show that aberrantly expressed TWIST1 and BET protein BRD4 cooperate to drive miR-214 e

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

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

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

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

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

31 lls via direct transcriptional repression of Twist1 and CD44.

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

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

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

35 such as BMP-TGFbeta, WNT, Notch, HIF1alpha, TWIST1 and HOX family genes, are regulated by shear stre

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

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

38 p62 binds to Twist1 and inhibits degradation of Twist1.

39 experiments show that TGIF1 associates with Twist1 and inhibits Twist1 expression and activity, and

40 Prkd1) is a direct transcriptional target of Twist1 and is not expressed in the normal mammary epithe

41 d consequently reduces the cellular level of TWIST1 and its downstream signaling.

42 Among them, ITGB1, TWIST1 and KRT6B are consistently up-regulated in metast

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

44 The levels of Twist1 and PDGFB are higher in PAE cells isolated from i

45 Hypoxia upregulates the levels of Twist1 and PDGFB in HPAE cells.

46 In patients with breast cancer, TWIST1 and PRKD1 expression correlated with metastatic r

47 unable to restore the level and signaling of TWIST1 and promote breast cancer progression.

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

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

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

51 the reduction in the level and signaling of TWIST1 and the suppression of breast cancer progression

52 Moreover, Twist1 and Twist2 contributed to enhance expression and

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

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

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

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

57 Consistently, Twist1 and Twist2 expression was increased after chronic

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

59 ken together, we identify mechanisms wherein Twist1 and Twist2 promote chromatin modifications, resul

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

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

62 lation upregulated the transcription factors Twist1 and Twist2, which bound to the promoters of the h

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

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

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

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

67 thelial-mesenchymal transition (CDH1, SNAI2, TWIST1, and beta catenin); ruxolitinib blocked these eff

68 tion and proteasome-dependent degradation of TWIST1, and consequently reduces the cellular level of T

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

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

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

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

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

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

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

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

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

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

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

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

81 These studies establish TWIST1 as a driver of resistance to EGFR TKIs and provid

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

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

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

85 ues of SPZ1 at positions 369 and 374, and of TWIST1 at positions 73 and 76, which are required for SP

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

87 A enhances IL-6 transcription through direct Twist1 binding to a conserved E-box element at the IL-6

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

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

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

91 ortance of acetylation signaling in the SPZ1-TWIST1-BRD4 axis in the mediation of EMT and its regulat

92 vitro and in vivo data, we propose that the TWIST1/BRD4/miR-214 regulatory loop is an important, tar

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

94 In macrophages, Twist1 can influence patterns of cytokine generation, bu

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

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

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

98 tions 73 and 76, which are required for SPZ1-TWIST1 complex formation and cancer cell migration in vi

99 d oncogenesis induced by the acetylated SPZ1-TWIST1 complex.

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

101 The transcription factor Twist1 controls diverse essential cellular functions thr

102 MYC and Twist1 cooperate and their sustained expression is requi

103 Checkpoint mRNAs targeted by AUF1 include Twist1, decay of which promotes myoblast development; Cy

104 matory cytokines, and other factors in these Twist1-deficient mice compared with wild-type controls a

105 We also treated wild-type and Twist1-deficient mice with an MMP13 inhibitor after unil

106 TWIST1 dependent upregulation of Mmp3 expression was sup

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

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

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

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

111 1, rendering the latter's reduced binding to TWIST1 during transdifferentiation of Wharton jelly-deri

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

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

114 el whereby conditional expression of MYC and Twist1 enables hepatocellular carcinoma (HCC) to metasta

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

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

117 gerated mesenchymal phenotype with prominent Twist1-expressing TICs.

118 at TGIF1 associates with Twist1 and inhibits Twist1 expression and activity, and this function is sup

119 As Twist1 expression has been associated with poor survival

120 Twist1 expression in MCF7 cells silenced Foxa1 expressio

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

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

123 Twist1 expression is associated with dysregulation of T

124 Furthermore, Twist1 expression is negatively correlated with Foxa1 in

125 TWIST1 expression led to increased tumour engraftment in

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

127 TWIST1 expression was increased in human OA knee cartila

128 Ectopic SPZ1 and TWIST1 expression, but not that of TWIST1 alone, enhance

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

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

131 gh its transactivating ability in increasing TWIST1 expression.

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

133 C into rEC using unique transcription factor TWIST1 for an efficacious cell transplantation therapy t

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

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

136 e EMT transcription factor TWIST1 to release TWIST1 from its cytoplasmic anchor G3BP2 to enter the nu

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

138 To study Twist1 functions in different macrophage subsets during

139 Therefore, MYC and TWIST1 generally appear to cooperate in human cancer to

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

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

142 Twist1 has a well-established role in inducing Epithelia

143 eas, blockade of Ccl2 and Il13 abrogated MYC/Twist1-HCC metastasis.

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

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

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

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

148 airs of proteins of the stromal MAOA-induced Twist1/IL-6/STAT3 pathway in clinical specimens.

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

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

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

152 y, genetic and pharmacological inhibition of TWIST1 in EGFR TKI-resistant EGFR-mutant cells increased

153 is highly positively correlated with that of TWIST1 in human triple-negative breast cancer patients.

154 Twist1 in infiltrating inflammatory macrophages but not

155 Moreover, deletion of Twist1 in infiltrating macrophages attenuated the expres

156 Twist1 in infiltrating myeloid cells mitigates interstit

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

158 Ablating Twist1 in Kras(G12D) ;Tgif1(KO) mice completely blunted

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

160 okine generation, but the role of macrophage Twist1 in renal fibrogenesis remains undefined.

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

162 ghlight the complex cell-specific actions of Twist1 in the pathogenesis of kidney fibrosis.

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

164 TKI resistance through targeting the EMT-TF, TWIST1, in EGFR-mutant NSCLC.

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

166 TWIST1, in turn, regulates endothelial gene transcriptio

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

168 alpha-parvin promotes G3BP2 interaction with TWIST1, increases ubiquitination and proteasome-dependen

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

170 Twist1 induced dramatic transcriptional changes in extra

171 TWIST1 induced matrix metalloproteinase 3 (MMP3) express

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

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

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

175 logic and genetic inhibition of Prkd1 in the Twist1-induced dissemination model demonstrated that Prk

176 udy provides a molecular explanation for how Twist1-induced dissemination works and demonstrates that

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

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

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

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

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

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

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

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

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

186 ic silencing of TWIST1 or treatment with the TWIST1 inhibitor, harmine, resulted in growth inhibition

187 o EGFR TKIs and provide rationale for use of TWIST1 inhibitors or BCL2 inhibitors as means to overcom

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

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

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

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

192 Twist1 is a known regulator of metastatic cell behaviors

193 TWIST1 is a transcription factor critical for developmen

194 Surprisingly, Twist1 is dispensable in endothelial cells but required

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

196 A-positive cells in the implanted gel, while Twist1 knockdown in PAE cells inhibits the effects.

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

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

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

200 Twist1 may shape the IPF phenotype and regulate inflamma

201 Our findings reveal an EPHA2/LYN/TWIST1 mechanotransduction pathway that responds to mech

202 such, pan-BCL2 inhibitor treatment overcame TWIST1-mediated EGFR TKI resistance and were more effect

203 TWIST1-mediated EGFR TKI resistance was due in part to T

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

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

206 have reported that the transcription factor Twist1 mediates hypoxia-induced PH.

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

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

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

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

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

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

213 V malformations, similar to humans harboring TWIST1 mutations.

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

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

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

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

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

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

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

221 We demonstrated that genetic silencing of TWIST1 or treatment with the TWIST1 inhibitor, harmine,

222 TWIST1 overexpression and DNM3OS amplification provides

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

224 Here, we have demonstrated that Twist1 overexpression increases the expression of platel

225 TWIST1 overexpression led to coenrichment of TWIST1 and

226 1 in the regenerated diabetic wound bed with TWIST1 overexpression or silencing (piLenti-TWIST1-shRNA

227 TWIST1 overexpression resulted in erlotinib and osimerti

228 el of autochthonous EGFR-mutant lung cancer, Twist1 overexpression resulted in erlotinib resistance a

229 ce and were more effective in the setting of TWIST1 overexpression.

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

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

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

233 Endothelial Twist1-PDGFB signaling plays a key role in alphaSMA-posi

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

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

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

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

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

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

240 ther, in 33 human cancers (n = 9502) MYC and TWIST1 predict poor survival (p=4.3x10(-10)), CCL2/IL13

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

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

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

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

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

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

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

248 1, a newly dscribed molecule, transactivates TWIST1 promoters, and that this SPZ1-TWIST axis mediates

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

250 Transplantation of stable TWIST1 rEC into a type 1 and 2 diabetic full-thickness s

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

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

255 negatively, in part, of antiangiogenic SFRP4 Twist1 reprogramming enhanced the endothelial lineage co

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

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

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

259 TWIST1 overexpression or silencing (piLenti-TWIST1-shRNA-GFP), respectively, further confirmed impro

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

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

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

267 However, the mechanism by which endothelial Twist1 stimulates SMC accumulation to distal PAs in PH r

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

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

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

271 s in the gel, while knockdown of endothelial Twist1 suppresses the effects.

272 iated EGFR TKI resistance was due in part to TWIST1 suppression of transcription of the pro-apoptotic

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 and targetable signaling node downstream of Twist1 that is required for epithelial invasion and diss

276 9 is necessary to block the up-regulation of TWIST1 that occurs in response to hypoxic stress.

277 thway consisting of alpha-parvin, G3BP2, and TWIST1 that regulates breast cancer progression and meta

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

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 phosphorylates the EMT transcription factor TWIST1 to release TWIST1 from its cytoplasmic anchor G3B

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

284 Instead, the transcription factor Twist1, transforming growth factor beta (TGFbeta), and Y

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

286 bial exposure in the intestinal environment, TWIST1, TWIST2, HDAC1, and HDAC3 were upregulated in hum

287 mportantly, complementing HDAC1 and HDAC3 in Twist1/Twist2-deficient monocyte-derived macrophages res

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

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

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

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

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

293 TWIST1 was required to maintain the mesenchymal phenotyp

294 two conditional mutant mouse models in which Twist1 was selectively ablated either in infiltrating, i

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

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

297 Conditional deletion of Twist1 (which encodes Twist) or Snai1 (which encodes Sna

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

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

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