ライフサイエンスコーパス: EpCAM

1 EpCAM accumulated on the lateral interfaces of human col

2 EpCAM appears to differentially regulate LC mobility/mig

3 EpCAM appears to promote LC migration from epidermis by

4 EpCAM is a known transcriptional target of the Wnt signa

5 EpCAM knockdown resulted in decreases in claudin-7 and c

6 EpCAM overexpression was 98% in both esophageal squamous

7 EpCAM stabilizes claudin-7 in IECs, and HAI-2 regulates

8 EpCAM upregulation occurs in HBV-mediated HCCs and hepat

9 EpCAM was detected in the nuclei of human HCC cells from

10 EpCAM(+) CD49f(+) cells also engraft into the subcutaneo

11 EpCAM(+) CD49f(hi) cells expressed cluster of differenti

12 EpCAM(+)MPs in patients with CRSwNP were no different fr

13 EpCAM-targeted MBs efficiently (85%) and rapidly (within

14 EpCAM-targeted MBs efficiently (88%) isolated frequent t

15 ssociated markers (e.g., CD44, CD24, ALDH-1, EpCAM, Lgr5), multipotency, and tumorigenicity following

16 In addition, EpCAM, especially intracellular domain of EpCAM (EpICD),

17 st that, in the absence of strong adjuvants, EpCAM-deficient LCs exhibit increased migration to regio

18 TJ formed readily after EpCAM knockdown; the acquisition of trans-epithelial ele

19 ibodies (mAbs) of varying affinities against EpCAM for both noninvasive and intraoperative detection

20 Although EpCAM knockdown decreased claudin-1 and claudin-7 protei

21 n analyses and index sorts, we found that an EpCAM(+) CD49f(hi) epithelial cell subpopulation from pr

22 roblasts were associated with E-Cadherin and EpCAM expression and expression of integrin alphavbeta6.

23 e identified by their expression of CD24 and EpCAM, suggesting the potential of exosomes for diagnost

24 has antigen-binding arms that engage CD3 and EpCAM and a constant domain that recruits Fc receptor-be

25 The exosome-associated markers CD63 and EpCAM were enriched in the isolated EVs while markers of

26 A knockdown suppresses CpG demethylation and EpCAM expression.

27 increase and become progressively GS(-) and EpCAM(-) .

28 ith elevated expression of Plk1, HOTAIR, and EpCAM.

29 ochemistry scores generated for Keratin7 and EpCAM demonstrated a good correlation with gene expressi

30 thm based on the combination of Keratin7 and EpCAM gene expression that stratified three groups of pa

31 ty (MSI), germline mutations in the MSH2 and EpCAM genes, somatic mutations in BRAF and KRAS, and the

32 Combining OCT4 and EpCAM selection can further enrich the meiotic-competent

33 SC marker expression (e.g., NANOG, OCT4, and EpCAM), expansion of SP, and acceleration of tumor growt

34 ed the expression of the folate receptor and EpCAM on lung carcinoma and breast adenocarcinoma cells,

35 s at pH 7.0, such as the folate receptor and EpCAM.

36 We quantified the size and EpCAM expression of over 2,500 CTCs from 38 patient samp

37 HLA-ABC-/CD49e- (putative spermatogonia) and EpCAM-/HLA-ABC+/CD49e+ (putative MOLT-4) cell fractions.

38 ll and epithelial markers, such as SSEA1 and EpCAM, respectively, are not predictive of reprogramming

39 Anti-EpCAM MBs efficiently (>77%) isolated rare mouse breast

40 e with 90+/-8% efficiency when using an anti-EpCAM-coated array.

41 Biotinylated anti-EpCAM antibody that specifically binds to human cancer c

42 the trifunctional antibody catumaxomab (anti-EpCAM x anti-CD3).

43 nic for T cell recruitment (catumaxomab anti-EpCAM/CD3 and blinatumomab anti-CD19/CD3), increase in t

44 were twice as bright as two commercial anti-EpCAM red fluorophore conjugates, APC and AlexaFluor(R)6

45 (30 mum x 150 mum) channels containing anti-EpCAM antibodies that is scalable in terms of throughput

46 A panel of hybridoma-derived anti-EpCAM mAbs was generated and screened.

47 been tested in phase 1 studies so far: anti-EpCAM BiTE((R)) AMG 110, anti-CEA BiTE((R)) MEDI-565/AMG

48 In vitro, RBCs modified with lipophilic anti-EpCAM or anti-CD45 antibodies efficiently bound to cance

49 antiepithelial cell adhesion molecule (anti-EpCAM), provides the specificity for CTC capture.

50 utilized for covalent immobilization of anti-EpCAM antibody.

51 Amino group on anti-EpCAM antibody was covalently bound with succinimidyl gr

52 pture efficiency of a surface with only anti-EpCAM.

53 es with either fibronectin, Matrigel or anti-EpCAM antibody.

54 )) coated with fibronectin, Matrigel or anti-EpCAM.

55 ls (PBMCs) were functionalized with the anti-EpCAM-lipid-CSANs, they were shown to selectively kill a

56 CV results confirm that the anti-EpCAM/LC-SPDP/Au based biosensor could detect MCF-7 cell

57 The anti-EpCAM/LC-SPDP/Au electrodes were exposed to solutions wi

58 These anti-EpCAM/LC-SPDP/Au electrodes were characterized using cyc

59 uman liver cancer cell line Hep3B using anti-EpCAM-CdTe- and anti-GPC3-ZnSe-coated silica nanoparticl

60 NPs were conjugated with anti-EpCAM antibody to the NP surface for immunospecific targ

61 gold electrodes and functionalized with anti-EpCAM.

62 s expressing liver stem cell markers such as EpCAM, CK19, CD133, and Sox9.

63 In a matrigel differentiation assay, EpCAM(+) CD49f(+) cells expanding in vitro underwent org

64 Physical interactions between EpCAM and claudins were required for claudin stabilizati

65 novel double-negative feedback loop between EpCAM and ERK that contributes to the regulation of EMT.

66 first time an intricate relationship between EpCAM-regulated transcription and altered biophysical pr

67 o antibodies directed to surface biomarkers (EpCAM and Slex) of human colorectal CTCs.

68 important translational implications as both EpCAM and ERK are currently being targeted in human clin

69 n NSCLC cell lines, positive for E-Cadherin, EpCAM and alphavbeta6 expression, activate normal fibrob

70 Specifically, CCND2, EpCAM, and IGFII expression was elevated at the prolifer

71 ted triple-marker-positive (CD44(+)/CD133(+)/EpCAM(+)) cells of human PC MiaPaCa-2 and L3.6pl cells b

72 analysis showed that CSLCs (CD44(+)/CD133(+)/EpCAM(+)) exhibit differential expression of more than 1

73 Notably, CD133(+)/EpCAM(+) cancer stem cells vanished from the catumaxomab

74 the triple-marker-negative (CD44(-)/CD133(-)/EpCAM(-)) cells.

75 nce-activated cell sorting-enriched CD133(-)/EpCAM(-) (double negative, DN), Huh-7 cells underwent a

76 We previously demonstrated that the CD133(-)/EpCAM(-) hepatoma subpopulation was more metastatic than

77 predominated over epithelial markers (CD133, EpCAM, and LGR5).

78 ion overexpressing CSC markers (CD44, CD166, EpCAM) for all cell lines.

79 ed distinct CD49f+/EpCAM+ progenitor, CD271+/EpCAM- basal, and ALDEFLUOR+ cell profiles.

80 CD49f(+)/EpCAM(-), CD44(+)/EpCAM(-), CD44(+)/CD24(-), or ALDEFLUOR-positive subpopu

81 h reduced expression of EZH2, Notch-1, CD44, EpCAM, and Nanog and increased expression of let-7, miR-

82 CD49f(+)/EpCAM(-), CD44(+)/EpCAM(-), CD44(+)/CD24(-), or ALDEFLUO

83 iated and highly clonogenic ALDH(+)/CD49f(+)/EpCAM(+) luminal progenitors, which express both basal c

84 PAM50 gene-set analyses of ALDH(+)/CD49f(+)/EpCAM(+) populations efficiently identified major and mi

85 ALDH(+)/CD49f(+)/EpCAM(+) tumor and normal cells clustered differently co

86 ary stem cell-enriched basal cells (CD49f(+)/EpCAM(-)/Lin(-)) expressed higher levels of ANTXR1 compa

87 of the same patients showed distinct CD49f+/EpCAM+ progenitor, CD271+/EpCAM- basal, and ALDEFLUOR+ c

88 In epithelial cells, EpCAM regulates expression and distribution of selected

89 nt prostate cancer, isolated via CellSearch (EpCAM(pos)/CK(pos)/CD45(neg)/DAPI(pos)) and subsequent F

90 demonstrated that active matriptase cleaves EpCAM after Arg80 and that loss of HAI-2 in IECs led to

91 -bearing mice enriched for CD133(+)/CXCR4(+)/EpCAM(-) CICs are highly tumorigenic and metastatic.

92 ough the generation of the CD133(+)/CXCR4(+)/EpCAM(-) subset.

93 re contiguous to the surrounding cytoplasmic EpCAM(+)/HNF-4alpha(-) ductular oval cells.

94 ensities (26%; P<0.05) on P14, and decreased EpCAM expression intensities on LCs as well (33%).

95 o effect on proliferation of STAT3-deficient EpCAM(+)CD45(-) LPCs.

96 the ability of EpCAM aptamer SYL3C to detect EpCAM expression in 170 cases of esophageal cancer (EC)

97 Further evaluation in different EpCAM-expressing cell lines is warranted as well as appl

98 ancer stem cell markers BAMBI, DKK1,2, DLK1, EpCAM, MYC, and proliferation genes CCNA1, CCND2, IGFII,

99 t the promoters of BAMBI, CCND2, DKK2, DLK1, EpCAM, and IGFII was demonstrated by chromatin immunopre

100 activates peritoneal T cells and eliminates EpCAM(+) tumor cells, establishing a molecular and cellu

101 can be caused by mutations in genes encoding EpCAM, a putative adhesion molecule, and HAI-2, a cell s

102 EpCAM-) breast cancer cells to an epithelial EpCAM+/high phenotype.

103 leotide microarrays showed that the expanded EpCAM(+) CD49f(+) gallbladder cells and IHBD cells exhib

104 In a competitive binding experiment, EpCAM aptamer generated a staining pattern similar to th

105 ls containing Matrigel(R) without expressing EpCAM.

106 HCC subset that is classified by an extreme EpCAM(+) AFP(+) gene expression signature and associated

107 or maintaining HCC stemness, is required for EpCAM(+) HCC spheroid formation as well as the maintenan

108 ring EMT, demonstrate an unexpected role for EpCAM in the regulation of ERK and define a novel double

109 1AP1 may serve as a key molecular target for EpCAM(+) AFP(+) HCC subtype.

110 RelA site is in a CpG island downstream from EpCAM transcriptional start site (TSS).

111 Germline EpCAM deletions were present in three of four patients w

112 (+)EpCAM(-) cells, we isolated them as GFP(+)EpCAM(-) cells from DDC-injured livers of Sox9-EGFP mice

113 C-like with high langerin, Birbeck granules, EpCAM, and E-cadherin expression under the same conditio

114 Level 0 single-cell buds are K19(+) /GS(+) /EpCAM(+) /Heppar1(-) .

115 morphologically hepatocytes (K19(-) /GS(+) /EpCAM(+) /Heppar1(+) ).

116 In hepatocytes, EpCAM is silenced by polycomb repressive complex 2 (PRC2

117 inistration to nude BALB/c mice bearing high EpCAM-expressing HT-29 colorectal cancer xenografts.

118 iate EpCAM) and promyelocytic leukemia HL60 (EpCAM-negative) xenografts.

119 Interestingly, the human EpCAM gene also has a CpG island downstream from its TSS

120 These results identify EpCAM as a substrate of matriptase and link HAI-2, matri

121 To determine if EpCAM regulates claudins in LC and immune responses to e

122 itical oncoprotein specifically activated in EpCAM(+) AFP(+) HCC.

123 e up-regulated in EpCAM(+)AFP(+) HCCs and in EpCAM(+) HCC cells isolated from AFP(+) tumors.

124 hromatin-remodeling factor Smarcd3/Baf60c in EpCAM- breast cancer cells gave the most robust transiti

125 In addition, HCC cells in EpCAM(+) spheroids are more resistant to chemotherapeuti

126 duced translocation and dendrite motility in EpCAM-deficient LC in vivo in contact allergen-treated m

127 miR-181 family members were up-regulated in EpCAM(+)AFP(+) HCCs and in EpCAM(+) HCC cells isolated f

128 in de-repression of PRC2 targets, including EpCAM and pluripotency genes.

129 lls, SOX2 bound the EPCAM promoter to induce EpCAM-p21(Cip1)-cyclin A2 signaling, encouraging cell pr

130 Herein we demonstrate HBx induces EpCAM expression via active DNA demethylation.

131 neck squamous cell cancer FaDu (intermediate EpCAM) and promyelocytic leukemia HL60 (EpCAM-negative)

132 To gain insight into EpCAM function in a physiologic context in vivo, we gene

133 e-activated cell sorting was used to isolate EpCAM(+) HCC cells, which were tested for hepatic stem/p

134 ar cell suspensions was performed to isolate EpCAM+/HLA-ABC-/CD49e- (putative spermatogonia) and EpCA

135 fluorescence-activated cell sorting-isolated EpCAM(+) HCC cells displayed hepatic cancer stem cell-li

136 However, tumor-derived Lineage-EpCAM-CD73+CD90+ cells led to the formation of vessels w

137 ir normal counterpart, tumor-derived Lineage-EpCAM-CD73+CD90+ cells showed enhanced expression of the

138 oth tumor-derived and matched normal Lineage-EpCAM-CD73+CD90+ cells supported the assembly of perfusa

139 These results conclusively link EpCAM expression to LC motility/migration and LC migrati

140 ted eDAR for recovery of cells that have low EpCAM expression and developed an immunofluorescence lab

141 of epithelial cells in the breast: luminal (EpCAM(+)) and basal/myoepithelial (CD10(+)).

142 1, CD14 and Gly-A) and the epithelial marker EpCAM.

143 ction strategies rely on cell surface marker EpCAM and intracellular cytokeratins (CKs) for isolation

144 ncreased the expression of stem cell markers EpCAM, Claudin7, and Oct4, as well as decreased E-cadher

145 -1, CD133, Dlk) and liver stem cell markers (EpCAM, CD14, CD24, CD49f); and negative for: hematopoiet

146 anuclearly, stem/progenitor surface markers (EpCAM, NCAM, CD133, CXCR4), and sometimes weakly adult l

147 te of matriptase and link HAI-2, matriptase, EpCAM, and claudin-7 in a functionally important pathway

148 ore, we hypothesized that HAI-2, matriptase, EpCAM, and claudin-7 were functionally linked.

149 e (EpCAM(+)) SHPC clusters showed membranous EpCAM(+)/HNF-4alpha(+) (hepatocyte nuclear factor-4alpha

150 d spiked-in cancer cells (taken from a model EpCAM(high) cell line) from blood at an efficiency of 95

151 cktail allowed us to reliably detect a model EpCAM(low) cell line for triple negative breast cancer,

152 e proinvasive cell surface adhesion molecule EpCAM.

153 ls in the epithelial cell adhesion molecule (EpCAM(+)) SHPC clusters showed membranous EpCAM(+)/HNF-4

154 ession of epithelial cell adhesion molecule (EpCAM(-)), which also shows the greatest in vitro invasi

155 lpha(neg) epithelial cell adhesion molecule (EpCAM(neg)) CD11b(+) langerin (Lang; CD207)(neg) DCs, bu

156 Epithelial cell adhesion molecule (EpCAM) (CD326) is a surface glycoprotein expressed by in

157 sed genes epithelial cell adhesion molecule (EpCAM) and pluripotency genes.

158 ainst the epithelial cell adhesion molecule (EpCAM) and the T-cell antigen CD3, is approved as intrap

159 ponses to Epithelial Cell Adhesion Molecule (EpCAM) antibody and other ligands coated on the sensor c

160 ated anti-epithelial cell adhesion molecule (EpCAM) antibody lead to complete tumour regression in mo

161 with anti-epithelial cell adhesion molecule (EpCAM) antibody.

162 ection of epithelial cell adhesion molecule (EpCAM) antigen, a common marker for tumors of epithelial

163 ession of epithelial cell adhesion molecule (EpCAM) has been implicated in advanced endometrial cance

164 e used an Epithelial Cell Adhesion Molecule (EpCAM) independent fluid biopsy based on cell morphology

165 The epithelial cell adhesion molecule (EpCAM) is closely correlated with the occurrence and dev

166 Epithelial cell adhesion molecule (EpCAM) is expressed at the basolateral membrane of most

167 Epithelial cell adhesion molecule (EpCAM) is highly expressed in epithelial-transformed neo

168 sitizers, epithelial cell adhesion molecule (EpCAM) on LCs promotes LC dendrite mobility and LC migra

169 s-linking epithelial cell adhesion molecule (EpCAM) on tumor cells with a cluster of differentiation

170 st either epithelial cell adhesion molecule (EpCAM) or epidermal growth factor receptor (EGFR) and th

171 eting epithelial cellular adhesion molecule (EpCAM) present on the MCF-7 cell membrane.

172 ing 4, an epithelial cell adhesion molecule (EpCAM) targeting MMC-immunoconjugate was prepared and du

173 s against epithelial-cell adhesion molecule (EpCAM) via magnetic-activated cell sorting (MACS).

174 enin, and epithelial cell adhesion molecule (EpCAM) were activated by HBx in vitro and in vivo.

175 CD86(lo), epithelial cell adhesion molecule (EpCAM)(hi), CD45(lo) bone marrow-derived peripheral anti

176 ession of epithelial cell adhesion molecule (EpCAM), a 40-kDa type I transmembrane protein found on e

177 , such as epithelial cell adhesion molecule (EpCAM), human epidermal growth factor receptor-2 (HER-2)

178 e marker, epithelial cell adhesion molecule (EpCAM), is also expressed in human fetal gonads and can

179 richrome, epithelial cell adhesion molecule (EpCAM), K19, CD34, glutamine synthetase (GS), and Ki-67.

180 ha, HNF6, Epithelial cell adhesion molecule (EpCAM), Leucine-rich repeated-containing G-protein coupl

181 ated that epithelial cell adhesion molecule (EpCAM), Prominin-1, and Keratin7 were significantly incr

182 n such as epithelial cell adhesion molecule (EpCAM), thereby recruiting T-cell activation to the tumo

183 ing these epithelial cell adhesion molecule (EpCAM)-expressing cells using antibody-coated microposts

184 generated epithelial cell adhesion molecule (EpCAM)-positive hepatocytes.

185 known as epithelial cell adhesion molecule (EpCAM).

186 including epithelial cell adhesion molecule (EpCAM).

187 levels of epithelial cell adhesion molecule (EpCAM; CD326), a cell-surface protein that is characteri

188 lial MPs (epithelial cell adhesion molecule [EpCAM](+)MPs, E-cadherin(+)MPs), platelet MPs (CD31(+)CD

189 em cells (epithelial cell adhesion molecule [EpCAM], neural cell adhesion molecule [NCAM], epithelial

190 pressing epithelial cell adhesion molecules (EpCAM) was achieved by functionalizing micropallet surfa

191 ere higher in young and old Foxn1Tg and more EpCAM+ MHC II(hi) TEC expressed Ki-67 in aged Foxn1Tg co

192 showing hepatocytic morphology appeared near EpCAM(+) ductular structures in the livers of mice fed 3

193 epithelial cell adhesion molecule-negative (EpCAM(-)) hepatocyte nuclear factor 4alpha-positive (HNF

194 epithelial cell adhesion molecule-negative (EpCAM-) breast cancer cells to an epithelial EpCAM+/high

195 ic method identifying HBEC as CD45 negative, EpCAM/pan-cytokeratin (pan-CK) double-positive populatio

196 cinoma (EACA) and 100% in metastasis, but no EpCAM overexpression was detected in undifferentiated EC

197 frequently in early-stage NSCLC using a non-EpCAM mediated approach with a wide range noted for a gi

198 and Prominin-1 (OR1.14, P = 0.002), but not EpCAM (OR1.16, P = 0.06), were identified as independent

199 Also, with the percentage of OCT4(+)/EpCAM(+) cells as readout, we demonstrated the synergist

200 Combining BMP4/WNT3A induction and OCT4/EpCAM selection can significantly increase the putative

201 y tested, for the first time, the ability of EpCAM aptamer SYL3C to detect EpCAM expression in 170 ca

202 s, we demonstrated that specific ablation of EpCAM resulted in increased ERK pathway activity and SNA

203 geneous and dynamic expression or absence of EpCAM and/or CKs in CTCs.

204 The absence of EpCAM in normal lymphatics makes it an attractive marker

205 were dramatically reduced in the absence of EpCAM, conditional knockout mice with EpCAM-deficient LC

206 d in increased (33%; P<0.05) accumulation of EpCAM(+) DCs.

207 munoprecipitation documented associations of EpCAM with claudin-7 and claudin-1 but not claudin-2 or

208 embly that allows highly specific capture of EpCAM (epithelial cell adhesion molecule) positive CTCs

209 of protein A/G enabled efficient capture of EpCAM antibody on the micropallet surface.

210 Cleavage of EpCAM decreased its ability to associate with claudin-7

211 nsduction triggered cell-surface cleavage of EpCAM, leading to nuclear internalization of its cytopla

212 atriptase activity and efficient cleavage of EpCAM.

213 solation techniques rely on the detection of EpCAM to discriminate CTCs from other cells in the blood

214 n, EpCAM, especially intracellular domain of EpCAM (EpICD), bound to and activated the promoter of re

215 Thus, genome editing of EpCAM could be associated with altering these nanomechan

216 Elevation of EpCAM enhanced tumorsphere formation and tumor initiatio

217 The enumeration of EpCAM-positive circulating tumor cells (CTCs) has allowe

218 , which correlated with direct expression of EpCAM by DC.

219 n and invasion, whereas forced expression of EpCAM resulted in decreased ERK pathway activity and SNA

220 inversely correlated with the expression of EpCAM.

221 onstrated by the simultaneous immunoassay of EpCAM and GPC3 antigens on the surface of the human live

222 behavior, consistent with the inhibition of EpCAM and Snail expression.

223 Knockdown of EpCAM in T84 and Caco-2 cells using shRNAs led to change

224 Knockdown of EpCAM inhibited the expressions of reprogramming factors

225 8) cancer cells expressing various levels of EpCAM and EGFR.

226 nes that express both high and low levels of EpCAM.

227 tumors shed CTCs that express high levels of EpCAM; others release cells that have a low level of the

228 Migration of EpCAM-deficient LC from skin explants was inhibited, but

229 Attenuated migration of EpCAM-deficient LC resulted in enhanced contact hypersen

230 ted protein 1 (Dkk1) decreased the number of EpCAM(+) DCs (21%; P<0.05).

231 Total numbers of EpCAM+ MHC II+ and MHC II(hi) thymic epithelial cells we

232 phogenesis and apical expression patterns of EpCAM, a hepatic stem/progenitor cell marker highly expr

233 tion of cells bears the surface phenotype of EpCAM+CD24+CD44+CD133-SCA1- and is closer in its propert

234 ients without malignancy for the presence of EpCAM(+) single cells.

235 Herein we show that in the presence of EpCAM-positive tumor targets, CatmAb markedly enhanced T

236 de important insights into the regulation of EpCAM expression during EMT, demonstrate an unexpected r

237 The capture and release of EpCAM expressing cancer cells using this approach was fo

238 In our studies on the role of EpCAM in cancer biology, we observed that EpCAM expressi

239 Here we report that transformation of EpCAM(+) epithelial cells results in the formation of co

240 (e.g., epithelial cell adhesion molecule or EpCAM) or size to separate them from blood cell populati

241 lecule-positive (EpCAM(+)) cells and overall EpCAM expression.

242 Overexpressed EpCAM was detected in severe dysplasia, but negative in

243 el population of lineage(neg/low), CD45(pos) EpCAM(pos), SCA1(pos), CD117(neg), CD138(neg), MHCII(neg

244 epithelial cell adhesion molecule-positive (EpCAM(+)) cells and overall EpCAM expression.

245 d by the finding that CD44+/CD24- and PROCR+/EpCAM- multi-potent stem cells were elevated significant

246 dividual knockdown was sufficient to promote EpCAM and E-cadherin expression.

247 in expression of the cell surface proteins, EpCAM/CD326 and NCAM/CD56.

248 Recently, EpCAM (CD326) has been identified as a cell surface prot

249 gical inhibition of the ERK pathway restored EpCAM expression.

250 We demonstrate the ability to select EpCAM positive CTCs from PDAC patients in high purity (>

251 n of SPRi with flow cytometry showed similar EpCAM expression on MCF7, SKBR3 and HS578T cells.

252 Sox9(+)EpCAM(-) cells proliferated and could differentiate to f

253 In addition, Sox9(+)EpCAM(-) cells formed cysts with a small central lumen i

254 Although Sox9(+)EpCAM(-) cells adjacent to expanding ducts likely furthe

255 nverting to cholangiocyte-like cells, Sox9(+)EpCAM(-) cells provide luminal space near expanded ductu

256 know the cellular characteristics of Sox9(+)EpCAM(-) cells, we isolated them as GFP(+)EpCAM(-) cells

257 These results suggest that Sox9(+)EpCAM(-) cells maintaining biphenotypic status can estab

258 the ability of contact allergen-stimulated, EpCAM-deficient LC to exit epidermis in vivo was delayed

259 oncogene-induced ERK2 activation suppressed EpCAM expression, whereas genetic or pharmacological inh

260 ter region, we observed that ERK2 suppresses EpCAM transcription directly by binding to a consensus E

261 Surprisingly, EpCAM appears to modulate ERK activity.

262 pregulation of miR-181, both of which target EpCAM.

263 nofluorescence-based technology that targets EpCAM to rank aliquots of blood for the presence or abse

264 d on these results, it can be concluded that EpCAM is suitable for use as an EC biomarker, therapeuti

265 l-surface adhesion, here we demonstrate that EpCAM is a regulatory molecule in which its internalizat

266 Furthermore, we demonstrate that EpCAM(+) HCC cells cultured as spheroids are more sensit

267 rative immunoprecipitation demonstrated that EpCAM bound tightly to claudin-7.

268 We demonstrated via FACS that EpCAM is expressed by human spermatogonia but not MOLT-4

269 tome analysis of single cells and found that EpCAM(+) cells from controls expressed transcripts thoug

270 of EpCAM in cancer biology, we observed that EpCAM expression is decreased in mesenchymal-like primar

271 We observed that EpCAM expression is decreased with activation of the ERK

272 Herein, we report that EpCAM regulates the composition and function of tight ju

273 or-initiated cells (TICs), but the role that EpCAM plays in the stemness properties of TICs is still

274 Here we show that EpCAM and reprogramming factors (c-Myc, Oct4, Nanog, and

275 These findings suggest that EpCAM modulates adhesion and TJ function by regulating i

276 Together, these findings suggest that EpCAM plays an important role in regulating cancer-initi

277 The EpCAM+/HLA-ABC-/CD49e- fraction was enriched for spermat

278 The EpCAM-/HLA-ABC+/CD49e+ fraction produced tumors followin

279 on into the human genome specifically at the EpCAM, CXCR4 and TFRC gene promoters.

280 ons with proteins and a layer containing the EpCAM antibodies.

281 ding to a consensus ERK2-binding site in the EpCAM promoter and indirectly through activation of EMT-

282 1 and ZEB1, which bind to E-box sites in the EpCAM promoter.

283 the cells, matching with the location of the EpCAM marker.

284 In detailed studies of the EpCAM promoter region, we observed that ERK2 suppresses

285 d by changes in histone modifications of the EpCAM promoter, a target of PRC2 and LSD1/Co-REST/HDAC1

286 rm (>passage 20) and clonal expansion of the EpCAM(+) CD49f(hi) cells in vitro.

287 ecificity for nonoverlapping epitopes on the EpCAM extracellular domain were chosen for further evalu

288 nriched in colony-forming cells, compared to EpCAM(+) CD49f(lo) cells.

289 Using EpCAM targeted MBs CTCs from metastatic cancer patients

290 umulated at the tumor cell surface in viable EpCAM-expressing tumor tissue.

291 Tumor uptake of (89)Zr-AMG 110 was EpCAM-specific and correlated with EpCAM expression.

292 s required for association of claudin-1 with EpCAM.

293 G 110 was EpCAM-specific and correlated with EpCAM expression.

294 we generated conditional knockout mice with EpCAM-deficient LC and characterized them.

295 nce of EpCAM, conditional knockout mice with EpCAM-deficient LCs and control LC dendrites docked with

296 munization of conditional knockout mice with EpCAM-deficient LCs with ovalbumin led to increased indu

297 s, we studied conditional knockout mice with EpCAM-deficient LCs.

298 was extensively evaluated and optimized with EpCAM-positive HCT116 cells seeded into whole blood.

299 atment of malignant ascites in patients with EpCAM-positive carcinomas.

300 that of antibody, but the binding sites with EpCAM were different.