ライフサイエンスコーパス: cytokeratin

1 mors were positive for the epithelial marker cytokeratin.

2 hrough p38 MAPK-dependent phosphorylation of cytokeratin.

3 e ultra-staged with immunohistochemistry for cytokeratin.

4 in, epithelial membrane antigen, and various cytokeratins.

5 n (EMA), Ber-EP4, AE1, AE3, and 8 individual cytokeratins.

6 nd increased phosphorylation of p38 MAPK and cytokeratins.

7 e expression of E-cadherin, desmoplakin, and cytokeratins.

8 ct cell types that express basal and luminal cytokeratins.

9 stromal Bmp4, epithelial Sox9, and columnar cytokeratins.

10 nue expression of Thy-1 and begin to express cytokeratins.

11 ted by p38 MAPK-dependent phosphorylation of cytokeratins.

12 s a bifunctional protein that binds to human cytokeratin 10 (K10) and fibrinogen (Fg).

13 Cytokeratin 10 (K10) and loricrin expression were then e

14 Cytokeratin 10, involucrin, loricrin, and filaggrin prot

15 ression of key structural proteins including cytokeratin-10 and loricrin, resulting in increased kera

16 corneal epithelial cells and the absence of cytokeratin 12 (K12) expression featured Cited2 deficien

17 l surface (conjunctivalized corneal surface: cytokeratin 12 [cK12]-negative and mucin 1 [MUC1]-positi

18 cal microscopy and impression cytology (PAS, cytokeratin 12, and cytokeratin 19) staining were perfor

19 els of mature cornea epithelial cell marker, cytokeratin 12.

20 d of stem cells, which were characterized by cytokeratin 14 (CK14) staining and enhanced tumor sphere

21 Cytokeratin 14 (CK14) was examined by immunohistochemist

22 binase (CreER(tam)) under the control of the cytokeratin 14 (K14) promoter (K14-CreER(tam)) and mice

23 IHC confirmed increased cytokeratin 14 expression in female bladders and additio

24 dings and revealed a significant increase in cytokeratin 14 expression in the urothelium of the femal

25 tionship between loss of FOXA1 and increased cytokeratin 14 expression.

26 20(OH)D3 stimulated involucrin and inhibited cytokeratin 14 expression.

27 Co-localization studies with cytokeratin 14 indicated that KCNQ1 is also expressed in

28 umor cells expressing markers of basal (p63, cytokeratin 14) and luminal (cytokeratin 8 and androgen

29 owed thinning of skin epithelium and loss of cytokeratin 14, an early marker of skin differentiation.

30 uently stained for pimonidazole, sirius red, cytokeratin 14, and hematoxylin-eosin for quantitative a

31 microtubules in mesenchymal cells increased cytokeratin 14-positive (K14+) progenitors and their dif

32 ders and additionally revealed enrichment of cytokeratin 14-positive basal cells in the hyperplastic

33 xpression of basal epithelial genes, such as cytokeratin-14 (K14) and p63.

34 We show that formation of the actin/cytokeratin/14-3-3sigma complex and cellular migration a

35 fiber (OF) immunosensor for the detection of cytokeratin 17 (CK17), a biomarker of interest for lung

36 AIRE with the intermediate filament protein cytokeratin 17 (K17) in the THP-1 monocyte cell line.

37 We have recently demonstrated that plasma cytokeratin 18 (CK-18) fragment levels correlate with th

38 necrosis in serum was quantified using serum cytokeratin 18 (CK18) M30 and M65 enzyme-linked immunoso

39 -122), glutamate dehydrogenase (GLDH), total cytokeratin 18 (K18), caspase cleaved K18, glutathione S

40 Serum cleaved cytokeratin 18 and caspase-3/7 decreased significantly.

41 ormal unperturbed RPE are immunoreactive for cytokeratin 18 and negative for cytokeratin 19, vimentin

42 ated with increased apoptosis (caspase 3 and cytokeratin 18 cleavage) in excised tumors.

43 of lactate dehydrogenase and caspase-cleaved cytokeratin 18 in the perfused medium.

44 zyme-linked immunosorbent assays for various cytokeratin 18 products (eg, M65, cell death, M30, and a

45 sin-converting enzyme 2 (hACE2) by the human cytokeratin 18 promoter (K18 hACE2) represent a suscepti

46 Notably, mice expressing hDPP4 with the cytokeratin 18 promoter developed progressive, uniformly

47 trol of the surfactant protein C promoter or cytokeratin 18 promoter that are susceptible to infectio

48 Elevated total cytokeratin 18 suggested the presence of necrotic cell d

49 , hepatocyte nuclear factor 4alpha, albumin, cytokeratin 18, and cytochrome P450 3A.

50 epithelial phenotype, expressing E-cadherin, cytokeratin 18, and desmin.

51 rum transaminases were normal in TASH, total cytokeratin 18, but not the caspase-cleaved fragment, wa

52 rly reactive RPE (7 days in culture) express cytokeratin 18, cytokeratin 19, and vimentin.

53 markers of colonic epithelial cells such as cytokeratin 18, zonula occludens-1, mucins-1 and -2, ant

54 strogen, and progesterone receptor-positive, cytokeratin 18-positive (ER(+)PR(+)CK18(+)) subtype, and

55 claudin 3, 4, and 7 and the luminal marker, cytokeratin 18.

56 ation of fibrosis-associated markers such as cytokeratins 18 and 19 and annexin 2, as determined both

57 say (ELISA), which detects a caspase-cleaved cytokeratin-18 (CK-18) fragment and thereby apoptotic ce

58 helial cell markers pan-cytokeratin (Pan-K), cytokeratin-18 (K-18), and occludin.

59 rting enzyme 2 (ACE2) receptor driven by the cytokeratin-18 (K18) gene promoter (K18-hACE2) as a mode

60 Total and caspase-cleaved cytokeratin-18 (M65 and M30) measured at admission and s

61 mined by alanine aminotransaminase [ALT] and cytokeratin-18 [CK-18]).

62 ch as increased expression of E-Cadherin and cytokeratin-18 and decreased expression of Snail.

63 2-derived peptide, alanine aminotransferase, Cytokeratin-18 and homeostasis model of insulin resistan

64 Colonies of cytokeratin-18 and human albumin-expressing cells were p

65 Levels of M30, a cleavage product of cytokeratin-18 caspase, are significantly increased in s

66 itative Insulin-Sensitivity Check Index, and cytokeratin-18 correlated with NASH.

67 lesterol and adiponectin concentrations, and cytokeratin-18 fragment elevation.

68 rum levels of M30 and M65 antigen (the total cytokeratin-18 fragment, a marker of apoptosis and necro

69 3 +/- 1.5 vs. 1.7 +/- 1.4; P = 0.004), serum cytokeratin-18 fragments (283 vs. 404 U/L; P < 0.001) an

70 Plasma levels of cytokeratin-18 fragments are reliable noninvasive marker

71 labeling-positive nuclei and accumulation of cytokeratin-18 fragments in the liver, was independent o

72 cytokines, markers of hepatocyte apoptosis (cytokeratin-18 fragments), and hepatic fibrogenesis (hya

73 ed low-density lipoproteins, adipokines, and cytokeratin-18 fragments, and an oral glucose tolerance

74 Cytokeratin-18 fragments, controlled attenuation paramet

75 ment of plasma lipoproteins, adipokines, and cytokeratin-18 fragments.

76 ment of plasma lipoproteins, adipokines, and cytokeratin-18 fragments.

77 ling-positive cells, caspase-3 activity, and cytokeratin-18 staining in the liver.

78 cirrhosis contained hepatocyte-derived MPs (cytokeratin-18(+)), whereas plasma from controls did not

79 tested M65 and M30 (circulating fragments of cytokeratin-18) and their respective fraction carried by

80 caspase-dependent apoptosis (caspase-cleaved cytokeratin-18) compared to control; caspase-dependent a

81 ll as the epithelial markers pancytokeratin, cytokeratin-18, and occludin, but not mesenchymal (CD44,

82 umin, alpha-fetoprotein, cytochrome P4502E1, cytokeratin-18, type-1 collagen, transforming growth fac

83 of persistent nodules and all HCCs expressed cytokeratin 19 (CK19), whereas 14% of remodeling nodules

84 roteins used clinically for staging disease (cytokeratin 19 [CK19]), identifying cancer stem cells (e

85 and expressed the biliary epithelial markers cytokeratin 19 and carbonic anhydrase IV.

86 n were evaluated by immunohistochemistry for cytokeratin 19 and Ki-67.

87 mine the threshold levels of mammaglobin and cytokeratin 19 correlating with metastasis greater than

88 001) and with the progenitor subtype of HCC (cytokeratin 19 expression, P = 0.031).

89 uamous cell carcinoma antigen (P = .03), and cytokeratin 19 fragment antigen 21-1 (P = .01) were mark

90 Baseline plasma carcinoembryonic antigen/cytokeratin 19 fragments biomarker signature was associa

91 els of epithelial cell adhesion molecule and cytokeratin 19 gene messenger RNAs.

92 2 and hepatic nuclear factor-4alpha, but not cytokeratin 19 or carbonic anhydrase IV.

93 f sex determining region Y-box (SOX)9(+) and cytokeratin 19(+) cells but fewer features of hepatocyte

94 mpression cytology (PAS, cytokeratin 12, and cytokeratin 19) staining were performed in the central c

95 (Col1A1), matrix metalloproteinase 2 (Mmp2), cytokeratin 19, alpha-smooth muscle actin (alpha-SMA), c

96 (7 days in culture) express cytokeratin 18, cytokeratin 19, and vimentin.

97 sociated with cholangiocyte differentiation (cytokeratin 19, connexin 43, integrin beta4, and gamma-g

98 arkers including gamma glutamyl transferase, cytokeratin 19, epithelial cellular adhesion molecule, c

99 tures and immunohistochemical markers (PD-1, cytokeratin 19, glutamine synthetase, and beta-catenin e

100 reactive for cytokeratin 18 and negative for cytokeratin 19, vimentin, and alpha-smooth muscle actin

101 ibroblastic RPE (35 days in culture) express cytokeratin 19, vimentin, and alphaSMA.

102 Cytokeratin 19-, A6- and alpha-fetoprotein-positive cell

103 d contain actin filaments, microtubules, and cytokeratin 19-based intermediate filaments.

104 hat increased LC3B was located mainly in the cytokeratin 19-labeled ductular reaction (DR) in human c

105 Cytokeratin 19-positive cells are detected surrounding t

106 the normal acinar compartment, and increased cytokeratin 19-positive metaplasias and immune cell infi

107 naling occupying an alpha-fetoprotein (AFP)+/cytokeratin-19 (CK-19)-positive progenitor cell niche fo

108 (DCAMKL-1), Lgr5, CD133, alpha-fetoprotein, cytokeratin-19 (CK19), Lin28, and c-Myc.

109 ted KO mice demonstrated significantly fewer cytokeratin-19 (CK19)-positive ductular reactions (P = 0

110 ons positive for the progenitor cell marker, cytokeratin-19 (Krt-19) and characterized by a higher pr

111 Intrahepatic biliary mass was detected by cytokeratin-19 and F4/80 to evaluate inflammation.

112 IBDM was detected by cytokeratin-19 expression and proliferation by Ki-67 imm

113 We determined whether cytokeratin-19 positive (K19(+)) cholangiocytes give ris

114 Rat ED14 FLSPC are alpha-fetoprotein(+)/cytokeratin-19(+) or alpha-fetoprotein(+)/cytokeratin-19

115 +)/cytokeratin-19(+) or alpha-fetoprotein(+)/cytokeratin-19(-) and contain all of the normal liver re

116 epithelial marker E-CADHERIN, biliary marker CYTOKERATIN-19, and mesenchymal markers VIMENTIN and alp

117 positive for the stem/progenitor cell marker cytokeratin-19, indicating that several HCC-associated a

118 In vivo, the DDC-stimulated number of cytokeratin-19-positive cells in the liver of wild-type

119 e NRF2 pathway accompanied the regression of cytokeratin-19-positive nodules, suggesting that activat

120 igen, epithelial cell adhesion molecule, and cytokeratin-19.

121 f MCC was confirmed by staining positive for cytokeratin 20 (CK20) and synaptophysin.

122 Needle biopsy revealed a cytokeratin 20-positive, high-grade neuroendocrine neopl

123 al cytoplasmic stain than the gold standard, cytokeratin 20.

124 owed a higher proliferation rate and greater cytokeratin 3(CK3) expression, indicating that this newl

125 nitiating marker CD44, the progenitor marker cytokeratin 5 (CK5) and are more resistant to standard e

126 n of de-differentiated cell markers CD44 and cytokeratin 5 (CK5), lose luminal markers ER and PR, and

127 ve breast cancers contain a subpopulation of cytokeratin 5 (CK5)-expressing cells that are therapy re

128 at express the intermediate filament protein cytokeratin 5 (CK5).

129 have discovered that a previously described cytokeratin 5 (K5)-Cre gene construct is expressed in ea

130 al cell markers, including tumor protein 63, cytokeratin 5 (KRT5), KRT6A, and KRT14.

131 tch signalling to activate the DeltaNp63 and cytokeratin 5 program, and subsequent Notch blockade pro

132 ivate a DeltaNp63 (a p63 splice variant) and cytokeratin 5 remodelling program after influenza or ble

133 ontain increased numbers of p63/AR-positive, cytokeratin 5-negative basal cells compared with WT or A

134 s, although none expressed the basal marker, cytokeratin 5.

135 ptor and ERBB2 expression, and expression of cytokeratin 5.

136 uclear hormone receptor and HER2 negativity, cytokeratin 5/6 and vimentin expression, and stem cell e

137 n epidermal growth factor receptor 2 (HER2), cytokeratin 5/6, epidermal growth factor receptor, and K

138 n of basal cells expressing Trp-63 (p63) and cytokeratins 5 (Krt5) and Krt14.

139 ed phenotype (basal v nonbasal, according to cytokeratins 5/6 and/or epidermal growth factor receptor

140 uminal breast cancer, progesterone induces a cytokeratin-5 (CK5)-positive basal cell-like population.

141 a-negative cancer cells expressing the basal cytokeratin-5 (CK5).

142 Runx1, Runx3, and cytokeratin-5 expression increased significantly in rege

143 e putative epithelial progenitor cell marker cytokeratin-5.

144 They ultimately differentiate into the cytokeratin 6-positive (K6) inner bulge cells in telogen

145 Knockdown of cytokeratin 6A markedly reduced the bactericidal activit

146 rich C-terminal fragments derived from human cytokeratin 6A were identified in bactericidal lysate fr

147 the unexpected role of a structural protein, cytokeratin 6A, in this process.

148 Two cytokeratin 7 (CK7) samples with a molecular weight rang

149 cystic disease fluid protein-15 (GCDFP-15), cytokeratin 7 (CK7), and smooth muscle actin (SMA).

150 xpressed markers of cholangiocytes including cytokeratin 7 and osteopontin, and the transcription fac

151 glands, apoptotic expression decreased while cytokeratin 7 remained positive.

152 8.18, proximal tubular CD10, distal tubular cytokeratin 7, and endothelial von Willebrand factor mar

153 7 eyes were stained with hematoxylin-eosin, cytokeratin 7, cytokeratin AE1/3, smooth muscle actin, v

154 Cytokeratin 7, EMA, and CD68 were found to be useful imm

155 D68, A-kinase anchoring protein 12 (AKAP12), cytokeratin 7, epithelial cell adhesion molecule (EPCAM)

156 all biopsy samples were stained positive for Cytokeratin 7, SOX2, Nestin, Vimentin, and CD44.

157 The transcriptome analysis of cytokeratin 7-positive (KRT7(+) ) DR cells uncovered int

158 ytes, based on the expression of albumin and cytokeratin 7.

159 plement 4d (C4d) and for biliary damage with cytokeratin 7.

160 colocalization of a predictive lumen marker, cytokeratin 7.

161 A classic cytokeratin 7/20 staining pattern was present in 23 case

162 in and eosin and by immunohistochemistry for cytokeratins 7 and 20, and Chromogranin A-proteins which

163 ssed intracellular and cell-surface proteins cytokeratin-7 (CK7) and fibroblast growth factor recepto

164 The DR was evaluated by cytokeratin-7 immunohistochemistry in liver biopsies, st

165 th a significant reduction in tumor size, in cytokeratin-7+ cells and by an anti-angiogenic effect.

166 ellate cell activation were assessed by anti-cytokeratin-7, anti-glutamine synthetase (GS), anti-cyto

167 tion of the secreted plasminogen activators (cytokeratin 8 and alpha-enolase).

168 of basal (p63, cytokeratin 14) and luminal (cytokeratin 8 and androgen receptor) epithelial cells, a

169 artially rescued Twist1-silenced ERalpha and cytokeratin 8 expression and reduced Twist1-induced inte

170 IL-8 by targeting its 3' UTR, and inhibited cytokeratin 8 via the cell cycle control protein cyclin

171 ased placental glutathione S-transferase and cytokeratin 8-18 activity; starting at 12 wk).

172 pithelial regeneration propose that distinct cytokeratin 8-expressing progenitor cells, arising from

173 In contrast, the cytokeratin 8-positive mammary cell population with prog

174 and by the specific expression of epithelial cytokeratin 8.18, proximal tubular CD10, distal tubular

175 d found to be CD45 negative and positive for cytokeratins 8, 18, and/or 19 and 4',6-diamidino-2-pheny

176 adhesions and a reduction in E-cadherin and cytokeratins 8/18 and 19.

177 Expression of epithelial markers including cytokeratin-8, E-cadherin, and prosurfactant protein B d

178 ained with hematoxylin-eosin, cytokeratin 7, cytokeratin AE1/3, smooth muscle actin, vimentin, and CD

179 l carcinomas positive for alpha-fetoprotein, cytokeratin AE1/AE3, and CD30.

180 istochemical analysis revealed expression of cytokeratin AE1/AE3, CD31, ERG, and FLI-1, with focal an

181 for OM using immunohistochemistry (IHC) for cytokeratin (AE1/AE3) and real-time reverse transcriptas

182 rapid growth, with the expression of biliary cytokeratins, alpha-fetoprotein, and c-Met by FIHC.

183 Coexpression of cytokeratin and human chromosome was observed at 7 and,

184 ochemical staining for tumor markers and for cytokeratin and mucin proteins were used to classify IPN

185 inal, and six oncocytic subtypes; results of cytokeratin and mucin staining were similar to those of

186 large cuboidal cells that were positive for cytokeratin and other markers characteristic of invasive

187 ibodies paired with immunohistochemistry for cytokeratin and surfactant identified pneumocytes and ep

188 nt proteins, we examined the contribution of cytokeratin and vimentin filaments to tumor cell microte

189 notype characterized by immunoreactivity for cytokeratins and endothelial markers.

190 emistry for human-specific breast epithelial cytokeratins and human-specific milk proteins in impregn

191 tive for DeltaNp63 and high molecular weight cytokeratins and negative for low molecular weight cytok

192 tive for DeltaNp63 and high molecular weight cytokeratins and positive for low molecular weight cytok

193 ally, in both cases, lesions had epithelial (cytokeratin(+)) and stromal (vimentin/CD10(+)) cell comp

194 children were immunostained for epithelial (cytokeratin) and mesenchymal (vimentin) EMT biomarkers,

195 ction (RET), Dolichos biflorus lectin, EndoA cytokeratin, and aquaporin 2.

196 and partial retention of RPE markers (MITF, cytokeratin, and CRALBP).

197 re likely to induce the expression of simple cytokeratins as has been shown for SV40 in other nonepit

198 of ERK1/2 similarly decreases the basal-like cytokeratins as well as migration.

199 cells were detected by an immunocytochemical cytokeratin assay in preoperatively taken bone marrow as

200 Combined, these data reveal a GABRP-ERK1/2-cytokeratin axis that maintains the migratory phenotype

201 nts (78%) had epithelial CTCs that expressed cytokeratin but not CD45.

202 An intermediate filament cytokeratin "cage" was not observed around KD ICI, makin

203 pericytic cells was lower in the presence of cytokeratin(+) cells in bone marrow.

204 Similar to the presence of cytokeratin(+) cells in the bone marrow, this MSC subpop

205 using basic histology and immunostaining for cytokeratin (CK) 10 and CK13.

206 tive" cancers lack steroid receptors but are cytokeratin (CK) 5-positive and require chemotherapy.

207 tissue-and differentiation-specific markers, cytokeratin (CK) 5/6, 13, and 14, to detect presence or

208 LT levels, AST levels, and caspase-3-cleaved cytokeratin (CK)-18 fragments at week 4 were assessed by

209 ession of epithelial markers (E-cadherin and cytokeratin (CK)-18) and an increased expression of mese

210 pindle-like morphology and expressing CD133, cytokeratin (CK)7, CK19, procollagen-alpha1(I), and Snai

211 tiation markers such as involucrin (IVL) and cytokeratin CK13 in a CSL-dependent fashion.

212 identify by immunohistochemical staining for cytokeratin CK5/6 or CK14 the basal-like subgroup in a s

213 oid cells of MECs were strongly positive for cytokeratin CK5/6, CK34betaE12, and P63; whereas negativ

214 cell surface marker EpCAM and intracellular cytokeratins (CKs) for isolation and identification, res

215 These cells stained positive for cytokeratin, confirming their epithelial origin, and als

216 cular endothelial-cadherin (VE-cadherin) and cytokeratins consistent with vasculogenic mimicry (VM),

217 xpress uroplakin II and low molecular weight cytokeratins, consistent with an umbrella cell phenotype

218 ar-weight cytokeratin, high-molecular-weight cytokeratin, cyclo-oxygenase-2, EMA, HER2, matrix metall

219 The absence of major cytokeratin derangements in the squamous papillomas may

220 h as beta-defensins, the cathelicidin LL-37, cytokeratin-derived antimicrobial peptides, and RNase7.

221 ments coaligned with microtentacles, whereas cytokeratin did not.

222 nhanced expression of E-cadherin, epithelial cytokeratins (e.g., CK-19), and tight junction proteins

223 specimens were characterized for epithelial (cytokeratins, E-cadherin) and mesenchymal (vimentin, N-c

224 on marker), anti-CD68 (macrophage), and anti-cytokeratin (epithelial marker).

225 recurrence, those with vimentin-positive and cytokeratin-expressing CTCs had decreased median time to

226 d extension correlated strongly with loss of cytokeratin expression and up-regulation of vimentin, as

227 growth and expansion as determined by human cytokeratin expression.

228 l peptide that redirects keratin 10 from the cytokeratin filament network to the nucleolus.

229 e disruption of actin, tubulin, vimentin, or cytokeratin filaments, suggesting that membrane fusion w

230 omarkers, hepatocyte growth factor (HGF) and cytokeratin fragment 18, in 954 hematopoietic cell trans

231 D from non-GVHD diarrhea better than HGF and cytokeratin fragment 18.

232 f tumor markers (neuron-specific enolase and cytokeratin fragment 21-1).

233 ubstrate and used for immobilization of anti-cytokeratin fragment-21-1 (anti-Cyfra-21-1) for the elec

234 These data suggest that epithelial cytokeratins function as endogenous antimicrobial peptid

235 Here we report that epithelial cytokeratins have innate defense properties because they

236 L2, caspase-9, CD34MVD, low-molecular-weight cytokeratin, high-molecular-weight cytokeratin, cyclo-ox

237 subjected to immunofluorescence for ICI and cytokeratin, high-throughput sequencing, and transmissio

238 sitive for CD34 and HHF-35, but negative for cytokeratin, HMB-45 and Melan-A.

239 entiation (E-cadherin, high molecular weight cytokeratins (Hmw CK) and CK5, vimentin) and lineage dif

240 ibody cocktail against high-molecular weight cytokeratin (HMWCK), p63, and alpha-methylacyl CoA racem

241 d an image-based computational method on pan-cytokeratin IHC stainings to quantify tumor fragmentatio

242 LNs (N0) were examined for OM, diagnosed by cytokeratin immunohistochemistry (IHC).

243 and eosin (H&E) negative LNs (N0) using pan-cytokeratin immunohistochemistry (pan-CK-IHC) is unknown

244 pN0 LNs were collected and assessed by using cytokeratin immunostaining in two serial histology secti

245 34, FAP (fibroblast activation protein), and cytokeratin in 220 tissue cores from 26 high-grade serou

246 taining showed similar staining patterns for cytokeratins in large cell acanthoma and normal conjunct

247 e immunohistochemical analysis of a range of cytokeratins in normal conjunctival epithelium, normal c

248 Ig-bound proteins yielding a predominance of cytokeratins, including several associated with a mesenc

249 d Eomes, and also the trophectoderm-specific cytokeratin intermediate filament, recognised by Troma1,

250 Positive staining for either cytokeratin is very significantly associated with that f

251 dentified with intracellular markers such as cytokeratins, is linked to resistance to specific target

252 Here, in analyzing the expression of basal cytokeratin (K) 14 in the secretory complex, we discover

253 ative LSC markers ABCG2, DeltaNp63alpha, and cytokeratin (K)14 were significantly higher in the SSEA4

254 d that, although ductal stem cells marked by cytokeratin K14 and Axin2 undergo a multipotency switch,

255 a novel transgenic (Tg) mouse model, using a cytokeratin K14 promoter to drive expression of the E6 a

256 MAML1 was targeted to the mouse esophagus by cytokeratin K14 promoter-driven Cre (K14Cre) recombinati

257 mmunostained to identify key biomarkers (pan-cytokeratin, Ki67, CD3).

258 on ( approximately 50%) stained for both pan-cytokeratin (KRT) markers and the common leukocyte marke

259 usions and expression of the BLBC-associated cytokeratins, KRT5, KRT6B, KRT14, and KRT17.

260 These results show that the basal cytokeratin-like carcinomas contain many of the MIPs and

261 mmunohistochemical stains, including AE1/AE3 cytokeratin, Lin28A, and CD45, were performed.

262 of a combination of cell surface receptors, cytokeratin markers, drug transporters and the efficient

263 ssociated vesicles are enmeshed in an apical cytokeratin meshwork and that Rab11a likely acts upstrea

264 determined by immunocytochemistry using pan-cytokeratin monoclonal antibodies.

265 No patients had cytokeratin-negative and vimentin-positive CTCs.

266 omeric probe showed that positive cells were cytokeratin-negative at 24 hours.

267 uster differentiation-44 (CD44)-positive but cytokeratin-negative, unlike the case in other regenerat

268 Our optrode targets a type of cytokeratins, overexpressed at the surface of cancer cel

269 identifying HBEC as CD45 negative, EpCAM/pan-cytokeratin (pan-CK) double-positive population after ex

270 (Ccsp), and the epithelial cell markers pan-cytokeratin (Pan-K), cytokeratin-18 (K-18), and occludin

271 ng distribution of the tumor cell marker pan-cytokeratin (panCK).

272 The papillomas displayed a normal cytokeratin pattern but exhibited a higher than normal P

273 ratins and positive for low molecular weight cytokeratins) phenotypes, with DeltaNp63 expression asso

274 r phagocytes in human gastric mucosa contain cytokeratin-positive and TUNEL-positive AEC material, in

275 aining and the loss of high molecular weight cytokeratin-positive basal epithelial cells.

276 The presence of cytokeratin-positive CTCs (P < 0.01), but not mesenchyma

277 The presence of cytokeratin-positive CTCs remained a significant indepen

278 In the TI, alpha8 integrin was localized to cytokeratin-positive epithelial cells and to interstitia

279 nchymal markers, including vimentin (VIM) in cytokeratin-positive epithelial cells metalloproteinase

280 factor Twist1 induced rapid dissemination of cytokeratin-positive epithelial cells.

281 2 to vimentin-positive decidual cells versus cytokeratin-positive interstitial trophoblasts.

282 PVR membranes and partially colocalized with cytokeratin-positive RPE cells.

283 against networks involving BRCA1, TP53, and cytokeratin proteins associated with a mesenchymal/basal

284 itial trophoblast (IT) markers, vimentin and cytokeratin, respectively.

285 f immunostaining markers (DAPI, amylase, and cytokeratins; Spearman correlation score = 0.86, 0.97, a

286 e PAX8 staining was superior to the variable cytokeratin staining in the ciliary epithelial neoplasms

287 ing EGFP from the Ret locus, and whole-mount cytokeratin staining.

288 cinoma, where lineage tracing indicates that Cytokeratin-Synaptophysin dual positive cells arise from

289 Higher percentages of Cytokeratin-Synaptophysin dual positive tumor cells corr

290 and express pRb, the epithelial cell marker cytokeratin that is expressed in the retinal pigmented e

291 fluorescence-labeled antibodies against pan-cytokeratin through flow cytometry.

292 ing a multiplexed assay for ALDH1, CD44, and cytokeratin to measure the coexpression of these protein

293 ns and structures, including those involving cytokeratins, topoisomerase-2-alpha, and post-translatio

294 ratins and negative for low molecular weight cytokeratins) versus luminal-like (negative for DeltaNp6

295 e using commercially available antibodies to cytokeratin, vimentin, and CD45.

296 tection of CTCs expressing both vimentin and cytokeratin was predictive of recurrence (P = 0.01).

297 Fibronectin and cytokeratin were accumulated along the stroma-to-stroma

298 taining and immunohistochemical staining for cytokeratin were used at two widely spaced additional ti

299 tion markers prosurfactant protein-C and pan-cytokeratins were passed to the opposing daughter cell,

300 (P = .20), the mean proliferation index with cytokeratin wide-spectrum was 2.55 vs 1.13 (P = .06), an