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1 1, cyclin G1, alpha smooth muscle actin, and cytokeratin 19).
2 and in some cells the liver stem cell marker cytokeratin 19.
3 solute copy numbers of the epithelial marker cytokeratin 19.
4 e cell surface in cells with lower levels of cytokeratin 19.
5  specifically apical cytokeratin, presumably cytokeratin 19.
6 MA and fibronectin expression and suppressed cytokeratin-19.
7 igen, epithelial cell adhesion molecule, and cytokeratin-19.
8                                              Cytokeratin 19-, A6- and alpha-fetoprotein-positive cell
9                         Some of these genes (cytokeratin 19, alpha smooth muscle actin, and kappa cas
10 (Col1A1), matrix metalloproteinase 2 (Mmp2), cytokeratin 19, alpha-smooth muscle actin (alpha-SMA), c
11 In addition, injured hepatocytes can express cytokeratin 19 and AE1, which normally are biliary inter
12 and expressed the biliary epithelial markers cytokeratin 19 and carbonic anhydrase IV.
13 o activation of duct-specific genes, such as cytokeratin 19 and cytokeratin 20, suggesting that alter
14 tudy we confirmed the apical distribution of cytokeratin 19 and expanded that observation to other ep
15 n were evaluated by immunohistochemistry for cytokeratin 19 and Ki-67.
16 press albumin and stained more intensely for cytokeratin 19 and laminin.
17 atures with mature bile duct epithelium (AE1/cytokeratin 19 and type IV collagenase positive) or HEP
18 +)/cytokeratin-19(+) or alpha-fetoprotein(+)/cytokeratin-19(-) and contain all of the normal liver re
19 nomas revealed strong expression of keratin, cytokeratin 19, and cytokeratin 20 in the cytoplasm of a
20  (7 days in culture) express cytokeratin 18, cytokeratin 19, and vimentin.
21 multaneously positive for alpha-fetoprotein, cytokeratin-19, and c-kit, indicating their progenitor p
22 epithelial marker E-CADHERIN, biliary marker CYTOKERATIN-19, and mesenchymal markers VIMENTIN and alp
23 xpress these stem cell markers together with cytokeratin 19, another putative stem cell marker in the
24 e microscopy the milk protein lactoferrin or cytokeratin 19, both markers of differentiation expresse
25           Cells that were still positive for cytokeratin-19 but actively producing type I collagen we
26 nce of known stem/progenitor markers such as cytokeratin 19, c-Kit, EpCAM, and activated Wnt-beta-cat
27 f sex determining region Y-box (SOX)9(+) and cytokeratin 19(+) cells but fewer features of hepatocyte
28 ptase polymerase chain reaction (RT-PCR) for cytokeratin 19 (CK-19) may be useful in the management o
29 d a quantitative system for the detection of cytokeratin 19 (CK-19) transcripts using reverse transcr
30  (AFP), gamma-glutamyl transpeptidase (GGT), cytokeratin 19 (CK-19), OC.2, and OV-6, all known marker
31 ence confocal microscopy was performed using cytokeratin 19 (CK-19; biliary cell marker) with either
32 by morphometry of liver sections stained for cytokeratin-19 (CK-19) and by proliferating cellular nuc
33 ed BEC, as well as each cell line, expressed cytokeratin-19 (CK-19), epithelial cell adhesion molecul
34 r antigen (PCNA)-positive cholangiocytes and cytokeratin-19 (CK-19)-positive ducts.
35 naling occupying an alpha-fetoprotein (AFP)+/cytokeratin-19 (CK-19)-positive progenitor cell niche fo
36 s human epithelial antigen-125 (HEA-125) and cytokeratin-19 (CK-19).
37 umin, and cells expressing AFP, albumin, and cytokeratins-19 (CK-19).
38 s were serially sectioned, immunostained for cytokeratin 19 (CK19), and sequentially photographed.
39 yte nuclear factor-3beta (HNF-3beta), GATA4, cytokeratin 19 (CK19), transthyretin, and alpha-fetoprot
40 of persistent nodules and all HCCs expressed cytokeratin 19 (CK19), whereas 14% of remodeling nodules
41 mponent of the active NF-kappa B complex, in cytokeratin 19 (CK19)-positive epithelial cells of ER-ne
42  epidermal growth factor receptor (EgfR) and cytokeratin 19 (CK19).
43  (DCAMKL-1), Lgr5, CD133, alpha-fetoprotein, cytokeratin-19 (CK19), Lin28, and c-Myc.
44 roteins used clinically for staging disease (cytokeratin 19 [CK19]), identifying cancer stem cells (e
45 sociated with cholangiocyte differentiation (cytokeratin 19, connexin 43, integrin beta4, and gamma-g
46 mine the threshold levels of mammaglobin and cytokeratin 19 correlating with metastasis greater than
47   Immunohistochemistry with ductal (keratin, cytokeratin 19, cytokeratin 20), acinar (chymotrypsin),
48                                The amount of cytokeratin 19 expression was related to clinicopatholog
49 001) and with the progenitor subtype of HCC (cytokeratin 19 expression, P = 0.031).
50 and the induction of alpha-actin and loss of cytokeratin 19 expression.
51                         IBDM was detected by cytokeratin-19 expression and proliferation by Ki-67 imm
52  several known genes, including mammaglobin, cytokeratin 19, fibronectin, and hair-specific type II k
53 uamous cell carcinoma antigen (P = .03), and cytokeratin 19 fragment antigen 21-1 (P = .01) were mark
54     Baseline plasma carcinoembryonic antigen/cytokeratin 19 fragments biomarker signature was associa
55 ly one protein, and phosphorylation released cytokeratin 19 from the complexes.
56  analysis identified four of these clones as cytokeratin 19, GATA-3, CD24 and glutathione-S-transfera
57 in urothelial cells under the control of the cytokeratin 19 gene (CK19) regulatory elements.
58 els of epithelial cell adhesion molecule and cytokeratin 19 gene messenger RNAs.
59 tures and immunohistochemical markers (PD-1, cytokeratin 19, glutamine synthetase, and beta-catenin e
60 omas showed strong expression of keratin and cytokeratin 19 in all neoplastic cells, expression of cy
61 nterestingly, colocalization of alphaSMA and cytokeratin-19 in bile duct epithelium was observed, sug
62 positive for the stem/progenitor cell marker cytokeratin-19, indicating that several HCC-associated a
63 s expressed cholangiocyte markers, including cytokeratin 19, integrin beta4, and aquaporin-1, but not
64 s of junctional E-cadherin localization, and cytokeratin 19 (K19) expression.
65 es the clinical significance of detection of cytokeratin 19 (K19) in the bone marrow of patients with
66 eatic ductal cells (PDCs) were purified from cytokeratin 19 (K19)-Ki-RAS(G12V) transgenic mice and co
67 ons positive for the progenitor cell marker, cytokeratin-19 (Krt-19) and characterized by a higher pr
68 hat increased LC3B was located mainly in the cytokeratin 19-labeled ductular reaction (DR) in human c
69  increased, whereas those for E-cadherin and cytokeratin 19 (markers for the epithelial phenotype) we
70 thioate oligodeoxy nucleotides that targeted cytokeratin 19 mRNA enabled us to obtain confluent monol
71 ymph nodes (six) had more than 106 copies of cytokeratin 19 mRNA per microg total RNA.
72 2 and hepatic nuclear factor-4alpha, but not cytokeratin 19 or carbonic anhydrase IV.
73      Rat ED14 FLSPC are alpha-fetoprotein(+)/cytokeratin-19(+) or alpha-fetoprotein(+)/cytokeratin-19
74 ssical oval cell markers (alpha-fetoprotein, cytokeratin-19, OV-1 antigen, a6 integrin, and connexin
75   The ductal blast-like cells do not express cytokeratin 19, oval cell antigen 270.38, or actin immun
76 ors were strongly immunoreactive for biliary cytokeratin 19, p185neu, and cyclooxygenase-2.
77  complexes containing both gamma-tubulin and cytokeratin 19, p34(cdc2) phosphorylated only one protei
78                        We determined whether cytokeratin-19 positive (K19(+)) cholangiocytes give ris
79               Enhanced NF-kappaB staining of cytokeratin 19-positive bile ducts and proliferating duc
80 tein within parenchyma and the appearance of cytokeratin 19-positive bile ductule-like cells (oval ce
81                                              Cytokeratin 19-positive cells are detected surrounding t
82 re shown by immunofluorescence to consist of cytokeratin 19-positive duct cells and hormone-positive
83        In vivo, the DDC-stimulated number of cytokeratin-19-positive cells in the liver of wild-type
84 taste buds at adulthood as a result of fewer cytokeratin-19-positive cells.
85 ional cells, forming duct-like structures of cytokeratin-19-positive cells.
86 e NRF2 pathway accompanied the regression of cytokeratin-19-positive nodules, suggesting that activat
87  can largely be accounted for by addition of cytokeratin-19-positive taste bud cells.
88 f markers expressed by bile duct epithelium (cytokeratin 19), produce TGFalpha and acidic FGF and ass
89 derations, there is parallel activity of the cytokeratin 19 promoter in the stem cell region of the g
90 e generated a novel mouse model in which the cytokeratin 19 promoter, specifically active in pancreat
91 re designed not to amplify either of the two cytokeratin 19 pseudogenes.
92                       This downregulation of cytokeratin 19 resulted in (a) decrease in the number of
93 ed 2-3 min after palpation (P<0.01) by human cytokeratin 19 RT-PCR of extracted RNA from 300 microl o
94 gon, and somatostatin, as well as peripheral cytokeratin-19 staining.
95 mpression cytology (PAS, cytokeratin 12, and cytokeratin 19) staining were performed in the central c
96  evidence of micrometastases had the highest cytokeratin 19 transcription level in a first lymph-node
97                        Median copy number of cytokeratin 19 transcription was significantly higher (>
98                                Expression of cytokeratin 19 (up to 1.1 x 10(5) copies per microg RNA)
99 e-oligonucleotide-mediated downregulation of cytokeratin 19, using two different antisense sequences,
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 was never expressed, but in some mice, human cytokeratin 19 was expressed, which may indicate bile du
103                             Transcription of cytokeratin 19 was found at a low level in just one of 3
104 fic genes (gamma-glutamyl transpeptidase and cytokeratin 19) was similar among the three subpopulatio

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