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1 claudin 3, 4, and 7 and the luminal marker, cytokeratin 18.
2 8, but in the presence of actin, AVP cleaved cytokeratin 18.
3 cells exhibited caspase-specific cleavage of cytokeratin 18.
4 ith a monoclonal antibody specific for human cytokeratin 18.
5 pase-3, and immunohistochemical staining for cytokeratin 18.
7 skeletal filaments: vimentin, cytokeratin 8, cytokeratin 18, actin, and hair type II basic keratin.
8 ormal unperturbed RPE are immunoreactive for cytokeratin 18 and negative for cytokeratin 19, vimentin
10 2-derived peptide, alanine aminotransferase, Cytokeratin-18 and homeostasis model of insulin resistan
12 ation of fibrosis-associated markers such as cytokeratins 18 and 19 and annexin 2, as determined both
15 tested M65 and M30 (circulating fragments of cytokeratin-18) and their respective fraction carried by
18 es in HeLa cells revealed AVP localized with cytokeratin 18, and this was followed by destruction of
19 ll as the epithelial markers pancytokeratin, cytokeratin-18, and occludin, but not mesenchymal (CD44,
21 rum transaminases were normal in TASH, total cytokeratin 18, but not the caspase-cleaved fragment, wa
25 We have recently demonstrated that plasma cytokeratin 18 (CK-18) fragment levels correlate with th
26 say (ELISA), which detects a caspase-cleaved cytokeratin-18 (CK-18) fragment and thereby apoptotic ce
28 necrosis in serum was quantified using serum cytokeratin 18 (CK18) M30 and M65 enzyme-linked immunoso
29 reased expression of HDAC1 target genes Bax, cytokeratin 18 (CK18), and p21(WAF1/CIP1), whereas maspi
31 vities, and immunohistochemical staining for cytokeratin 18 cleavage products indicated no activation
33 ropeptide Y receptor Y1, p21 WAF-1, p55 PIK, cytokeratin 18 (cloned twice), fructose-1,6-biphosphatas
34 cells express cytokeratins 5 and 14, but not cytokeratin 18, consistent with a basal epithelial cell
38 brils with active caspase-3, caspase-cleaved cytokeratin-18, death-effector-domain containing DNA-bin
39 amplification loop to facilitate cleavage of cytokeratin-18, disruption of the cytoskeleton and the e
40 of differentiation as shown by expression of cytokeratin 18, E-cadherin, thyroglobulin, TTF-1 and Pax
43 rum levels of M30 and M65 antigen (the total cytokeratin-18 fragment, a marker of apoptosis and necro
44 3 +/- 1.5 vs. 1.7 +/- 1.4; P = 0.004), serum cytokeratin-18 fragments (283 vs. 404 U/L; P < 0.001) an
46 labeling-positive nuclei and accumulation of cytokeratin-18 fragments in the liver, was independent o
49 cytokines, markers of hepatocyte apoptosis (cytokeratin-18 fragments), and hepatic fibrogenesis (hya
50 ed low-density lipoproteins, adipokines, and cytokeratin-18 fragments, and an oral glucose tolerance
60 alpha, ERbeta, cytokeratin 14 (basal cells), cytokeratin 18 (luminal cells), and dorsolateral protein
61 enterocyte proliferation and migration, (2) cytokeratin-18 M30-immunohistochemistry to compare level
63 strogen, and progesterone receptor-positive, cytokeratin 18-positive (ER(+)PR(+)CK18(+)) subtype, and
64 zyme-linked immunosorbent assays for various cytokeratin 18 products (eg, M65, cell death, M30, and a
66 trol of the surfactant protein C promoter or cytokeratin 18 promoter that are susceptible to infectio
69 umin, alpha-fetoprotein, cytochrome P4502E1, cytokeratin-18, type-1 collagen, transforming growth fac
70 cirrhosis contained hepatocyte-derived MPs (cytokeratin-18(+)), whereas plasma from controls did not
71 re used to identify five proteins, including cytokeratin 18, which is the product of the most highly
72 markers of colonic epithelial cells such as cytokeratin 18, zonula occludens-1, mucins-1 and -2, ant
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