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1 s remained unaltered, including cyclin E and keratin 8.
2 ine-to-histidine mutations at position 53 of keratin 8.
3 Tumors were further classified by markers keratin 8/18 (K18, KRT18), keratin 14 (K14, KRT14) and e
6 e effect of small heat shock proteins on the keratin 8/18 intermediate filament cytoskeleton using a
8 rates expression of NP markers FoxF1, Pax-1, keratin-8/18, carbonic anhydrase-12, and NC markers brac
12 blocked normal differentiation, and induced keratin 8, a marker of malignant conversion, but did not
15 runcates the last 14 amino acids; 8 missense keratin 8 and 18 alterations; and several new polymorphi
17 a time-dependent disassembly-degradation of keratin 8 and 18 proteins, which was associated with an
20 cytoskeletal intermediate filament proteins keratin 8 and keratin 18 (K8/K18) is associated with cir
22 osis, but the importance of mutations in the keratin 8 and keratin 18 genes in such patients is uncle
23 of TEC subsets during ontogeny, we analyzed keratin 8 and keratin 5 expression at several stages of
24 duction of epithelial markers E-cadherin and keratin-8 and down-regulation of mesenchymal markers N-c
25 patibility complex transcription factors and keratin-8 and therefore may allow immune evasion and est
31 eral liver diseases and consist primarily of keratins 8 and 18 (K8/K18) and ubiquitin that are cross-
35 major keratins in the pancreas and liver are keratins 8 and 18 (K8/K18), but their function seemingly
37 -Denk bodies (MDBs), which are aggregates of keratins 8 and 18 (K8/K18), ubiquitin, and the ubiquitin
39 demonstrated the constitutive expression of keratins 8 and 18 and induced expression of keratin 19,
40 n, the transfectants containing vimentin and keratins 8 and 18 demonstrated an increase in focal adhe
41 nimal models, the absence of heteropolymeric keratins 8 and 18 or the presence of mutant keratins in
43 ich included several keratins, in particular keratins 8 and 18 which are regulated through the ras si
44 h up-regulation of epithelial markers (i.e., keratins 8 and 18) and down-regulation of mesenchymal ma
48 ue-type plasminogen activator (tPA), AFP and keratins 8 and 19 is inhibited, whilst brachyury and myo
49 position 61 (a highly conserved glycine) of keratin 8, and 2 had tyrosine-to-histidine mutations at
50 actor) was both necessary and sufficient for keratin 8 cleavage in chlamydia-infected cells, suggesti
52 increase in p62 and Hsp25 levels as well as keratin 8 cross-linking that is normally associated with
54 ontrols: keratin 18 deletion (delta64-71), a keratin 8 frameshift that truncates the last 14 amino ac
56 Mutations that introduced disulfide bonds (keratin 8 G61C or R453C) decreased keratin solubility, p
64 ated ectopic expression in cardiomyocytes of keratin 8 (K8) and keratin 18 (K18), two epithelial-spec
66 Using stable CACO-2 transfectants expressing keratin 8 (K8) antisense RNA under a tetracycline-respon
76 of intestinal keratins is unknown, although keratin 8 (K8)-null mice develop colitis, hyperplasia, d
77 Keratins are essential for MDB formation and keratin 8 (K8)-overexpressing transgenic mice are predis
78 2 and keratin overexpression, with a greater keratin 8 (K8)-to-keratin 18 (K18) ratio, which are crit
82 l tissues such as liver and pancreas express keratins 8 (K8) and 18 (K18) as their major intermediate
85 was not affected, but hsc hsp70, hsp90beta, keratin 8, keratin 18 and caveolin-1 were deregulated fo
86 ents in simple epithelial cells, cleavage of keratin 8 may increase the solubility of the host cell c
87 -associated mutations have been described in keratin 8 or 18 (K8/18) which are the major keratin pair
88 ach to identify proteins that associate with keratins 8 or 18 (K8/K18) in a pervanadate-dependent man
90 ge-committed basal Lgr5-positive and luminal keratin-8-positive cells of the adult mouse mammary glan
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