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1 ratins 6, 13, 14, and 19; and the absence of keratin 1.
4 r subset involves the type II keratin chains keratin 1, 2e, 5, or 6 crosslinked to several protein pa
5 sion of several epithelial markers including keratins 1, 5, 10, and 14 while increasing expression of
6 y isolated infundibula were found to express keratins 1, 5, 6, 16, and 17, as determined by immunohis
7 amino acid substitution in the 1A domain of Keratin 1, a known target for human mutations that cause
9 ssed markers of skin differentiation such as Keratin 1 and 10 instead of Keratin 12, a marker of corn
13 of human keratinocytes induces expression of keratin 1 and keratin 10 genes, early markers of termina
14 leading to the reduced tumorigenesis because keratin 1 and keratin 10, two keratins that indicate the
19 smoglein 1 (Dsg1), desmocollin 1 (Dsc1), and keratins 1 and 10 (K1/K10), in a dose-dependent manner i
21 ed expression of the differentiation markers keratins 1 and 10 induced by high calcium in the medium.
22 the A-FOS virus reversed the suppression of keratins 1 and 10 transcripts and protein, which is char
23 differentiation markers (e.g., profilaggrin, keratins 1 and 10) as well as certain pro-apoptotic gene
24 ns of the head and tail domains of epidermal keratins 1 and 10, based on all-atom 3D simulations of k
26 o epidermal-like structures, which expressed keratins 1 and 6, filaggrin, loricrin and involucrin.
27 stimulating an early differentiation marker (keratin 1) and suppressing later markers (profilaggrin,
28 ifferentiation (such as desmoglein-1 [Dsg1], keratin-1, and loricrin) and abrogated MAL/SRF signaling
29 affecting the tail domains of keratin-10 or keratin-1, and Suzuki et al. expand the mutation spectru
31 f the early (spinous) differentiation marker keratin 1 decreased in response to 1, 25(OH)2D3 over 12-
36 iation of primary keratinocytes, we measured keratin-1 expression and transglutaminase activity, mark
38 mutation in the exon 6 splice donor site of keratin 1 (G4134A) that segregates with a palmoplantar k
40 t ras under the control of the keratin 10 or keratin 1 gene promoters, the formation of these lesions
42 ulated two early markers of differentiation, keratin 1 (K1) and keratin 10 (K10) but had a minimal ef
43 nt aggregates in these areas are composed of keratin 1 (K1) and keratin 10 (K10), and several K1 and
47 albumin (K212, K414, K199, and K351), human keratin 1 (K211 and K355), human keratin 10 (K163), bovi
48 of epidermal differentiation markers such as keratin 1, keratin 10, and loricrin, with or without the
49 rrant expression of differentiation markers, keratin 1, keratin 6, loricrin, and filaggrin in ML.myc2
50 esidues, which would spatially constrain the keratin 1/keratin 10 end domains to allow filament compa
52 markers assayed by immunoblotting, including keratin 1, loricrin, filaggrin, involucrin, TGK, and SPR
54 and p27), a marker of early differentiation (keratin 1), mediators of apoptosis (caspases 3 and 8), a
55 nital ichthyosiform erythroderma also due to keratin 1 mutations, which show widespread and severe ep
56 sis, frequently associated with mutations in keratin 1 or 10 that result in disruption of the keratin
58 enic mouse model (HK1.bcl-2) using the human keratin 1 promoter to target the expression of a human b
60 er keratin 14 and the differentiation marker keratin 1 was evident in Aurora-A(-/-) epidermis, there
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