コーパス検索結果 (1語後でソート)
通し番号をクリックするとPubMedの該当ページを表示します
1 f polzeta) was deleted in tissues expressing keratin 5.
2 luminal marker keratin 8/18 and basal marker keratin 5.
5 tochemical staining showed that nestin, GFP, keratin 5/8, and keratin 15 colocalize in the hair folli
8 creased and decreased promoter activities of keratin 5, a proliferative marker, and involucrin, a dif
10 the undifferentiated epithelial cell markers keratin 5 and 14 but not the differentiation marker kera
11 y a role in the suprabasal repression of the keratin 5 and 14 genes because keratin 14 mRNA expressio
14 mSG cells exhibited progenitor cell markers (keratin 5 and nanog) as well as acinar-specific markers-
19 tified and simple epithelial tissues express keratins 5 and 14, and keratins 8 and 18, respectively.
20 is caused by dominant-negative mutations in keratins 5 and 14, which are specifically expressed in t
21 , and markers of keratinocyte proliferation (keratins 5 and 6), and differentiation (small proline-ri
22 disorder caused by mutations in keratins K5 (keratin 5) and K14 (keratin 14), with fragility of basal
24 on-sense mutation, overexpressed a truncated keratin 5, and showed a disorganized and collapsed kerat
27 of IGF-1 is under the control of the bovine keratin 5 (BK5) promoter and is directed to either the m
29 ress a subset of basal cell genes, including keratin 5, but no longer express high levels of either T
33 expanding set of genetic variants including keratin 5 (encoded by KRT5), an intermediate filament-fo
34 mentation (mutation P25L in the V1 domain of keratin 5), epidermolysis bullosa simplex with migratory
35 ne or more layers of intermediate cells, and keratin 5-expressing basal cells (K5-BCs), which are con
36 Pten-deficient prostate lesions arising from keratin 5-expressing basal cells in a temporally control
38 s during ontogeny, we analyzed keratin 8 and keratin 5 expression at several stages of fetal developm
40 Expression of mutant ras from a truncated keratin 5 gene promoter, which directs expression to the
41 subsets regulate the expression of IL-7 and keratin 5 in adult cortical epithelium, suggesting that
42 k of keratin filaments (with type II partner keratin 5) in skin keratinocytes analyzed by static and
43 xpression decreased the promoter activity of keratin 5, increased that of keratin 10 and enhanced the
44 The pattern of expression of keratin 1 and keratin 5 indicated that epidermal differentiation was n
45 proliferating cell nuclear antigen and mouse keratin 5 indicated that these increases were due to a m
46 t cases of EBS, point mutations occur in the keratin 5 (K5) and K14 genes expressed in the basal laye
49 in mouse skin carcinogenesis, we used bovine keratin 5 (K5) and keratin 6 (K6) promoter elements to d
51 s in the intermediate filament (IF) proteins keratin 5 (K5) or keratin 14 (K14) cause epidermolysis b
52 lex (EBS) results from dominant mutations in keratin 5 (K5) or keratin 14 (K14) genes, encoding the i
56 ressing the E2F4 gene under the control of a keratin 5 (K5) promoter were developed, and their phenot
59 ressing the E2F1 gene under the control of a keratin 5 (K5) promoter, we previously demonstrated that
65 regulated the expression of p63, Trim29, and keratin 5 (K5), which serve as diagnostic markers for hu
67 combinase expressed under the control of the keratin-5 (K5) promoter resulted in a delay in the first
69 ares features with normal urothelium such as keratin 5 (KRT5), P-cadherin (P-Cad), and epidermal grow
70 in pigmentation associated with mutations in keratin 5 (KRT5), protein O-fucosyltransferase 1 (POFUT1
71 R-196a with its in silico-predicted targets, keratin 5 (KRT5), small proline-rich protein 2C (SPRR2C)
73 change predicts the synthesis of a truncated keratin 5, missing 119 amino acids, including the entire
76 ost cases of EBS are due to mutations in the keratin 5 or 14 gene (K5 and K14), whose products copoly
77 s caused by expression of either an abnormal keratin 5 or an abnormal keratin 14 protein, which compr
78 ound to harbor heterozygous mutations in the keratin 5 or keratin 14 genes, KRT5 and KRT14, respectiv
81 ing loss of gangliogenesis, innervation, and keratin 5-positive (K5+) epithelial progenitors in the S
82 mutants display premature differentiation of keratin 5-positive (Krt5(+)) basal cells and ectopic exp
83 ery of the PNA-Antp, chromosomally modified, keratin 5-positive basal keratinocytes persist for at le
87 to the gradual appearance of matriptase in a keratin-5-positive proliferative cell compartment during
90 xpressing RasGRP1 in the epidermis under the keratin 5 promoter (K5.RasGRP1) are prone to developing
91 wild-type TGFbeta1 in the epidermis using a keratin 5 promoter (K5.TGFbeta1(wt)) developed inflammat
93 ice overexpressing CDK4 under control of the keratin 5 promoter (K5CDK4 mice) develop epidermal hyper
95 1 overexpression is controlled by the bovine keratin 5 promoter and recapitulates the paracrine expos
96 udy, we show that when Edn3 is driven by the keratin 5 promoter and thereby placed proximal to melano
97 Transgenic mice (K5-PKC alpha) in which the keratin 5 promoter directs the expression of protein kin
98 nic (Tg) mice over-expressing Cx26 driven by keratin 5 promoter had an unexpected mammary phenotype:
99 under the control of an epithelial-specific keratin 5 promoter to determine whether the absence of E
100 tional expression system by using the bovine keratin 5 promoter to drive expression of the tetracycli
102 a Cre transgene under control of the bovine keratin 5 promoter we achieved 100% recombination of the
103 l layer of the forestomach epithelium by the keratin 5 promoter were used to investigate whether AZ o
104 expression of COX-2, under the control of a keratin 5 promoter, is sufficient to cause transitional
105 ess a Smad7 transgene under the control of a keratin 5 promoter, were resistant to radiation-induced
115 nocyte-specific CtBP1 transgenic mice with a keratin-5 promoter (K5.CtBP1) to probe the pathological
117 ng a desmoglein-3 mouse model (Dsg3(-/-)) or keratin 5-specific reporter mice, the investigators show
118 cantly higher total E-cadherin and decreased keratin 5 staining than epithelium of placebo-treated mi
120 shift mutation c1649delG in the V2 domain of keratin 5), striate palmoplantar keratoderma (PPK), and
121 keratosis in both patients suggests that the keratin 5 tail domain may have unrecognized, but importa
122 e model that expresses an epidermal-targeted keratin-5-UCP3 (K5-UCP3) transgene and exhibits signific
123 sgenics to delete Fgfr2b in cells expressing keratin 5, we show that mice lacking epidermal Fgfr2b su
WebLSDに未収録の専門用語(用法)は "新規対訳" から投稿できます。