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1 f polzeta) was deleted in tissues expressing keratin 5.
2 luminal marker keratin 8/18 and basal marker keratin 5.
3 axome consists of a marginal ring containing keratin 5 10-nm-thick filaments and F-actin.
4 amous phenotype with increased expression of keratins 5/6 and beta-catenin.
5 ription factor NFAT2 to induce expression of keratin (5, 7, and 8) filaments.
6 tochemical staining showed that nestin, GFP, keratin 5/8, and keratin 15 colocalize in the hair folli
7                   Here, we demonstrated that keratin 5, a 58 kD protein required for formation of 8 n
8                                      Because keratin 5, a keratin associated with basal cells, was de
9 creased and decreased promoter activities of keratin 5, a proliferative marker, and involucrin, a dif
10                           The genes encoding keratin 5 and 14 are highly expressed in the basal cell
11 the undifferentiated epithelial cell markers keratin 5 and 14 but not the differentiation marker kera
12 y a role in the suprabasal repression of the keratin 5 and 14 genes because keratin 14 mRNA expressio
13  the expression of the proliferation markers keratin 5 and cyclin D1.
14                                          The keratin 5 and keratin 14 genes encode proteins that form
15 mSG cells exhibited progenitor cell markers (keratin 5 and nanog) as well as acinar-specific markers-
16 ne both induced changes in the expression of keratins 5 and 10, consistent with the inhibition of pro
17                                              Keratins 5 and 14 (K5 and K14), the main pairing occurri
18                         For IFs comprised of keratins 5 and 14 (K5 and K14), which occur in basal ker
19                         For IFs comprised of keratins 5 and 14 (K5, K14), found in basal keratinocyte
20                                              Keratins 5 and 14 are expressed as a pair in basal cells
21 tified and simple epithelial tissues express keratins 5 and 14, and keratins 8 and 18, respectively.
22  is caused by dominant-negative mutations in keratins 5 and 14, which are specifically expressed in t
23 , and markers of keratinocyte proliferation (keratins 5 and 6), and differentiation (small proline-ri
24 disorder caused by mutations in keratins K5 (keratin 5) and K14 (keratin 14), with fragility of basal
25 in a dramatic redistribution of desmoplakin, keratin 5, and chromogranin A proteins.
26 on-sense mutation, overexpressed a truncated keratin 5, and showed a disorganized and collapsed kerat
27                                Four-week-old keratin 5/AZ and wild-type (Wt) littermates were placed
28             Specifically, after low-dose IR, keratin 5(+) basal hair bulb progenitors, rather than bu
29  of IGF-1 is under the control of the bovine keratin 5 (BK5) promoter and is directed to either the m
30  driven by human keratin 14 (HK14) or bovine keratin 5 (BK5) promoters, respectively.
31 ress a subset of basal cell genes, including keratin 5, but no longer express high levels of either T
32 airway stem cells expressing Trp63 (p63) and keratin 5, called DASC(p63/Krt5), to this process.
33 xpressing mouse strains under the control of keratin 5, CD4, and retinoic acid receptor-related orpha
34                               Using either a keratin 5-Cre recombinase (K5-Cre) cross or an MMTV-NIC
35                          We used a truncated keratin 5 (DeltaK5) promoter to assess the potential rol
36 opment in vivo with a doxycycline-inducible, keratin 5-driven transgene encoding TSLP (K5-TSLP).
37  expanding set of genetic variants including keratin 5 (encoded by KRT5), an intermediate filament-fo
38 mentation (mutation P25L in the V1 domain of keratin 5), epidermolysis bullosa simplex with migratory
39 es an injury-induced tissue niche containing keratin 5(+) epithelial cells and plastic Pdgfra(+) mese
40 ne or more layers of intermediate cells, and keratin 5-expressing basal cells (K5-BCs), which are con
41 Pten-deficient prostate lesions arising from keratin 5-expressing basal cells in a temporally control
42        Unchallenged mice developed tumors in keratin 5-expressing tissues with age, consistent with t
43 s during ontogeny, we analyzed keratin 8 and keratin 5 expression at several stages of fetal developm
44 ocervix and uterine cavity were monitored by keratin 5 expression with immunohistochemistry.
45    Expression of mutant ras from a truncated keratin 5 gene promoter, which directs expression to the
46  subsets regulate the expression of IL-7 and keratin 5 in adult cortical epithelium, suggesting that
47 k of keratin filaments (with type II partner keratin 5) in skin keratinocytes analyzed by static and
48 xpression decreased the promoter activity of keratin 5, increased that of keratin 10 and enhanced the
49   The pattern of expression of keratin 1 and keratin 5 indicated that epidermal differentiation was n
50 proliferating cell nuclear antigen and mouse keratin 5 indicated that these increases were due to a m
51 t cases of EBS, point mutations occur in the keratin 5 (K5) and K14 genes expressed in the basal laye
52                    One mTEC subset expresses keratin 5 (K5) and K14, but fails to bind Ulex europaeus
53 c disorders of the basal epidermal keratins, keratin 5 (K5) and keratin 14 (K14).
54 in mouse skin carcinogenesis, we used bovine keratin 5 (K5) and keratin 6 (K6) promoter elements to d
55 al dominant condition caused by mutations in keratin 5 (K5) or K14.
56 s in the intermediate filament (IF) proteins keratin 5 (K5) or keratin 14 (K14) cause epidermolysis b
57 lex (EBS) results from dominant mutations in keratin 5 (K5) or keratin 14 (K14) genes, encoding the i
58 aithfully recapitulate the strong endogenous keratin 5 (K5) promoter and/or enhancer activity.
59                                          The keratin 5 (K5) promoter drives transgenic expression to
60 tic protein (BMP) antagonist noggin from the keratin 5 (K5) promoter in the epidermis.
61 ressing the E2F4 gene under the control of a keratin 5 (K5) promoter were developed, and their phenot
62 c mice expressing Myc under the control of a keratin 5 (K5) promoter were generated.
63  mice expressing E2F1 under the control of a keratin 5 (K5) promoter were generated.
64 ressing the E2F1 gene under the control of a keratin 5 (K5) promoter, we previously demonstrated that
65 targeted to squamous epithelial tissues by a keratin 5 (K5) promoter.
66 f transgenic mice expressing E2F3a through a keratin 5 (K5) promoter.
67 chieved by Cre recombinase expression from a keratin 5 (K5) promoter.
68 f the Cre recombinase under the control of a keratin 5 (K5) promoter.
69  produce BCCs when overexpressed by use of a Keratin 5 (K5) promoter.
70 regulated the expression of p63, Trim29, and keratin 5 (K5), which serve as diagnostic markers for hu
71 y breeding conditional Perp knockout mice to keratin 5 (K5)-Cre transgenic mice.
72 combinase expressed under the control of the keratin-5 (K5) promoter resulted in a delay in the first
73  In this study, we analyzed the structure of keratin 5/keratin 14 filaments within ghost mouse kerati
74 ade a series of point substitutions with the keratin 5/keratin 14 IF system.
75 d upregulation of Ifng and downregulation of keratin 5 (Krt5) and Krt14 even after complete macroscop
76  kinase (ERK)-driven proliferation of mostly keratin 5 (KRT5)(+)/KRT14(-) intermediate cells.
77 , including forkhead box protein J1 (FOXJ1), keratin 5 (KRT5), and secretoglobin family 1A member 1 (
78 ares features with normal urothelium such as keratin 5 (KRT5), P-cadherin (P-Cad), and epidermal grow
79 hemidesmosome-associated proteins, including keratin 5 (KRT5), plectin (PLEC), integrin alpha 6 (ITGa
80 in pigmentation associated with mutations in keratin 5 (KRT5), protein O-fucosyltransferase 1 (POFUT1
81 R-196a with its in silico-predicted targets, keratin 5 (KRT5), small proline-rich protein 2C (SPRR2C)
82 eading to the development and persistence of keratin 5+ (Krt5+) epithelial cells in the alveolar pare
83                        We identified type II keratin 5, lamin A, the cytoplasmic domain of integrin b
84 change predicts the synthesis of a truncated keratin 5, missing 119 amino acids, including the entire
85 ignificantly accelerate tumor development in keratin 5 Myc transgenic mice.
86                     Expression of an altered keratin 5, of predicted mass and pI for the product of t
87 ost cases of EBS are due to mutations in the keratin 5 or 14 gene (K5 and K14), whose products copoly
88 s caused by expression of either an abnormal keratin 5 or an abnormal keratin 14 protein, which compr
89 ound to harbor heterozygous mutations in the keratin 5 or keratin 14 genes, KRT5 and KRT14, respectiv
90                                       Mutant keratins 5 or 14 are implicated in the etiology of epide
91 heath of the hair follicle, as well as other keratin 5 positive tissues.
92 ing loss of gangliogenesis, innervation, and keratin 5-positive (K5+) epithelial progenitors in the S
93 mutants display premature differentiation of keratin 5-positive (Krt5(+)) basal cells and ectopic exp
94 ery of the PNA-Antp, chromosomally modified, keratin 5-positive basal keratinocytes persist for at le
95 re decreased the number and morphogenesis of keratin 5-positive epithelial progenitor cells.
96 elial morphogenesis and proliferation of the keratin 5-positive progenitor cells.
97 lumen layer of multi-ciliated and a layer of Keratin-5-positive basal cells.
98 to the gradual appearance of matriptase in a keratin-5-positive proliferative cell compartment during
99 sociated keratin 6A, but not of steady-state keratin 5, potentiated keratinocyte migration and wound
100 in epidermis were generated using the bovine keratin 5 promoter (BK5).
101 al component of the NF-kappaB pathway, under keratin 5 promoter (K5-Ikkbeta).
102 xpressing RasGRP1 in the epidermis under the keratin 5 promoter (K5.RasGRP1) are prone to developing
103  wild-type TGFbeta1 in the epidermis using a keratin 5 promoter (K5.TGFbeta1(wt)) developed inflammat
104                     Our recent study using a keratin 5 promoter (K5.TGFbeta1(wt)) showed that transge
105 ice overexpressing CDK4 under control of the keratin 5 promoter (K5CDK4 mice) develop epidermal hyper
106 sgenic mice carrying the CDK6 gene under the keratin 5 promoter (K5CDK6).
107 1 overexpression is controlled by the bovine keratin 5 promoter and recapitulates the paracrine expos
108 udy, we show that when Edn3 is driven by the keratin 5 promoter and thereby placed proximal to melano
109  Transgenic mice (K5-PKC alpha) in which the keratin 5 promoter directs the expression of protein kin
110 nic (Tg) mice over-expressing Cx26 driven by keratin 5 promoter had an unexpected mammary phenotype:
111  under the control of an epithelial-specific keratin 5 promoter to determine whether the absence of E
112 tional expression system by using the bovine keratin 5 promoter to drive expression of the tetracycli
113                                          The keratin 5 promoter was used with a tetracycline-inducibl
114  a Cre transgene under control of the bovine keratin 5 promoter we achieved 100% recombination of the
115 l layer of the forestomach epithelium by the keratin 5 promoter were used to investigate whether AZ o
116  expression of COX-2, under the control of a keratin 5 promoter, is sufficient to cause transitional
117 ess a Smad7 transgene under the control of a keratin 5 promoter, were resistant to radiation-induced
118 arrying the CDK4 gene under the control of a keratin 5 promoter.
119 hich carry cyclin D2 or D3 genes driven by a keratin 5 promoter.
120 ators, tTA and rTA, are linked to the bovine keratin 5 promoter.
121 sal layer of mouse epidermis with the bovine keratin 5 promoter.
122  the human cyclin D1 gene driven by a bovine keratin 5 promoter.
123 1 to basal epidermal keratinocytes using the keratin 5 promoter.
124 ecific myosin light-chain 2 or skin-specific keratin 5 promoter.
125 follicles under the regulation of the bovine keratin 5 promoter.
126 ycline transactivator tTA from the epidermal keratin 5 promoter.
127 nocyte-specific CtBP1 transgenic mice with a keratin-5 promoter (K5.CtBP1) to probe the pathological
128 cyclin in squamous epithelia from the bovine keratin-5 promoter.
129 ng a desmoglein-3 mouse model (Dsg3(-/-)) or keratin 5-specific reporter mice, the investigators show
130 cantly higher total E-cadherin and decreased keratin 5 staining than epithelium of placebo-treated mi
131  mouse skin biopsies was determined based on Keratin 5 staining.
132 shift mutation c1649delG in the V2 domain of keratin 5), striate palmoplantar keratoderma (PPK), and
133 keratosis in both patients suggests that the keratin 5 tail domain may have unrecognized, but importa
134 e model that expresses an epidermal-targeted keratin-5-UCP3 (K5-UCP3) transgene and exhibits signific
135 sgenics to delete Fgfr2b in cells expressing keratin 5, we show that mice lacking epidermal Fgfr2b su
136           Basal cell markers such as p63 and keratin 5 were not expressed by the masses of PIN-like l
137 ressing the BMP antagonist noggin (promoter: keratin 5) were generated.

 
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