ライフサイエンスコーパス: keratin-14

1 ific differentiation markers (keratin-10 and keratin-14).

2 hESCs and murine embryos express p63 before keratin 14.

3 ns, also recognized skin antigens, including keratin 14.

4 en activator receptor (uPAR); fibronectin 1; keratins 14, 18, and 19; vimentin; transforming growth f

5 We characterized Raf-keratin-14-3-3 associations and show that Raf associates

6 del that allows focal activation of a mutant keratin 14 allele in epidermal stem cells upon topical a

7 staining revealed supra-basal expression of keratin 14 and decreased expression of differentiation-a

8 Both basal cell types up-regulate keratin 14 and generate a broadly distributed, abundant,

9 nd an increase in luminal cells that express keratin 14 and integrin-alpha6, a phenotype that is usua

10 n markers characteristic of its final state (keratin 14 and involucrin).

11 f other epithelially expressed genes such as keratin 14 and the desmoglein genes DSG1 and DSG3.

12 ugh the expression of the basal layer marker keratin 14 and the differentiation marker keratin 1 was

13 urface but increased total protein levels of keratin-14 and beta1 integrins.

14 terminal differentiation including decreased keratin-14 and increased involucrin expression.

15 abasal cells were misaligned and coexpressed keratins 14 and 10.

16 cer cells led to cell blebbing and a loss of keratins 14 and 18, in addition to the upregulation of v

17 Keratins 14 and 5 are the structural hallmarks of the ba

18 MO (smoothened), p63, SLUG (snail-2), KER14 (keratin-14) and VIM (vimentin)).

19 ion, we chose one of the identified targets, keratin 14, and prepared recombinant proteins encompassi

20 the migrating front of epidermis stained for keratin 14, but only the basal cells expressed collagena

21 s on cell-cell adhesion in vivo, we utilized keratin-14 cre-recombinase (K14-cre) to inactivate Flcn

22 is study, we crossed Fam20C(fl/fl) mice with keratin 14-Cre (K14-Cre) transgenic mice to specifically

23 s of FTase and GGTase-I, respectively) and a keratin 14-Cre transgene to create mice lacking FTase or

24 Using the keratin 14-Cre transgene, we bred mice lacking the expre

25 ce bearing the floxed C/EBPalpha allele with keratin-14-Cre mice generate C/EBPalpha conditional knoc

26 P expression in the enamel epithelium with a keratin 14-driven transgene corrects the defect in bone

27 ith a floxed fak allele under the control of keratin-14-driven Cre fused to a modified estrogen recep

28 s type 16 (HPV16) under control of the human keratin-14 enhancer/promoter (K14-HPV16 transgenic mice)

29 thelium demonstrated that two multipotential keratin 14-expressing cells (K14ECs) function as progeni

30 generates mitochondrial oxidative stress in keratin 14-expressing epidermal stem/progenitor cells in

31 overexpression of TSP-1 in the skin, using a keratin 14 expression cassette.

32 In addition, we show that decreased mutant keratin 14 expression resulted in normal morphology and

33 Keratin 14 expression, a basal keratinocyte marker, was

34 All flow-sorted cells were positive for keratin 14 expression, and negative for keratin 1, loric

35 ith PMA treatment, but A23187 did not affect keratin 14 expression.

36 Keratin 14-Fyn (K14) transgenic mice were derived to cha

37 ggesting that POU domain factors may repress keratin 14 gene expression by interfering with the activ

38 /p300 co-activators are strong activators of keratin 14 gene expression, acting through sequences clo

39 essing NT4 in skin, under the control of the keratin 14 gene promoter, were examined.

40 The region of the keratin 14 gene sufficient and required for repression b

41 The keratin 5 and keratin 14 genes encode proteins that form the primary s

42 r heterozygous mutations in the keratin 5 or keratin 14 genes, KRT5 and KRT14, respectively, whereas

43 t)) in epidermal basal cells driven by human keratin 14 (HK14) or bovine keratin 5 (BK5) promoters, r

44 se model of epithelial carcinogenesis [i.e., keratin 14-human papillomavirus 16 (K14-HPV16) transgeni

45 Virgin female keratin 14-human papillomavirus 16 transgenic mice were

46 Iron was increased up to 2-fold in hair of keratin 14-human transferrin receptor (hTfR) transgenics

47 es of point substitutions with the keratin 5/keratin 14 IF system.

48 expression of involucrin and keratins-10 and keratins-14 in the epidermis, indicating their stimulato

49 d in the central alpha-helical rod domain of keratin 14 is necessary for the formation of a stable pe

50 ate filament (IF) proteins keratin 5 (K5) or keratin 14 (K14) cause epidermolysis bullosa simplex (EB

51 from dominant mutations in keratin 5 (K5) or keratin 14 (K14) genes, encoding the intermediate filame

52 homotypic disulfide bond involving Cys367 in keratin 14 (K14) occurs in an atomic-resolution structur

53 BS are due to dominantly acting mutations in keratin 14 (K14) or K5, the type I and II intermediate f

54 due to dominantly acting mutations in either keratin 14 (K14) or K5, the type I and II intermediate f

55 ne-bound form of OVA in skin under the human keratin 14 (K14) promoter (K14-mOVA mice).

56 o the basal layer of the epidermis using the keratin 14 (K14) promoter (K14.MCM7).

57 2 directed to these sites in the skin by the keratin 14 (K14) promoter produces prominent hair follic

58 We have used the keratin 14 (K14) promoter to re-express a class II MHC a

59 ing membrane ovalbumin (mOVA), driven by the keratin 14 (K14) promoter, developed GVHD-like mucocutan

60 a downstream effector of Ras, driven by the keratin 14 (K14) promoter, has been used to test the hyp

61 Using a previously described human keratin 14 (K14) promoter, we created mice expressing a

62 terminus, E6(Delta 146-151), from the human keratin 14 (K14) promoter.

63 (CreER(tam)) under the control of the human keratin 14 (K14) promoter.

64 cken ovalbumin (OVA), under the control of a keratin 14 (K14) promoter.

65 ibitor noggin or BMP4 under the control of a keratin 14 (K14) promoter.

66 17-kDa IL-1 alpha in the epidermis under the keratin 14 (K14) promoter.

67 several Msx-regulated genes (Bmp4, Fgf8, and keratin 14 (K14)) in BlC groups, including MSX1, MSX2, a

68 We previously generated keratin 14 (K14)-A(beta)b mice expressing MHC class II o

69 oraphane (SF) ameliorates skin blistering in keratin 14 (K14)-deficient mice, correlating with the in

70 We identified a population of keratin 14 (K14)-expressing progenitor epithelial cells

71 utoreactive TCR-Tg CD8 T cells (OT-I cells), keratin 14 (K14)-mOVA(high) Tg mice developed autoreacti

72 basal epidermal keratins, keratin 5 (K5) and keratin 14 (K14).

73 in type II (KtyII) K5 and its type I partner keratin 14 (K14).

74 pressed the epithelial cytoskeletal protein, keratin 14 (K14).

75 sified by markers keratin 8/18 (K18, KRT18), keratin 14 (K14, KRT14) and estrogen receptor (ER, ESR1)

76 responses in keratinocyte cell lines lacking keratin 14 (K14-null mutation).

77 ther the Tyrosinase-Related Protein-1 or the keratin-14 (K14) promoter, the latter with and without a

78 derived from inversion heterozygotes, and a keratin-14 (K14) promoter-driven agouti minigene was int

79 al cells by regulatory elements of the human keratin-14 (K14) promoter.

80 Immunostaining for Keratin-14 (K14) was used to delineate Hertwig's epithel

81 Tg) murine model of autoimmunity by crossing keratin-14 (K14)-soluble chicken ovalbumin (sOVA) mice,

82 We have generated a transgenic (Tg) mouse [keratin-14 (K14)-survivin] with skin expression of survi

83 The type I keratins 14 (K14) and 16 (K16) are distinct in their ass

84 ypoplastic, displaying reduced expression of Keratin 14, Keratin 1 and markers of proliferation.

85 We found that keratin 14 (KRT14) marks the most primitive differentiat

86 s, we used a transgenic mouse model in which keratin 14 (KRT14) promoter-mediated overexpression of N

87 We report a mutation in the gene encoding keratin 14 (KRT14) that changes the predicted amino acid

88 Keratin 14 (KRT14, a biomarker in esophageal tumorigenes

89 nomas that express high levels of C/EBPbeta, keratin-14, matrix metalloproteinase-3, and beta-catenin

90 Keratin 14-mediated Cre recombinase expression induced e

91 ession of the keratin 5 and 14 genes because keratin 14 mRNA expression persists in suprabasal cells

92 epidermal growth factor receptor, c-myc, and keratin 14 mRNAs comparable with the parental BC-1-Ep ke

93 fter removal of rapamycin and expressed more keratin 14, N-Cadherin, DeltaNp63 and ABCG2, and less ke

94 or pool is further divided into two subsets, keratin 14-negative and -positive.

95 and conditional deletion of Prdm1 in either Keratin 14- or Foxn1-expressing cells in mice resulted i

96 ined by cross-breeding experiments employing keratin 14-parathyroid hormone-related protein mice and

97 l types of hair were 30-40% shorter in adult keratin 14-parathyroid hormone-related protein mice as c

98 The dorsal skin of the keratin 14-parathyroid hormone-related protein mouse was

99 se exostosin glycosyltransferase 1 (Ext1) in keratin 14-positive cells from P21.

100 on the Spdef promoter and that treatment of keratin 14-positive cells with TGFbeta inhibited SPDEF a

101 Gain of function of Spdef in keratin 14-positive epithelia resulted in the ectopic fo

102 phenotype was associated with a decrease in keratin 14-positive myoepithelial cells in PyMT(mgko) tu

103 g growth factor beta receptor II (Tgfbr2) in keratin 14-positive stratified epithelia causes ocular s

104 was directed in its expression by the human keratin 14 promoter (hK14) to the basal layer of the epi

105 in vivo using transgenic mice driven by the keratin 14 promoter (K14).

106 nes for human papillomavirus type 16 under a keratin 14 promoter (K14-HPV16 mice) develop cervical ca

107 of transgenic mice under the control of the keratin 14 promoter and beta-catenin activity was induce

108 A keratin 14 promoter construct was used to produce transg

109 wing mating Tgf-beta3 heterozygous mice with Keratin 14 promoter directed Smad2 transgenic mice (K14-

110 ilized a transgenic mouse model in which the keratin 14 promoter drives expression of the entire HPV8

111 ronic VEGF overexpression in vivo, we used a keratin 14 promoter expression cassette containing the g

112 GF-2 in epidermal keratinocytes, driven by a keratin 14 promoter expression construct.

113 These studies underscore the utility of the keratin 14 promoter for expressing foreign transgenes in

114 optotic gene bcl-xL under the control of the keratin 14 promoter have significantly shorter hair than

115 nt negative c-jun (TAM-67) controlled by the keratin 14 promoter in ICR mice were used to determine t

116 o demonstrate that the activity of the human keratin 14 promoter remains high in adult skin and that

117 HrP-knockout mice under the direction of the keratin 14 promoter reversed the abnormalities seen in P

118 The keratin 14 promoter targeted the receptor primarily to b

119 Using the keratin 14 promoter to target expression of an activated

120 n of hair growth directly, we used the human keratin 14 promoter to target human vitamin D receptor e

121 nant negative mutant c-jun driven by a human keratin 14 promoter was co-transfected with AP-1 or NF-k

122 The human keratin 14 promoter was used to direct expression of mut

123 ling in murine limb development in vivo, the keratin 14 promoter was used to drive expression of the

124 lomavirus (HPV) type 16 under control of the keratin 14 promoter were analyzed by comparative genomic

125 ukemia virus long terminal repeat (LTR), the keratin 14 promoter, or the involucrin promoter was not

126 ing growth factor alpha under control of the keratin 14 promoter, Stat3 was constitutively activated.

127 overexpress COX-2 under control of the human keratin 14 promoter, which allows for expression in the

128 periments, both Skn-1a and Tst-1 repress the keratin 14 promoter, with the POU domain being sufficien

129 cted a transgene (K14-ARGE) encoding a human keratin 14 promoter-driven AR gene.

130 targeted expression of a transgene encoding keratin 14 promoter-driven human amphiregulin to the bas

131 tenin binding site, under the control of the keratin 14 promoter.

132 ress Smad2 in epidermis under the control of keratin 14 promoter.

133 ssion, acting through sequences close to the keratin 14 promoter.

134 thelial cells under the control of the human keratin 14 promoter.

135 Cepsilon) in their epidermis using the human keratin 14 promoter.

136 Cdelta (T7-PKCdelta) regulated by the human keratin 14 promoter.

137 transgene expressed under the control of the keratin 14 promoter.

138 he basal layer of the epidermis by the human keratin 14 promoter.

139 the basal layer of mouse epidermis using the keratin 14 promoter.

140 ermal keratinocytes under the control of the keratin 14 promoter.

141 ing progerin in epidermis under control of a keratin 14 promoter.

142 tical epithelial cells (cEC) using the human keratin 14 promoter.

143 g the 2C and HY ligands under control of the keratin 14 promoter.

144 ated Ras fusion in transgenic mice using the keratin 14 promoter.

145 ncogenes of HPV16 under control of the human keratin-14 promoter (K14-HPV16 transgenic mice) and nont

146 -specific expression of RIP4 using the human keratin-14 promoter (K14-RIP4).

147 r root sheath under the control of the human keratin-14 promoter (K14/Bcl-2).

148 he murine epidermis under the control of the keratin-14 promoter and showed that E7 is carcinogenic i

149 e expressing survivin under the control of a keratin-14 promoter developed normally, without histolog

150 hat overexpress PTHrP by virtue of the human keratin-14 promoter displayed a thickened ventral epider

151 Cre transgene under the control of the human keratin-14 promoter show robust Cre expression in the am

152 rate in bitransgenic mice expressed from the keratin-14 promoter to enhance carcinoma development in

153 -jun (TAM67), under the control of the human keratin-14 promoter, is expressed specifically in the ba

154 n-1 in mouse epidermis, under control of the keratin-14 promoter.

155 erexpression of Foxn1 is driven by the human keratin-14 promoter.

156 l expressing Shh in basal epithelium under a Keratin-14 promoter.

157 sing soluble OVA (sOVA) under control of the keratin-14 promoter.

158 E7 oncogenes, under the control of the human keratin-14 promoter/enhancer.

159 under the control of the nestin, albumin, or keratin-14 promoters, all of which turn on during embryo

160 either an abnormal keratin 5 or an abnormal keratin 14 protein, which compromises the structure and

161 inal, middle, and C-terminal portions of the keratin 14 protein.

162 stochemistry showed that metallothionein and keratin 14 proteins were overexpressed in zinc-deficient

163 kin and although an increase was observed in keratin 14-PTHrP transgenic animals, their epidermis did

164 ed by overexpression of a Smad2 transgene in Keratin 14-synthesizing MEE cells following mating Tgf-b

165 The keratin-14-TAM67 transgene was expressed in the epidermi

166 , BMP antagonist noggin was used to generate keratin 14-targeted transgenic mice.

167 stage, whereas a forth cluster that included keratin 14 tended to be associated with tumor size.

168 d the basal layer of mouse epidermis using a keratin 14 vector (K14.MYC2).

169 f many genes, including trefoil factor 1 and keratin 14, were inhibited by greater than 90% by TCDD.

170 nd of biomarkers such as S100A8, S100A7, and keratin 14, which reflect the antimicrobial and hyperpro

171 utations in keratins K5 (keratin 5) and K14 (keratin 14), with fragility of basal keratinocytes leadi