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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 n between invasion and protein expression of Keratin 14, a known biomarker for poor prognosis, with p
7 e changes as well as increased expression of keratin 14, a marker of immature keratinocytes.
8 del that allows focal activation of a mutant keratin 14 allele in epidermal stem cells upon topical a
9  staining revealed supra-basal expression of keratin 14 and decreased expression of differentiation-a
10            Both basal cell types up-regulate keratin 14 and generate a broadly distributed, abundant,
11 nd an increase in luminal cells that express keratin 14 and integrin-alpha6, a phenotype that is usua
12 n markers characteristic of its final state (keratin 14 and involucrin).
13 f other epithelially expressed genes such as keratin 14 and the desmoglein genes DSG1 and DSG3.
14 ugh the expression of the basal layer marker keratin 14 and the differentiation marker keratin 1 was
15 urface but increased total protein levels of keratin-14 and beta1 integrins.
16 terminal differentiation including decreased keratin-14 and increased involucrin expression.
17 abasal cells were misaligned and coexpressed keratins 14 and 10.
18 cer cells led to cell blebbing and a loss of keratins 14 and 18, in addition to the upregulation of v
19                                              Keratins 14 and 5 are the structural hallmarks of the ba
20 MO (smoothened), p63, SLUG (snail-2), KER14 (keratin-14) and VIM (vimentin)).
21 ion, we chose one of the identified targets, keratin 14, and prepared recombinant proteins encompassi
22 are heterogeneous and identify and isolate a keratin 14- and cadherin-3-positive subpopulation suffic
23     The authors show that hemicentin-1 binds keratin 14 at the protein level and that silencing HMCN1
24 vivo models of metastasis, we establish that keratin-14+ breast cancer cells are vulnerable to NK cel
25 the migrating front of epidermis stained for keratin 14, but only the basal cells expressed collagena
26 s on cell-cell adhesion in vivo, we utilized keratin-14 cre-recombinase (K14-cre) to inactivate Flcn
27 is study, we crossed Fam20C(fl/fl) mice with keratin 14-Cre (K14-Cre) transgenic mice to specifically
28 with loxP-flanked PRPK alleles, crossed with keratin 14-Cre (K14.Cre) mice.
29 s of FTase and GGTase-I, respectively) and a keratin 14-Cre transgene to create mice lacking FTase or
30                                    Using the keratin 14-Cre transgene, we bred mice lacking the expre
31                               Here, by using Keratin 14-Cre-driven ablation of Tet genes in skin epit
32 ce bearing the floxed C/EBPalpha allele with keratin-14-Cre mice generate C/EBPalpha conditional knoc
33 P expression in the enamel epithelium with a keratin 14-driven transgene corrects the defect in bone
34 ith a floxed fak allele under the control of keratin-14-driven Cre fused to a modified estrogen recep
35 s type 16 (HPV16) under control of the human keratin-14 enhancer/promoter (K14-HPV16 transgenic mice)
36 ion mass spectrometry imaging and identified keratin 14-expressing (K14-expressing) keratinocytes exe
37 thelium demonstrated that two multipotential keratin 14-expressing cells (K14ECs) function as progeni
38  generates mitochondrial oxidative stress in keratin 14-expressing epidermal stem/progenitor cells in
39 e genetically deleted AMPK within all adult, keratin 14-expressing KCs of mice.
40 ed a mouse with a deletion of p63 exon 13 in keratin-14-expressing tissues and employed transcriptome
41 overexpression of TSP-1 in the skin, using a keratin 14 expression cassette.
42   In addition, we show that decreased mutant keratin 14 expression resulted in normal morphology and
43                                              Keratin 14 expression, a basal keratinocyte marker, was
44      All flow-sorted cells were positive for keratin 14 expression, and negative for keratin 1, loric
45 ith PMA treatment, but A23187 did not affect keratin 14 expression.
46 tudy, we analyzed the structure of keratin 5/keratin 14 filaments within ghost mouse keratinocytes by
47  excessively targeting intermediate filament keratin-14 for proteasomal degradation, ultimately causi
48                                              Keratin 14-Fyn (K14) transgenic mice were derived to cha
49 ggesting that POU domain factors may repress keratin 14 gene expression by interfering with the activ
50 /p300 co-activators are strong activators of keratin 14 gene expression, acting through sequences clo
51 essing NT4 in skin, under the control of the keratin 14 gene promoter, were examined.
52                            The region of the keratin 14 gene sufficient and required for repression b
53                            The keratin 5 and keratin 14 genes encode proteins that form the primary s
54 r heterozygous mutations in the keratin 5 or keratin 14 genes, KRT5 and KRT14, respectively, whereas
55 t)) in epidermal basal cells driven by human keratin 14 (HK14) or bovine keratin 5 (BK5) promoters, r
56        To test this, we used the preclinical keratin-14-HPV8 transgenic mouse model, which develops s
57 se model of epithelial carcinogenesis [i.e., keratin 14-human papillomavirus 16 (K14-HPV16) transgeni
58                                Virgin female keratin 14-human papillomavirus 16 transgenic mice were
59   Iron was increased up to 2-fold in hair of keratin 14-human transferrin receptor (hTfR) transgenics
60 es of point substitutions with the keratin 5/keratin 14 IF system.
61 expression of involucrin and keratins-10 and keratins-14 in the epidermis, indicating their stimulato
62 d in the central alpha-helical rod domain of keratin 14 is necessary for the formation of a stable pe
63 ate filament (IF) proteins keratin 5 (K5) or keratin 14 (K14) cause epidermolysis bullosa simplex (EB
64 from dominant mutations in keratin 5 (K5) or keratin 14 (K14) genes, encoding the intermediate filame
65 homotypic disulfide bond involving Cys367 in keratin 14 (K14) occurs in an atomic-resolution structur
66 BS are due to dominantly acting mutations in keratin 14 (K14) or K5, the type I and II intermediate f
67 due to dominantly acting mutations in either keratin 14 (K14) or K5, the type I and II intermediate f
68 ne-bound form of OVA in skin under the human keratin 14 (K14) promoter (K14-mOVA mice).
69 o the basal layer of the epidermis using the keratin 14 (K14) promoter (K14.MCM7).
70 2 directed to these sites in the skin by the keratin 14 (K14) promoter produces prominent hair follic
71                             We have used the keratin 14 (K14) promoter to re-express a class II MHC a
72 ing membrane ovalbumin (mOVA), driven by the keratin 14 (K14) promoter, developed GVHD-like mucocutan
73  a downstream effector of Ras, driven by the keratin 14 (K14) promoter, has been used to test the hyp
74           Using a previously described human keratin 14 (K14) promoter, we created mice expressing a
75 17-kDa IL-1 alpha in the epidermis under the keratin 14 (K14) promoter.
76  terminus, E6(Delta 146-151), from the human keratin 14 (K14) promoter.
77  (CreER(tam)) under the control of the human keratin 14 (K14) promoter.
78 cken ovalbumin (OVA), under the control of a keratin 14 (K14) promoter.
79 ibitor noggin or BMP4 under the control of a keratin 14 (K14) promoter.
80            The intermediate filament protein keratin 14 (K14) provides vital structural support in ba
81 and development, epithelial cells expressing keratin 14 (K14) Sox2, Sox9, Sox10, and Trp63 give rise
82 several Msx-regulated genes (Bmp4, Fgf8, and keratin 14 (K14)) in BlC groups, including MSX1, MSX2, a
83                      We previously generated keratin 14 (K14)-A(beta)b mice expressing MHC class II o
84 oraphane (SF) ameliorates skin blistering in keratin 14 (K14)-deficient mice, correlating with the in
85                We identified a population of keratin 14 (K14)-expressing progenitor epithelial cells
86 utoreactive TCR-Tg CD8 T cells (OT-I cells), keratin 14 (K14)-mOVA(high) Tg mice developed autoreacti
87 pressed the epithelial cytoskeletal protein, keratin 14 (K14).
88 basal epidermal keratins, keratin 5 (K5) and keratin 14 (K14).
89 h EBS caused by mutations in KRT14, encoding keratin 14 (K14).
90 in type II (KtyII) K5 and its type I partner keratin 14 (K14).
91 sified by markers keratin 8/18 (K18, KRT18), keratin 14 (K14, KRT14) and estrogen receptor (ER, ESR1)
92 responses in keratinocyte cell lines lacking keratin 14 (K14-null mutation).
93 ther the Tyrosinase-Related Protein-1 or the keratin-14 (K14) promoter, the latter with and without a
94  derived from inversion heterozygotes, and a keratin-14 (K14) promoter-driven agouti minigene was int
95 al cells by regulatory elements of the human keratin-14 (K14) promoter.
96                           Immunostaining for Keratin-14 (K14) was used to delineate Hertwig's epithel
97 Tg) murine model of autoimmunity by crossing keratin-14 (K14)-soluble chicken ovalbumin (sOVA) mice,
98   We have generated a transgenic (Tg) mouse [keratin-14 (K14)-survivin] with skin expression of survi
99                                   The type I keratins 14 (K14) and 16 (K16) are distinct in their ass
100 ypoplastic, displaying reduced expression of Keratin 14, Keratin 1 and markers of proliferation.
101                                We found that keratin 14 (KRT14) marks the most primitive differentiat
102 s, we used a transgenic mouse model in which keratin 14 (KRT14) promoter-mediated overexpression of N
103    We report a mutation in the gene encoding keratin 14 (KRT14) that changes the predicted amino acid
104                                              Keratin 14 (KRT14, a biomarker in esophageal tumorigenes
105 t affect injury severity or proliferation of keratin 14(+) (KRT14(+)) basal progenitors or other urot
106 nomas that express high levels of C/EBPbeta, keratin-14, matrix metalloproteinase-3, and beta-catenin
107                                              Keratin 14-mediated Cre recombinase expression induced e
108 ession of the keratin 5 and 14 genes because keratin 14 mRNA expression persists in suprabasal cells
109 epidermal growth factor receptor, c-myc, and keratin 14 mRNAs comparable with the parental BC-1-Ep ke
110  stability by overexpression of the dominant keratin 14 mutation R416P inhibited the normal mechanica
111 fter removal of rapamycin and expressed more keratin 14, N-Cadherin, DeltaNp63 and ABCG2, and less ke
112 or pool is further divided into two subsets, keratin 14-negative and -positive.
113  and conditional deletion of Prdm1 in either Keratin 14- or Foxn1-expressing cells in mice resulted i
114 ined by cross-breeding experiments employing keratin 14-parathyroid hormone-related protein mice and
115 l types of hair were 30-40% shorter in adult keratin 14-parathyroid hormone-related protein mice as c
116                       The dorsal skin of the keratin 14-parathyroid hormone-related protein mouse was
117 se exostosin glycosyltransferase 1 (Ext1) in keratin 14-positive cells from P21.
118  on the Spdef promoter and that treatment of keratin 14-positive cells with TGFbeta inhibited SPDEF a
119                 Gain of function of Spdef in keratin 14-positive epithelia resulted in the ectopic fo
120  phenotype was associated with a decrease in keratin 14-positive myoepithelial cells in PyMT(mgko) tu
121 g growth factor beta receptor II (Tgfbr2) in keratin 14-positive stratified epithelia causes ocular s
122  was directed in its expression by the human keratin 14 promoter (hK14) to the basal layer of the epi
123  in vivo using transgenic mice driven by the keratin 14 promoter (K14).
124 nes for human papillomavirus type 16 under a keratin 14 promoter (K14-HPV16 mice) develop cervical ca
125  of transgenic mice under the control of the keratin 14 promoter and beta-catenin activity was induce
126                                            A keratin 14 promoter construct was used to produce transg
127 wing mating Tgf-beta3 heterozygous mice with Keratin 14 promoter directed Smad2 transgenic mice (K14-
128 ilized a transgenic mouse model in which the keratin 14 promoter drives expression of the entire HPV8
129 ronic VEGF overexpression in vivo, we used a keratin 14 promoter expression cassette containing the g
130 GF-2 in epidermal keratinocytes, driven by a keratin 14 promoter expression construct.
131  These studies underscore the utility of the keratin 14 promoter for expressing foreign transgenes in
132 optotic gene bcl-xL under the control of the keratin 14 promoter have significantly shorter hair than
133 nt negative c-jun (TAM-67) controlled by the keratin 14 promoter in ICR mice were used to determine t
134 o demonstrate that the activity of the human keratin 14 promoter remains high in adult skin and that
135 HrP-knockout mice under the direction of the keratin 14 promoter reversed the abnormalities seen in P
136                                          The keratin 14 promoter targeted the receptor primarily to b
137                                    Using the keratin 14 promoter to target expression of an activated
138 n of hair growth directly, we used the human keratin 14 promoter to target human vitamin D receptor e
139 nant negative mutant c-jun driven by a human keratin 14 promoter was co-transfected with AP-1 or NF-k
140                                    The human keratin 14 promoter was used to direct expression of mut
141 ling in murine limb development in vivo, the keratin 14 promoter was used to drive expression of the
142 lomavirus (HPV) type 16 under control of the keratin 14 promoter were analyzed by comparative genomic
143 ukemia virus long terminal repeat (LTR), the keratin 14 promoter, or the involucrin promoter was not
144 ing growth factor alpha under control of the keratin 14 promoter, Stat3 was constitutively activated.
145 overexpress COX-2 under control of the human keratin 14 promoter, which allows for expression in the
146 periments, both Skn-1a and Tst-1 repress the keratin 14 promoter, with the POU domain being sufficien
147 cted a transgene (K14-ARGE) encoding a human keratin 14 promoter-driven AR gene.
148  targeted expression of a transgene encoding keratin 14 promoter-driven human amphiregulin to the bas
149 ated Ras fusion in transgenic mice using the keratin 14 promoter.
150 tenin binding site, under the control of the keratin 14 promoter.
151 ress Smad2 in epidermis under the control of keratin 14 promoter.
152 ssion, acting through sequences close to the keratin 14 promoter.
153 thelial cells under the control of the human keratin 14 promoter.
154 Cepsilon) in their epidermis using the human keratin 14 promoter.
155  Cdelta (T7-PKCdelta) regulated by the human keratin 14 promoter.
156 transgene expressed under the control of the keratin 14 promoter.
157 he basal layer of the epidermis by the human keratin 14 promoter.
158 the basal layer of mouse epidermis using the keratin 14 promoter.
159 ermal keratinocytes under the control of the keratin 14 promoter.
160 ing progerin in epidermis under control of a keratin 14 promoter.
161 tical epithelial cells (cEC) using the human keratin 14 promoter.
162 g the 2C and HY ligands under control of the keratin 14 promoter.
163 ncogenes of HPV16 under control of the human keratin-14 promoter (K14-HPV16 transgenic mice) and nont
164 -specific expression of RIP4 using the human keratin-14 promoter (K14-RIP4).
165 r root sheath under the control of the human keratin-14 promoter (K14/Bcl-2).
166 he murine epidermis under the control of the keratin-14 promoter and showed that E7 is carcinogenic i
167 e expressing survivin under the control of a keratin-14 promoter developed normally, without histolog
168 hat overexpress PTHrP by virtue of the human keratin-14 promoter displayed a thickened ventral epider
169 Cre transgene under the control of the human keratin-14 promoter show robust Cre expression in the am
170 rate in bitransgenic mice expressed from the keratin-14 promoter to enhance carcinoma development in
171 -jun (TAM67), under the control of the human keratin-14 promoter, is expressed specifically in the ba
172 n-1 in mouse epidermis, under control of the keratin-14 promoter.
173 erexpression of Foxn1 is driven by the human keratin-14 promoter.
174 l expressing Shh in basal epithelium under a Keratin-14 promoter.
175 sing soluble OVA (sOVA) under control of the keratin-14 promoter.
176 E7 oncogenes, under the control of the human keratin-14 promoter/enhancer.
177 under the control of the nestin, albumin, or keratin-14 promoters, all of which turn on during embryo
178  either an abnormal keratin 5 or an abnormal keratin 14 protein, which compromises the structure and
179 inal, middle, and C-terminal portions of the keratin 14 protein.
180 stochemistry showed that metallothionein and keratin 14 proteins were overexpressed in zinc-deficient
181 kin and although an increase was observed in keratin 14-PTHrP transgenic animals, their epidermis did
182 ed by overexpression of a Smad2 transgene in Keratin 14-synthesizing MEE cells following mating Tgf-b
183                                          The keratin-14-TAM67 transgene was expressed in the epidermi
184 , BMP antagonist noggin was used to generate keratin 14-targeted transgenic mice.
185 stage, whereas a forth cluster that included keratin 14 tended to be associated with tumor size.
186 d the basal layer of mouse epidermis using a keratin 14 vector (K14.MYC2).
187        As desmin is the cardiac homologue of keratin-14, we hypothesized that KLHL24- N28 leads to ex
188 f many genes, including trefoil factor 1 and keratin 14, were inhibited by greater than 90% by TCDD.
189 nd of biomarkers such as S100A8, S100A7, and keratin 14, which reflect the antimicrobial and hyperpro
190 utations in keratins K5 (keratin 5) and K14 (keratin 14), with fragility of basal keratinocytes leadi

 
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