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1 dy was to determine the role of mitoStat3 in epidermal keratinocytes.
2 tes the proliferation and differentiation of epidermal keratinocytes.
3 kin tissue environment has limited effect on epidermal keratinocytes.
4 ostasis, we conditionally knocked out SRF in epidermal keratinocytes.
5 rganotypic three-dimensional cultures of rat epidermal keratinocytes.
6 normal human fibroblasts and neonatal human epidermal keratinocytes.
7 g-term ex vivo expansion of functional human epidermal keratinocytes.
8 ted the effect of Mg(2+) on TRPV3 in primary epidermal keratinocytes.
9 ages, and myelomonocytic cells as well as in epidermal keratinocytes.
10 n HSV-1 infection and their interaction with epidermal keratinocytes.
11 re produced by placenta, adrenal glands, and epidermal keratinocytes.
12 ar signals mediating cell differentiation in epidermal keratinocytes.
13 o cellular components of the skin, including epidermal keratinocytes.
14 , and modulating TGF-beta signaling in mouse epidermal keratinocytes.
15 als for UVB irradiation-induced apoptosis in epidermal keratinocytes.
16 further elaborate the desmosome proteome in epidermal keratinocytes.
17 ontact or were physically separated from the epidermal keratinocytes.
18 del, correlating with K17 induction in basal epidermal keratinocytes.
19 e also attenuated by chrysin pretreatment of epidermal keratinocytes.
20 l regulator that promotes differentiation in epidermal keratinocytes.
21 ortant roles in the survival and motility of epidermal keratinocytes.
22 ance of proliferation and differentiation in epidermal keratinocytes.
23 ted in cSCC cells compared with normal human epidermal keratinocytes.
24 adhesion molecule expression and function in epidermal keratinocytes.
25 lammatory skin and in the differentiation of epidermal keratinocytes.
26 EP2 to the plasma membrane of differentiated epidermal keratinocytes.
27 et of the TNF alpha-regulated genes in human epidermal keratinocytes.
28 d the expression of endogenous TRPC in human epidermal keratinocytes.
29 CCL20 and antimicrobial peptide release from epidermal keratinocytes.
30 C/EBPalpha is abundantly expressed in mouse epidermal keratinocytes.
31 cells responded more quickly to therapy than epidermal keratinocytes.
32 a) is an important regulator of apoptosis in epidermal keratinocytes.
33 results were obtained by using normal human epidermal keratinocytes.
34 ory neurons but are highly expressed in skin epidermal keratinocytes.
35 kappa B (NF-kappaB) pathways in normal human epidermal keratinocytes.
36 omplex regulation of Col7a1 transcription in epidermal keratinocytes.
37 s the predominant species expressed in basal epidermal keratinocytes.
38 imus block activation of calcineurin/NFAT in epidermal keratinocytes.
39 T1 was predominantly nuclear in normal basal epidermal keratinocytes.
40 al differentiation and hyperproliferation of epidermal keratinocytes.
41 d that p63 promotes glycolytic metabolism in epidermal keratinocytes.
42 ependent fashion with predominant effects on epidermal keratinocytes.
43 ons is an enhancer element that is active in epidermal keratinocytes.
44 yaluronan synthase (HAS) activation in human epidermal keratinocytes.
45 cutaneous IL-33 reduces REG3A expression in epidermal keratinocytes.
46 xygen species and extensive apoptosis of the epidermal keratinocytes.
47 dermal junction and accompanying necrosis of epidermal keratinocytes.
48 is a water and glycerol channel expressed in epidermal keratinocytes.
49 intermediate filament (IF) network of basal epidermal keratinocytes.
50 of intercellular adhesions between mammalian epidermal keratinocytes.
51 nt directional migration in undifferentiated epidermal keratinocytes.
52 mice lacking p53-mediated POMC induction in epidermal keratinocytes.
54 rough specific toll-like receptors (TLRs) in epidermal keratinocytes, a DFE-induced murine atopic der
56 , the major autoantigen in PV, cause loss of epidermal keratinocyte adhesion, resulting in blisters a
59 date the role of IL-6 in skin wound healing, epidermal keratinocyte and dermal fibroblast cells were
60 L2 and of IFNgamma-induced CCL8 and CXL10 by epidermal keratinocytes and (3) thereby limited the recr
62 and MARCO reduced SNA uptake in normal human epidermal keratinocytes and 3D rafts after topical appli
66 t STRA6 is constitutively expressed in human epidermal keratinocytes and dermal fibroblasts and is re
67 hich inactivates cortisol), was expressed in epidermal keratinocytes and dermal fibroblasts in human
72 mobility group box 1 (HMGB1) from UV-damaged epidermal keratinocytes and driven by Toll-like receptor
74 (ERK) activation in both normal human adult epidermal keratinocytes and five of seven SCCHN cell lin
75 ed the role of several coactivators in human epidermal keratinocytes and found that, although these c
77 proapoptotic and proinflammatory actions on epidermal keratinocytes and has been implicated in the p
78 3 channel (TRPV3) is abundantly expressed in epidermal keratinocytes and has important roles in senso
79 ng cyclin-dependent kinase 4 (Cdk4) in human epidermal keratinocytes and human mammary epithelial cel
80 a transporter-directed RNAi screen in human epidermal keratinocytes and identified SLC22A20 (OAT6) a
82 leading to the accumulation of mutations in epidermal keratinocytes and immunosuppression, which con
84 d that C/EBPalpha is induced in normal human epidermal keratinocytes and in the epidermis of human su
85 zed by IgG autoantibodies (AuAbs) binding to epidermal keratinocytes and inducing this devastating di
87 cation is the final differentiative step for epidermal keratinocytes and involves dramatic cell conde
88 ncrease in H2O2 was observed in normal human epidermal keratinocytes and its production was inhibited
90 ied indeed a functioning GFRP/GTPCHI axis in epidermal keratinocytes and melanocytes in the cytosol,
91 of 0.05-J/cm(2) reduced melanin pigments in epidermal keratinocytes and melanocytes, compared to unt
92 rolled by skin-specific factors derived from epidermal keratinocytes and not by resident dendritic ce
93 reted cysteine-rich protein, is expressed by epidermal keratinocytes and sebocytes and serves as an a
95 nal diacylglycerol/phorbol ester receptor in epidermal keratinocytes and suggest that activation of t
96 hat HVEM and LTbetaR were expressed on human epidermal keratinocytes and that LIGHT could directly pr
97 that AQP3 has a pro-differentiative role in epidermal keratinocytes and that PLD2 activity is necess
98 sly shown that RasGRP1 is expressed in mouse epidermal keratinocytes and that transgenic mice overexp
99 itin sulfate proteoglycan 4) was detected in epidermal keratinocytes and the cardiac conduction syste
100 creased SIRT1 protein levels in normal human epidermal keratinocytes and the immortalized keratinocyt
102 pholipase-A2 type X (sPLA2-X) is released by epidermal keratinocytes and we have shown that lysophosp
103 of Agouti transcripts and protein in primary epidermal keratinocytes, and BMP signaling positively re
104 --a stimulus of angiogenesis--is produced by epidermal keratinocytes, and elevated levels have been f
105 of wound repair, predominantly expressed in epidermal keratinocytes, and peaked in the subsequent pr
106 these cells fail to transdifferentiate into epidermal keratinocytes, and there was no improvement in
107 potent chemotactic and mitogenic factor for epidermal keratinocytes, and these properties are centra
108 sions, and migration and that differentiated epidermal keratinocytes are a component of the stem cell
112 higher levels of endogenous bcl-2 protein in epidermal keratinocytes as assessed by immunoblotting an
113 alterations in growth and differentiation of epidermal keratinocytes, as well as a marked increase in
114 city accompanied by MIF release in mouse ear epidermal keratinocytes, as well as in human keratinocyt
117 nal in TPA-induced shedding of TNFalpha from epidermal keratinocytes; (b) PKCepsilon-mediated signals
119 the transcriptional activity of NFkappaB in epidermal keratinocytes, both under basal treatment and
120 s cell carcinoma (SCC) are both derived from epidermal keratinocytes but are phenotypically diverse.
121 physiology of the cornified cell envelope in epidermal keratinocytes but may reside in the challenges
122 inally thought of as a disorder primarily of epidermal keratinocytes, but is now recognised as one of
123 , the results indicate that HSV enters human epidermal keratinocytes, but not neurons, by a low-pH, e
125 intrinsic sensory transduction mechanisms in epidermal keratinocytes can directly elicit AP firing in
127 ltaNp63alpha overexpression in primary human epidermal keratinocytes causes decreased cell proliferat
129 A treatment was observed in the immortalized epidermal keratinocyte cell line NHEK-HPV, whereas PMA d
131 isplayed increased DMBA-induced apoptosis in epidermal keratinocytes compared to wild-type mice.
136 ction of ODC activity did not rescue primary epidermal keratinocyte cultures isolated from ODCER2 mic
137 the culmination of signals exchanged between epidermal keratinocytes, dermal fibroblasts and leukocyt
140 mber, functions as an important regulator of epidermal keratinocyte differentiation and survival.
141 order chromatin remodeling in the context of epidermal keratinocyte differentiation in the skin.
148 ologous or allogeneic dermal fibroblasts and epidermal keratinocytes directly into an injured area, r
151 domain (TRADD)-dependent TNFR1 signaling in epidermal keratinocytes drives skin inflammation in Shar
152 cluding bone and cartilage, but not in basal epidermal keratinocytes, exhibit normal epidermal differ
154 holipid classes was measured in normal human epidermal keratinocytes exposed to cumene hydroperoxide
157 ere was a paracellular barrier defect in rat epidermal keratinocytes expressing a Ppp2r2a siRNA.
158 g, the dermal fibroblast has advantages over epidermal keratinocytes for delivering C7 to DEB patient
161 ts on matched primary dermal fibroblasts and epidermal keratinocytes from human donors on three bioma
163 phenotype through the transgenic delivery of epidermal keratinocyte growth factors or inflammatory me
164 induced skin cancer using immortalized human epidermal keratinocyte (HaCaT) cells through repetitive
165 212 murine cell line keratinocytes and human epidermal keratinocytes (HEK), express cell-surface GITR
166 sion was evaluated in cytokine-treated human epidermal keratinocytes (HEK)s, murine PAM 212 cell line
167 vels of miR-205 and miR-184 in primary human epidermal keratinocytes (HEKs) and corneal epithelial ke
168 Elevating FIH-1 levels in primary human epidermal keratinocytes (HEKs) and human corneal epithel
169 variants that are expressed in primary human epidermal keratinocytes (HEKs) and the biochemical activ
170 ions of select target genes in primary human epidermal keratinocytes (HEKs) using chromatin immunopre
174 th layered autologous dermal fibroblasts and epidermal keratinocytes in a hydrogel carrier showed rap
175 nking activities in cultured human and mouse epidermal keratinocytes in a modified in situ assay.
176 crease in integrin alpha9beta1 expression in epidermal keratinocytes in cutaneous and corneal wounds.
177 nstream signaling is strongly induced within epidermal keratinocytes in cutaneous psoriatic lesions,
178 for effects on human dermal fibroblasts and epidermal keratinocytes in monolayer culture, and for ef
180 eta(-/-) mice exhibit increased apoptosis in epidermal keratinocytes in response to carcinogen treatm
181 ar function of Merlin in AJ establishment in epidermal keratinocytes in vitro and confirm that a role
186 e transcription factor, AHR, in normal human epidermal keratinocytes increased AHR binding in the gen
188 in a variety of cell lines and primary human epidermal keratinocytes, indicating that the protein was
189 ith loss of Connexin 26 and Connexin 30 from epidermal keratinocyte intercellular junctions and accum
191 he sonic hedgehog (shh) signaling pathway in epidermal keratinocytes is a primary event leading to th
192 otype whereby intercellular adhesion between epidermal keratinocytes is disrupted, adversely affectin
195 esults not only reveal how UV irradiation of epidermal keratinocytes is sensed by the innate immune s
196 utaneous wounds, the number of proliferating epidermal keratinocytes is significantly reduced in K14-
197 sults indicate that the inhibition of JNK in epidermal keratinocytes is sufficient to initiate their
198 tingly, the prolonged expression of Snail in epidermal keratinocytes is sufficient to recapitulate ea
199 neage-committed human cells, including human epidermal keratinocytes, JARID2 predominantly exists as
200 (PKC) isoforms have been associated with the epidermal keratinocyte (KC) granular layer differentiati
201 ripheral blood mononuclear cells (PBMCs) and epidermal keratinocytes (KC) from patients with psoriasi
204 During malignant transformation in skin, epidermal keratinocytes (KCs) frequently acquire the cap
205 und that IFN-beta was abundantly produced by epidermal keratinocytes (KCs) in psoriasis and during wo
210 sufficient retinoic acid synthesis by keloid epidermal keratinocytes may contribute to the pathogenes
213 of cSCC cell lines (n = 8) and normal human epidermal keratinocytes (n = 11) with real-time quantita
214 tutively expressed in cultured normal canine epidermal keratinocytes (NCEKs), and its expression leve
215 easible to discriminate between normal human epidermal keratinocytes (NHEK) and dermal fibroblasts (N
216 n peroxide (H(2)O(2)) levels in normal human epidermal keratinocytes (NHEK) and melanocytes (mel) wer
217 ific keratins K1, K10 and K2 in normal human epidermal keratinocytes (NHEK) and two important cell li
218 melanin effectively prevented neonatal human epidermal keratinocytes (NHEK) from G2/M phase arrest un
219 ifferentiated or differentiated normal human epidermal keratinocytes (NHEK) in culture, but is dramat
220 yme was detected in cultures of normal human epidermal keratinocytes (NHEK) in response to Ca(2+)-ind
221 owed that EGCG treatment of the normal human epidermal keratinocytes (NHEK) inhibits ultraviolet (UV)
222 ation of DNA ligase in cultured normal human epidermal keratinocytes (NHEK) on exposure to the DNA-da
223 how that a single low-dose exposure of human epidermal keratinocytes (NHEK) to an FS20 light source i
227 ration and apoptosis studies in normal human epidermal keratinocytes (NHEKs) were conducted by MTT (3
233 was significantly elevated (17-fold) in the epidermal keratinocytes of 7,12-dimethylbenz[a]anthracen
234 are intrinsic to cutaneous neurons and that epidermal keratinocytes only modulate this transduction.
237 carcinogen-treated transgenic skin, whereas epidermal keratinocyte proliferation in vitro was not af
238 No significant differences in TPA-induced epidermal keratinocyte proliferation were observed in C/
239 and displayed no detectable abnormalities in epidermal keratinocyte proliferation, differentiation, o
241 differentiation in monolayer cultures of rat epidermal keratinocytes (REKs), but high PpIX signals we
242 cycle exit and differentiation of suprabasal epidermal keratinocytes require nuclear IkappaB kinase a
243 homeostasis and terminal differentiation of epidermal keratinocytes required for formation of the sk
244 differentiation-mitosis checkpoint in human epidermal keratinocytes, resulting in impaired cell divi
245 in the maturation and activity of ADAM17 in epidermal keratinocytes, resulting in significantly upre
246 X receptor (RXR)-alpha and RXR-beta in mouse epidermal keratinocytes (RXR-alphabeta(ep-/-)) or a topi
247 factor-2 in skin of mice lacking RXRalpha in epidermal keratinocytes (RXRalpha(ep-/-) mice), which in
248 s bacterial supernatant-treated normal human epidermal keratinocytes, S1PR1 knockdown reduced IL36G,
249 xpressed only by thymic epithelial cells and epidermal keratinocytes, Skint-1 drives specifically the
251 T pathway as new molecular targets of CsA in epidermal keratinocytes, suggesting a previously unknown
252 ression of CTIP2 was ablated specifically in epidermal keratinocytes, suggests that CTIP2 functions i
253 Fra-1 and Fra-2) that are key controllers of epidermal keratinocyte survival and differentiation, and
256 ls of VEGF protein and mRNA were observed in epidermal keratinocytes than in oral keratinocytes after
257 e to microbial component-mimicking agents in epidermal keratinocytes that form the physical barrier o
258 tive correlations included the morphology of epidermal keratinocytes, the appearance of nests of nevu
259 ling after a calcium switch in primary human epidermal keratinocytes, the loss of this receptor did n
262 in-specific factor(s) derived primarily from epidermal keratinocytes, thereby providing a mechanism f
263 alpha-2-glycoprotein is normally produced by epidermal keratinocytes, these studies raise the possibi
264 ifferentiation and inhibits proliferation in epidermal keratinocytes through interaction with the vit
265 tips, where they are transferred to adjacent epidermal keratinocytes through pathways that involve mi
266 ore, we propose that loss of cell contact in epidermal keratinocytes through reactive oxygen species-
267 ns resulting from exposure of cultured human epidermal keratinocytes to arsenite and antimonite in co
268 expression of KLK5 and KLK7 in normal human epidermal keratinocytes to better understand how these m
269 fic IQGAP requirement in vivo, we engineered epidermal keratinocytes to express individual IQGAP prot
270 epidermal growth factor (EGF) stimulation of epidermal keratinocytes to initiate the cell migration c
272 se characterized by reduced adherence of the epidermal keratinocytes to the underlying dermis, and is
274 itochondrial apoptotic signaling pathways in epidermal keratinocytes, triggering apoptosis and afford
275 In transgenic mice overexpressing Bmx in epidermal keratinocytes, tumors induced by a two-stage c
276 ed transgenic mice that overexpress TRPV3 in epidermal keratinocytes under the control of the keratin
278 The major cell type of the epidermis, the epidermal keratinocyte, undergoes a carefully choreograp
281 tional responses to ultraviolet radiation in epidermal keratinocytes using microarray chips containin
282 geted the overexpression of RasGRP1 to basal epidermal keratinocytes using the keratin 5 promoter.
283 ion in ultraviolet-B-irradiated normal human epidermal keratinocytes was also assessed and correlated
284 rehensively the JNK-regulated genes in human epidermal keratinocytes, we compared the transcriptional
285 16) E6 and E7 gene-immortalized normal human epidermal keratinocytes, we demonstrated intracellular a
287 ma on human skin cells, primary normal human epidermal keratinocytes were exposed to ultraviolet-B ra
289 recently shown expression of RasGRP1 in the epidermal keratinocytes where it can mediate Ras activat
290 integrin alpha3beta1 is highly expressed in epidermal keratinocytes, where it regulates both cell-au
292 demonstrated that treatment of normal human epidermal keratinocytes with cis-UCA resulted in increas
294 To address this issue, we treated human epidermal keratinocytes with five EFNAs individually and
295 day revealed a functional circadian clock in epidermal keratinocytes with hundreds of transcripts reg
296 as altered differentiation and activation of epidermal keratinocytes with increased expression of hai
297 fibroblasts led to increased invasiveness of epidermal keratinocytes with pre-malignant features.
298 However, direct treatment of normal human epidermal keratinocytes with S1P increased the expressio
299 e presence of functional opioid receptors on epidermal keratinocytes, with attendant regulation of ke
300 tured human skin, or isolated cultured human epidermal keratinocytes, with triiodothyronine (100 pmol