ライフサイエンスコーパス: epidermal

1 Measuring the opening shape of the epidermal actin cortex after laser nano-ablation, we ass

2 .ROCK(er)) were crossed with mice expressing epidermal-activated ras(Ha) (HK1.ras(1205)).

3 ibutes to the development and maintenance of epidermal alterations in psoriasis.

4 bility barrier induced similar elevations in epidermal and serum cytokine levels in normal and athymi

5 well as normalization of antibodies against epidermal and tissue transglutaminases.

6 ity barrier defect, which may originate from epidermal and/or peripheral changes in lipid and energy

7 was associated with acanthosis, disorganized epidermal architecture, and downregulation of several di

8 erent conduits of reduced path length across epidermal atrichoblast cell files.

9 it is the largest and most accessible organ, epidermal autografts and tissue-engineered skin equivale

10 junctivitis, relates to an intact epithelial/epidermal barrier during early childhood.

11 ted with execution of the genetic program of epidermal barrier formation, to a fully inactive conditi

12 of lamellar bodies, which are essential for epidermal barrier formation.

13 macrophages, and their skin also maintained epidermal barrier function compared with wild-type mice.

14 lthough both conditions are characterized by epidermal barrier impairment, AD also exhibits signs of

15 ated with generalized scaling, erythema, and epidermal barrier impairment.

16 obial activity but do not obviously regulate epidermal barrier integrity.

17 Null mutations in filaggrin (FLG), a key epidermal barrier protein, strongly predispose to AE; ho

18 p63 is a master regulator of epidermal biology, sustaining stemness and renewal capac

19 suggests a role for energetic metabolism in epidermal biology.

20 y fluid loss and higher mortality in a trans-epidermal body fluid loss test.

21 Using the ablation of epidermal caspase-8 as a model of wound healing in Mus m

22 In this study, we survey the epidermal cell differentiation in a systematic manner by

23 erived dendritic cell/inflammatory dendritic epidermal cell differentiation.

24 ost-transcriptional regulators of plant root epidermal cell fate.

25 ly reproducing plants, a single somatic, sub-epidermal cell in an ovule is selected to differentiate

26 80B1 mutants, underscoring the aberrant root epidermal cell patterning.

27 ence imaging that cdc-42 is not required for epidermal cell polarization or junction assembly, but ra

28 c plaques by inducing epidermal hyperplasia, epidermal cell proliferation, and recruitment of leukocy

29 o elongation, a process driven by asymmetric epidermal cell shape changes.

30 Cultured epidermal cell sheets (CES) containing undifferentiated

31 thway has the potential to similarly pattern epidermal cell types, we expanded the expression domain

32 This mutation decreases epidermal cell width but not length, and probably also r

33 insights into the regulation and function of epidermal cell-immune cell interactions and into how com

34 growth behavior was carried out by culturing epidermal cells and proliferation was quantified via via

35 rstitial-type DCs and inflammatory dendritic epidermal cells appearing in dermatitis/eczema lesions,

36 pathogen showing direct penetration of leaf epidermal cells comparable to G. orontii.

37 Expansion of ARF3 expression into lateral epidermal cells in a TAS3 ta-siRNA-insensitive mutant le

38 Guard cells and epidermal cells of hornworts show striking similarities

39 hanisms underlying nuclear movements in root epidermal cells remains limited.

40 s activation of many wound response genes in epidermal cells surrounding wound sites.

41 haped structure surrounds an opening between epidermal cells that facilitates the exchange of gases b

42 ith microbes that do not directly enter leaf epidermal cells were seemingly unaltered or showed even

43 icrotubule array architecture in light-grown epidermal cells with explicit reference to array pattern

44 The TEX1 protein was present in epidermal cells, but not in the germline, and, through T

45 itive activation of beta-catenin in adjacent epidermal cells, initiating the follicle gene expression

46 taneous squamous cell carcinoma, cSCC) human epidermal cells.

47 ariations in wall stiffness between adjacent epidermal cells.

48 We find that ATML1 is expressed in all epidermal cells.

49 rmination of cell division of the underlying epidermal cells.

50 ne comprising pObs and adjacent motile basal epidermal cells.

51 acid transporter primarily expressed in root epidermal cells.

52 dopsis plants and Nicotiana benthamiana leaf epidermal cells.

53 naling in Arabidopsis (Arabidopsis thaliana) epidermal cells; however, the immune signals that imping

54 This co-movement likely depends on epidermal cellular protrusions that directly contact pOb

55 , and imperceptible packaging with conformal epidermal contact.

56 or deficient in IL1-beta developed multiple epidermal cysts after chronic UVB exposure.

57 T cells would be differentially regulated by epidermal cytokine induction of specific IRF-controlled

58 Here, we explore the mechanism of acute epidermal damage in radiation dermatitis.

59 adherens junctions is pivotal for the acute epidermal damage in radiation dermatitis.

60 cally with ionizing radiation to promote the epidermal damage.

61 we assessed the potential autocrine role of epidermal-derived eicosanoids in FLG-associated versus F

62 p63 is a transcription factor essential for epidermal development and homeostasis.

63 In this short review, the roles of miRNA in epidermal development, psoriasis, cutaneous squamous cel

64 The epidermal differentiation complex (EDC) locus consists o

65 the same co-expression module, mapped to the epidermal differentiation complex, and exhibited differe

66 istically, Dnmt3a promotes the expression of epidermal differentiation genes by interacting with thei

67 DC and the transcriptional activation during epidermal differentiation suggested a cis-regulatory mec

68 f phosphoproteomic changes that occur during epidermal differentiation, and identifies RIPK-PKP1 sign

69 fected by TRAF3IP2 silencing are involved in epidermal differentiation, with early differentiation ge

70 ) and IV (FLG/FLG) HEEs showed impaired late epidermal differentiation.

71 and were enriched for genes associated with epidermal differentiation.

72 er capture Hi-C (CHi-C) was performed during epidermal differentiation.

73 ein1 (Dsg1) and Desmoplakin (Dp), to promote epidermal differentiation.

74 h between inflammatory diseases with similar epidermal disruption and overlapping epithelial inflamma

75 and serum inflammatory cytokines induced by epidermal dysfunction.

76 Epidermal dysmaturation, neutrophil exocytosis, perivasc

77 Recent development of epidermal electronics provides an enabling means to cont

78 pled with upregulation of genes that promote epidermal/epithelial cell barrier function.

79 Using human epidermal equivalents (HEEs) generated with keratinocyte

80 ast, the semidominant MED5b mutation reduced epidermal fluorescence4-3 (ref4-3) results in dwarfism a

81 glycerol channel, plays an important role in epidermal function, with studies showing its involvement

82 variety of molecular pathways, including the epidermal growth factor (EGF) pathway.

83 sforming growth factor alpha (TGF-alpha) and epidermal growth factor (EGF) share the same EGF recepto

84 Epidermal growth factor (EGF) was found to stimulate CAR

85 directed against the four highly constrained epidermal growth factor (EGF)-like domains of Pfs25 bloc

86 Heparin-binding epidermal growth factor (EGF)-like growth factor (HBEGF)

87 osphorylation site of NFAT3 was critical for epidermal growth factor (EGF)-stimulated cell transforma

88 ich correlated with increased invadopodia in epidermal growth factor (EGF)-stimulated cells.

89 reduces Ras membrane localization, inhibits epidermal growth factor (EGF)-stimulated Ras signaling a

90 tically engineered BLNs, which display human epidermal growth factor (hEGF) or anti-HER2 Affibody as

91 diac myofibroblasts secrete milk fat globule-epidermal growth factor 8 (MFG-E8), which promotes apopt

92 nation of IRDye 800-labeled therapeutic anti-epidermal growth factor antibody (cetuximab) showed sign

93 nted with a p38 MAPK signaling inhibitor and epidermal growth factor co-treatment.

94 cation, through engagement and activation of epidermal growth factor receptor (EGFR) and integrins on

95 on, Th2 cells required the expression of the epidermal growth factor receptor (EGFR) and of its ligan

96 Mutations in K-Ras and epidermal growth factor receptor (EGFR) are mutually exc

97 or receptor bound 2 (GRB2) to phosphorylated epidermal growth factor receptor (EGFR) as a model syste

98 Epidermal growth factor receptor (EGFR) family members p

99 ressed in keratinocytes, where together with epidermal growth factor receptor (EGFR) forms a signalin

100 The role of epidermal growth factor receptor (EGFR) inhibition in ch

101 Reversible epidermal growth factor receptor (EGFR) inhibitors promp

102 Epidermal growth factor receptor (EGFR) interacts with i

103 The specific targeting of oncogenic mutant epidermal growth factor receptor (EGFR) is a breakthroug

104 The epidermal growth factor receptor (EGFR) is a clinically

105 The epidermal growth factor receptor (EGFR) is a receptor ty

106 paring the concurrent administration of anti-epidermal growth factor receptor (EGFR) monoclonal antib

107 Here, using a beta-cell specific epidermal growth factor receptor (EGFR) null mouse, we s

108 8% (96/348) of patients were found to harbor epidermal growth factor receptor (EGFR) or Kristen rat s

109 epithelial cells had elevated ligand-induced epidermal growth factor receptor (EGFR) phosphorylation.

110 ogeneous expression of amplified and mutated epidermal growth factor receptor (EGFR) presents a subst

111 Epidermal growth factor receptor (EGFR) regulates many c

112 ular endothelial growth factor (VEGFR)-2 and epidermal growth factor receptor (EGFR) signaling by enh

113 Epidermal growth factor receptor (EGFR) signaling is a k

114 In addition, epidermal growth factor receptor (EGFR) signaling is reg

115 Aberrant epidermal growth factor receptor (EGFR) signaling is wid

116 Focusing on the epidermal growth factor receptor (EGFR) signaling networ

117 Despite decades of research in the epidermal growth factor receptor (EGFR) signalling field

118 l-validated solid tumor targets, such as the epidermal growth factor receptor (EGFR) that effectively

119 Current anti-epidermal growth factor receptor (EGFR) therapy for oral

120 Here, we find that LOX regulates the epidermal growth factor receptor (EGFR) to drive tumour

121 improved progression-free survival with the epidermal growth factor receptor (EGFR) tyrosine kinase

122 Stimulation of the epidermal growth factor receptor (EGFR) with EGF, the be

123 regulate chloride secretion, centred on the epidermal growth factor receptor (EGFr), are discussed.

124 the wound repair pathway, controlled by the epidermal growth factor receptor (EGFR), is critical to

125 ve been reported to regulate the function of epidermal growth factor receptor (EGFR), the effect of p

126 ell lines, which was accompanied by enhanced epidermal growth factor receptor (EGFR)-mediated mitogen

127 ing brain and leptomeningeal metastases-from epidermal growth factor receptor (EGFR)-mutant non-small

128 rsor cells, a well-characterized paradigm of epidermal growth factor receptor (EGFR)-Ras-ERK signalin

129 (SRS), whole-brain radiotherapy (WBRT), and epidermal growth factor receptor (EGFR)-tyrosine kinase

130 ped them into siRNA carriers targeted to the epidermal growth factor receptor (EGFR).

131 e demonstrated that RCN2 interacted with the epidermal growth factor receptor (EGFR).

132 es ErbB signaling by inhibiting formation of epidermal growth factor receptor (EGFR)/human epidermal

133 on of glioblastoma cells expressing a mutant epidermal growth factor receptor (EGFRvIII) is responsib

134 ons between the catalytically impaired human epidermal growth factor receptor (HER3/ERBB3) and its ca

135 pidermal growth factor receptor (EGFR)/human epidermal growth factor receptor 2 (HER2) and HER2/HER3

136 By simultaneously targeting the human epidermal growth factor receptor 2 (HER2) expressed by c

137 e receptor expression and negative for human epidermal growth factor receptor 2 (HER2) overexpression

138 sed, histopathologic classification of human epidermal growth factor receptor 2 (HER2) status in wome

139 rican Pathologists recommendations for human epidermal growth factor receptor 2 (HER2) testing in bre

140 or for the detection and estimation of human epidermal growth factor receptor 2 (HER2), a biomarker f

141 A-like tumors, 70.5% of luminal B-like human epidermal growth factor receptor 2 (HER2)-negative tumor

142 patient has hormone receptor-positive, human epidermal growth factor receptor 2 (HER2)-negative, node

143 In human epidermal growth factor receptor 2 (HER2)-positive breas

144 In neoadjuvant trials, treatment of human epidermal growth factor receptor 2 (HER2)-positive breas

145 r- and progesterone receptor-negative, human epidermal growth factor receptor 2 (HER2)-positive breas

146 edict the efficacy of chemotherapy and human epidermal growth factor receptor 2 (HER2, encoded by the

147 ecular subtypes: luminal A, luminal B, human epidermal growth factor receptor 2 enriched, and basal l

148 l aptamer-based assay for detection of human epidermal growth factor receptor 2 protein (HER2) cancer

149 egimens based on estrogen receptor and human epidermal growth factor receptor 2 status was also asses

150 eptor+, progesterone receptor+, and/or human epidermal growth factor receptor 2+ tumors.

151 proved IDFS in patients with high-risk human epidermal growth factor receptor 2-negative breast cance

152 For 145 human epidermal growth factor receptor 2-negative patients you

153 ry toxicity of trastuzumab therapy for human epidermal growth factor receptor 2-overexpressing (HER2-

154 umors (21% v 6%; P = .08), but not for human epidermal growth factor receptor 2-positive (luminal and

155 r adjuvant treatment of node-positive, human epidermal growth factor receptor 2-positive early-stage

156 esponse to RT, although, in our study, human epidermal growth factor receptor 2-positive tumors seeme

157 The human epidermal growth factor receptor 3 (HER3) is an interest

158 ression of MAN2A1-FER in 4 cell lines led to epidermal growth factor receptor activation of BRAF, MEK

159 d EV release and mitogenic content including epidermal growth factor receptor and c-Src.

160 ted metastasis suppressor interacts with the epidermal growth factor receptor and mediates its downst

161 Members of the epidermal growth factor receptor family (ErbB family) po

162 Purpuric drug eruptions caused by epidermal growth factor receptor inhibitors are uncommon

163 systemic antibiotic treatment; the doses of epidermal growth factor receptor inhibitors were also ch

164 aracterize purpuric skin eruptions caused by epidermal growth factor receptor inhibitors.

165 y rarely been reported in patients receiving epidermal growth factor receptor inhibitors.

166 the FER kinase inhibitor crizotinib and the epidermal growth factor receptor kinase inhibitor canert

167 Eps15 (epidermal growth factor receptor pathway substrate 15)-h

168 ol myristate acetate, Gq/11-coupled GPCR, or epidermal growth factor receptor stimulation promotes be

169 (PI3K) mediate the increase independently of epidermal growth factor receptor transactivation.

170 Epidermal growth factor receptor tyrosine kinase inhibit

171 tation, disease progression after first-line epidermal growth factor receptor tyrosine kinase inhibit

172 The epidermal growth factor receptor tyrosine kinase inhibit

173 binding fragments F(ab')2 and Fab) targeting epidermal growth factor receptor were labeled with Alexa

174 and c78(f/+) pancreata leads to reduction of epidermal growth factor receptor, which is critical for

175 The transcriptional regulation of the human epidermal growth factor receptor-2 (HER2) contributes to

176 ptors, including estrogen receptor and human epidermal growth factor receptor-2.

177 mmatory cytokine TNFalpha and ligands of the epidermal growth factor receptor.

178 Following gut epithelial damage, epidermal growth factor receptor/mitogen-activated prote

179 tective antigen, PA) which was redirected to Epidermal Growth Factor Receptors (EGFR) or to human EGF

180 ion of the ERK pathway in Gnb5(-/-) cells by epidermal growth factor restored M3R-stimulated insulin

181 This compound was used to link epidermal growth factor to genome-free MS2 viral capsids

182 agen matrix with and without the presence of epidermal growth factor to probe the intracellular mecha

183 O-Linked fucose modifications on Notch1 epidermal growth factor-like (EGF) domains 8 and 12 enga

184 Epidermal growth factor-like (EGF) repeats are also smal

185 Here we identify heparin-binding epidermal growth factor-like growth factor (HBEGF) as a

186 Heparin-binding epidermal growth factor-like growth factor promotes neur

187 ) and PCA-Tr (also known as delta/notch-like epidermal growth factor-related receptor [DNER]; 0.006%)

188 herin, which prevents secretion of mitogenic epidermal growth factors (EGFs) by repressing transcript

189 alterations, are barriers to effective anti-epidermal-growth-factor-receptor (EGFR) therapy.

190 ata from corneal epithelium were compared to epidermal hair follicle stem cell RNA-Seq to identify ge

191 d by qPCR corresponding to genes involved in epidermal homeostasis and dermal repair.

192 Epidermal homeostasis depends on a balance between stem

193 Epidermal homeostasis under normal and healing condition

194 nt role of the epigenetic regulator Ash1l in epidermal homeostasis.

195 (EGFR) forms a signaling complex regulating epidermal homeostasis.

196 all, or homeotic)-like (Drosophila)] develop epidermal hyperplasia and impaired epidermal stratificat

197 Steroids (particularly clobetasol) restored epidermal hyperplasia and terminal differentiation versu

198 ment of mature psoriatic plaques by inducing epidermal hyperplasia, epidermal cell proliferation, and

199 genic mice exhibited a significantly reduced epidermal hyperplasia, oxidative skin damage, and photoc

200 keratinocyte-derived inflammatory mediators, epidermal hyperproliferation, and increased neutrophil i

201 Establishment of dorsal-ventral epidermal identities and functions, in response to BMP s

202 To identify the epidermal initiating signals produced by DLX3-null kerat

203 After epidermal injury, barrier repair requires activation of

204 with neuropathic pain often show changes in epidermal innervation, although it remains to be elucida

205 s a complex interplay between these distinct epidermal integrins.

206 Here, the first epidermal-iontronic interface (EII) is successfully intr

207 ce of 3 or more atypical cells at the dermal-epidermal junction (DEJ) by RCM correlated with hyperpla

208 lture media and also localized to the dermal-epidermal junction in organotypic skin culture.

209 inophils induced separation along the dermal-epidermal junction of ex vivo skin.

210 of cSCC cell lines (n = 8) and normal human epidermal keratinocytes (n = 11) with real-time quantita

211 X receptor (RXR)-alpha and RXR-beta in mouse epidermal keratinocytes (RXR-alphabeta(ep-/-)) or a topi

212 itin sulfate proteoglycan 4) was detected in epidermal keratinocytes and the cardiac conduction syste

213 Terminally differentiating epidermal keratinocytes express a large number of struct

214 How p63 regulates metabolism in epidermal keratinocytes is incompletely understood, and

215 ore, we propose that loss of cell contact in epidermal keratinocytes through reactive oxygen species-

216 During terminal differentiation of the epidermal keratinocytes, the nucleus undergoes programme

217 al differentiation and hyperproliferation of epidermal keratinocytes.

218 d that p63 promotes glycolytic metabolism in epidermal keratinocytes.

219 ependent fashion with predominant effects on epidermal keratinocytes.

220 interactions of the head and tail domains of epidermal keratins 1 and 10, based on all-atom 3D simula

221 Compensation exhibited by adult GC receptor epidermal knockout mice demonstrated that keratinocyte-d

222 Use of GC receptor epidermal knockout mice with adrenalectomy allowed for t

223 al type 2 conventional DC subsets and not by epidermal Langerhans cells.

224 ic cells results in only one cell in the sub-epidermal layer differentiating into the megaspore mothe

225 that changes in stomatal development of the epidermal layer lead to coupled changes in the underlyin

226 rt of the keratinized cells of the cornified epidermal layer.

227 on of the critical barrier function of upper epidermal layers, causatively linked to environmental st

228 Epidermal LC and CD34LC express AhR and AhRR.

229 Notably, topical application of epidermal lipids from wild-type onto Pnpla1-mutant mice

230 hanges downstream of FLG deficiency in human epidermal living skin-equivalent (LSE) models and valida

231 ks the effect of epilation on follicular and epidermal melanocyte regeneration as well as skin and ha

232 on in zebrafish was associated with abnormal epidermal morphogenesis.

233 The influence of upregulated KLK5 on epidermal morphology was investigated using an in vivo s

234 Stevens-Johnson syndrome and toxic epidermal necrolysis (SJS/TEN) are rare but severe adver

235 Toxic epidermal necrolysis (TEN) and Stevens-Johnson Syndrome

236 Stevens-Johnson syndrome (SJS) and toxic epidermal necrolysis (TEN) are rare but life-threatening

237 Stevens-Johnson syndrome (SJS) and toxic epidermal necrolysis (TEN) are rare but life-threatening

238 uch as Stevens-Johnson syndrome (SJS), toxic epidermal necrolysis (TEN), or drug rash with eosinophil

239 ugh rare, Stevens-Johnson syndrome and toxic epidermal necrolysis remain among the most devastating o

240 ents with Stevens-Johnson syndrome and toxic epidermal necrolysis.

241 could similarly be associated with a loss of epidermal nerve fiber density (ENFD).

242 Epidermal nerve fiber density, the primary outcome, is a

243 data suggest that the pathology of the P2X3 epidermal nerve fibers can be selectively linked to neur

244 Multicellular glandular trichomes are epidermal outgrowths characterized by the presence of a

245 In agreement, low epidermal PAR3 and high P-cadherin expression correlate

246 Normal sun-exposed skin contains numerous epidermal patches that stain positive for p53 protein (p

247 The epidermal patterning factor (EPF) family of secreted sig

248 a a signaling cascade, which includes mobile EPIDERMAL PATTERNING FACTOR (EPF) peptides to enforce st

249 pment and germination, cuticle formation and epidermal patterning, vascular development, programmed c

250 urrent episodes of palmoplantar erythema and epidermal peeling.

251 CGI-58 die postnatally and exhibit a severe epidermal permeability barrier defect, which may origina

252 pecific Pnpla1-deficient neonates die due to epidermal permeability barrier defects with severe trans

253 ults show first that acute disruption of the epidermal permeability barrier in young mice leads not o

254 -MS/MS, transepidermal water loss (TEWL) and epidermal pH.

255 fy an unexpected non-cell autonomous role of epidermal polarity proteins, molecular determinants of c

256 This study presents a novel sustained epidermal powder delivery technology (sEPD) for safe, ef

257 at hair follicles is locally directed by an epidermal prepattern.

258 Tissue homeostasis of skin is sustained by epidermal progenitor cells localized within the basal la

259 Here we show that in the developing skin, epidermal progenitor cells of mice lacking p63 transcrip

260 y increases proliferative capacity of p63(+) epidermal progenitor cells, while preserving their abili

261 ound to be the most highly expressed PRMT in epidermal progenitors and the most downregulated PRMT du

262 we develop skin grafts from mouse and human epidermal progenitors that were engineered by CRISPR-med

263 soriasis-like phenotype severity and reduced epidermal proliferation and thickness in both the Rac1(V

264 Lgr6 downregulation in vivo causes increased epidermal proliferation with expanded lineage tracing fr

265 rtantly, we highlight disconnect between the epidermal proteome and transcriptome, emphasizing the ut

266 that GLI2 overexpression supported long-term epidermal regeneration in 3D organotypic cultures, and r

267 ence for a role of claudin-1 and occludin in epidermal regeneration with potential clinical importanc

268 ect of upregulated KLK5 on the expression of epidermal-related proteins and cytokines in keratinocyte

269 vestigation into the role of IL-1 ligands in epidermal repair and innate immune response after damagi

270 ganic layers, including continuous fields of epidermal scales and intact horn sheaths capping the bod

271 ion and to define conditions inducing dermal-epidermal separation (DES).

272 Dermal-epidermal separation by IL-5-activated eosinophils depen

273 Dermal-epidermal separation was assessed by light microscopy st

274 This Hh/Smo activity is driven by epidermal Sonic hedgehog a (Shha) rather than Ob-derived

275 Using epidermal specific TC-PTP knockout (K14Cre.Ptpn2(fl/fl))

276 Epidermal-specific deletion of the homeobox transcriptio

277 uit led to the identification of CNE 923, an epidermal-specific enhancer that was found to mediate ch

278 nt mice and found that PNPLA1 is crucial for epidermal sphingolipid synthesis.

279 t with the role of beta-catenin and SNAIL in epidermal stem cell maintenance.

280 iferation with expanded lineage tracing from epidermal stem cells positive for Lgr6 expression.

281 the robust number of Caenorhabditis elegans epidermal stem cells, known as seam cells, as a readout.

282 deployed in clinical applications, and skin epidermal stem/progenitor cells for generating such graf

283 ] develop epidermal hyperplasia and impaired epidermal stratification upon aging.

284 ients and murine models revealed an impaired epidermal structure, ascribed to aberrant secretion of l

285 knockdown may be responsible for an abnormal epidermal structure.

286 as 2.7 mm in depth with no ulceration of the epidermal surface.

287 The epidermal tattoo and textile sensors display a good repr

288 rnified envelope-1 (Lce1) family involved in epidermal terminal differentiation and of anticancer gen

289 Keratinocyte (KC) hyper-proliferation and epidermal thickening are characteristic features of psor

290 s to compound-driven reductions in erythema, epidermal thickening, and tissue cytokine levels.

291 y also resulted in a significant increase in epidermal thickness and hyperproliferation following exp

292 ts with psoriasis vulgaris, and it decreases epidermal thickness as well as T cell infiltration in th

293 AD correlated with immune (IL-13, IL-22) and epidermal (thickness, K16) measures in lesional and, eve

294 signature, deviating from previously studied epidermal tissues.

295 mis and upper dermis, exposing the powder to epidermal tissues.

296 inhibitory factor protects from nonmelanoma epidermal tumors by regulating the number of antigen-pre

297 pus erythematosus lesions showed significant epidermal up-regulation of IL-6 compared with control vi

298 Although rescue of epidermal wound closure in the absence of macrophages pr

299 ation, differentiation, and migration and in epidermal wound healing and barrier repair.

300 the large polygonal cells that were found in epidermal xenomas from flatfish from the Pacific Northwe