ライフサイエンスコーパス: keratinocyte

1 ding of melanin transfer from melanocytes to keratinocytes.

2 ubstitutions in UVB-irradiated primary human keratinocytes.

3 and differentiation of overlying epithelial keratinocytes.

4 ng human papillomavirus replication in human keratinocytes.

5 vivo expansion of functional human epidermal keratinocytes.

6 acting on rapidly proliferating hair matrix keratinocytes.

7 of inflammatory chemokines and cytokines by keratinocytes.

8 lls, but with interferon-kappa production by keratinocytes.

9 an TGM1, to deliver functional human TGM1 to keratinocytes.

10 SCF activates a transient c-kit receptor in keratinocytes.

11 ot Dsg1 molecules binding strength in murine keratinocytes.

12 uamous carcinoma cells and TERT-immortalized keratinocytes.

13 n-induced differentiation of mouse and human keratinocytes.

14 enuated by chrysin pretreatment of epidermal keratinocytes.

15 laborate the desmosome proteome in epidermal keratinocytes.

16 e signaling molecules, including T cells and keratinocytes.

17 dine dimers in Melan-A melanocytes and HaCaT keratinocytes.

18 the regulation of the NF-kappaB responses in keratinocytes.

19 C cells compared with normal human epidermal keratinocytes.

20 responsible for the endothelial response to keratinocytes.

21 nization and dynamics of keratin IFs in skin keratinocytes.

22 cept of nerve endings passing freely between keratinocytes.

23 nhibiting epithelial differentiation of skin keratinocytes.

24 lly restored melanin transfer to neighboring keratinocytes.

25 heir striking convergence in mouse and human keratinocytes.

26 cells and suppressed apoptosis of irradiated keratinocytes.

27 icIL-1Ra1 represents the major isoform in keratinocytes.

28 d melanocytes compared to surrounding bulbar keratinocytes.

29 ulation of caspase-1 and LUBAC activities in keratinocytes.

30 sion by suppressing IkappaBzeta induction in keratinocytes.

31 ed the number of mutations in UVB-irradiated keratinocytes.

32 mental systems to efficiently infect primary keratinocytes.

33 ion by signal transduction pathways in human keratinocytes.

34 induced by CARD14(E138A) signalling only in keratinocytes.

35 were unable to establish stable episomes in keratinocytes.

36 antimicrobial peptide release from epidermal keratinocytes.

37 ermal IL-23 injections and in IL-17A-treated keratinocytes.

38 regulated kinase signaling pathways in human keratinocytes.

39 and function in differentiating Krt14 C373A keratinocytes.

40 m of the IFNK gene driving its expression in keratinocytes.

41 ion of CIB1 to study the function of CIB1 in keratinocytes.

42 sions and in rafts derived from immortalized keratinocytes.

43 B-induced DNA damage in both melanocytes and keratinocytes.

44 ular functions through S1PR1-5, expressed by keratinocytes.

45 BE and delayed TJ formation in primary human keratinocytes.

46 ene expression of mast cells, monocytes, and keratinocytes.

47 nges could be replicated by IFN treatment of keratinocytes.

48 important modulators of melanin transfer to keratinocytes, a key process for epidermal UV photoprote

49 e miR-17~92 cluster or miR-19b alone in mice keratinocytes accelerated wound closure in vivo.

50 y showed significant decreases in markers of keratinocyte activation, epidermal thickness, KRT16 and

51 Here, we asked whether keratinocyte activity is also required for normal cold a

52 ng cellular constructs based on fibroblasts, keratinocytes alone or in combination have been develope

53 ugh recent studies have shown that epidermal keratinocytes also participate in sensory transduction,

54 the early response to dithranol belonged to keratinocyte and epidermal differentiation pathways and

55 We also noted aberrant keratinocyte and fibroblast migration in the Rhamm-null

56 Normal human epidermal keratinocytes and 3D raft treatment with SR-A inhibitors

57 reduced SNA uptake in normal human epidermal keratinocytes and 3D rafts after topical application, af

58 nism of SNA uptake in normal human epidermal keratinocytes and 3D skin equivalents.

59 s a skin-tropic virus that infects epidermal keratinocytes and causes chickenpox.

60 In vitro, OSM promoted invasiveness of keratinocytes and cuSCC cells and suppressed apoptosis o

61 ce the understanding of HPV control in human keratinocytes and development of NMSC.

62 the loss of S100A8 enhances proliferation of keratinocytes and disrupts keratinocyte differentiation.

63 omic repeats (CRISPR)-generated mutant fetal keratinocytes and Drosophila.

64 ES was generated from human keratinocytes and fibroblasts and was initially devoid o

65 ation by increasing migration of skin cells (keratinocytes and fibroblasts) and immune cells (neutrop

66 Rather, IFN-lambda activates keratinocytes and mesangial cells to produce chemokines

67 Blockage of TEAD activity by TEADi in human keratinocytes and mouse skin leads to reduced proliferat

68 Cultured keratinocytes and organotypic skin equivalents depleted

69 mechanism underlying efficient apoptosis in keratinocytes and provide further evidence of a cross-ta

70 pa is constitutively expressed in uninfected keratinocytes and responds only weakly to pattern recogn

71 e synaptic character of the contacts between keratinocytes and sensory neurons and their involvement

72 By providing selective communication between keratinocytes and sensory neurons, synaptic-like contact

73 tional approaches in cocultures of epidermal keratinocytes and sensory neurons.

74 involvement in sensory communication between keratinocytes and sensory neurons.

75 LAT1 expression is increased in keratinocytes and skin-infiltrating lymphocytes of psori

76 Furthermore, in vitro experiments with human keratinocytes and synovial fibroblasts were conducted.

77 These peptides were not toxic to human keratinocytes and the S. capitis extract did not kill ot

78 rproliferation, a reduced adherence of basal keratinocytes, and a gradual decrease in the stemness of

79 rons triggers necroptosis in RIPK1-deficient keratinocytes, and epidermis-specific deletion of MLKL p

80 HPVs infect human keratinocytes, and we previously reported that both PTPN

81 An increased rate of in situ keratinocyte apoptosis, which might contribute to skin h

82 migration and that differentiated epidermal keratinocytes are a component of the stem cell niche tha

83 aumbauer et al., 2015) has demonstrated that keratinocytes are also critical for normal mechanotransd

84 and human papillomavirus (HPV)-immortalized keratinocytes are altered in the presence of HPV genomes

85 er studies, we show that HPV16 E7-expressing keratinocytes are highly sensitive to metabolic stress i

86 sal layer of the epidermis where replicating keratinocytes are located.

87 addition, we show that galectin-8 levels in keratinocytes are positively correlated with the ability

88 Keratinocytes are the most abundant cell type in the epi

89 Conditional knockout of miR-17~92 in keratinocytes as well as injection of miR-19a/b and miR-

90 Incubation of normal human epidermal keratinocytes at 4(o)C or with sodium azide prevented SN

91 nally knocked out mice, we demonstrated that keratinocytes' autocrine production of SCF activates a t

92 f which the latter two are key regulators of keratinocyte biology.

93 for understanding TM disorders and modeling keratinocyte biology.

94 cinoma (SCC) are both derived from epidermal keratinocytes but are phenotypically diverse.

95 and contributes to the hyperproliferation of keratinocytes by maintaining centrosome integrity during

96 ntrols the terminal differentiation of HaCaT keratinocytes by modulating DeltaNp63alpha expression.

97 (95% CI) per 30 nmol = 1.42 (1.17-1.72)) and keratinocyte cancer (KC) (SRR (95% CI) per 30 nmol/L = 1

98 ite OTRs (HR 4.4, 95% CI 3.5-5.7, P < .001): keratinocyte cancers were more common in white OTRs (P <

99 In vitro studies with keratinocytes cannot fully model the complex viral and h

100 To improve the understanding of keratinocyte carcinogenesis, it is critical to understan

101 While 75% of all keratinocyte carcinoma (4 million annual cases in the Un

102 jor challenges faced when treating high-risk keratinocyte carcinoma (KC) is the unpredictable subclin

103 d biological pathways potentially altered in keratinocyte carcinoma, including enriched epidermal dev

104 Treatment of keratinocyte carcinomas requires an assessment of the ex

105 mentation with vitamin D or calcium prevents keratinocyte carcinomas, also known as nonmelanoma skin

106 Keratinocyte carcinomas, including basal and squamous ce

107 performance for preoperative demarcation of keratinocyte carcinomas.

108 ell extrusions, during which extruding outer keratinocytes carry out an entosis-like engulfment and e

109 A keratinocyte cell culture system using HaCat cells was e

110 ase 1/11-, caspase 8-, and RIPK3-independent keratinocyte cell death accompanied by the release of bo

111 re, we found that PABPN1 deficiency inhibits keratinocyte cell growth, which can be rescued by ectopi

112 These exhibited cytopathicity to a keratinocyte cell line and mediated pathological damage

113 -gamma], interleukin-1beta [IL-1beta], IL-6, keratinocyte chemoattractant [KC], and IL-10) were measu

114 Using calcium imaging, we determined that keratinocyte cold activity is conserved across mammalian

115 (differentiated) cells occurred in expanding keratinocyte colonies and in response to differentiation

116 nsory transduction, the mechanism underlying keratinocyte communication with intraepidermal nerve end

117 Human keratinocyte conditioned media spiked with recombinant c

118 ype of mesenchymal HNSCC and its normal oral keratinocyte counterpart.

119 This fully human keratinocyte culture system is 'regulatory friendly' and

120 cytosis, under basal conditions in monolayer keratinocyte cultures.

121 Our data suggest that upon keratinocyte damage icIL-1Ra1 acts extracellularly as an

122 Intercellular adhesion of keratinocytes depends critically on desmosomes that, dur

123 host T cells in skin explants and against a keratinocyte-derived cell line.

124 Until recently, studies were restricted to keratinocyte-derived cell lines immortalized by HPV due

125 esis of AD, particularly what is the role of keratinocyte-derived cytokine TSLP and Langerhans cells

126 Evidently, IL-17-induced release of keratinocyte-derived inflammatory mediators is a key dri

127 Epidermal keratinocytes dialogue with sensory neurons through en p

128 In addition, Pkp1- or 3-deficient keratinocytes did not exhibit changes in Dsg3 binding on

129 ated the expression of genes associated with keratinocyte differentiation (e.g., KRT1, GRHL2, SPRR4).

130 terized by dysregulation of genes related to keratinocyte differentiation and itch signaling.

131 t and demonstrate that these signals control keratinocyte differentiation in proliferating cells inde

132 n cancer development, immune regulation, and keratinocyte differentiation in SCC susceptibility.

133 nformin suppresses tumor growth and promotes keratinocyte differentiation in the 7,12-dimethylbenz[a]

134 Abnormal keratinocyte differentiation is fundamental to pathologi

135 o dithranol, rapid decrease in expression of keratinocyte differentiation regulators (e.g. involucrin

136 of individual lipid species in the onset of keratinocyte differentiation remains unknown.

137 antitumor activity of phenformin to promote keratinocyte differentiation that warrants future transl

138 HPV16 E7 and PTPN14 CRISPR knockout repress keratinocyte differentiation-related genes.

139 may significantly impact in vitro studies of keratinocyte differentiation.

140 etically silences critical genes involved in keratinocyte differentiation.

141 4 binding by HPV16 E7 and HPV18 E7 represses keratinocyte differentiation.

142 naling reverses the effects of phenformin on keratinocyte differentiation.

143 ntiated, and the HPV life cycle depends upon keratinocyte differentiation.

144 riptional node regulated by YAP1/TAZ-TEAD in keratinocyte differentiation.

145 proliferation of keratinocytes and disrupts keratinocyte differentiation.

146 iR-335 was identified as a potent inducer of keratinocyte differentiation; it exerts this effect by d

147 LAT1 deletion in keratinocytes does not dampen the inflammatory response

148 s expressed in several cell types, including keratinocytes, epidermal Langerhans cells (LC), and derm

149 We demonstrate that proliferating keratinocyte epithelial cell clusters display waves of o

150 Further, SLE keratinocytes exhibited increased binding to S. aureus.

151 ion, such as filaggrin and loricrin, and SLE keratinocytes exhibited increased S. aureus-binding inte

152 The digestion of double-stranded RNA from keratinocytes exposed to UVB blocked the capacity of the

153 Keratinocytes express many pattern recognition receptors

154 S-induced NF model, mice lacking hepcidin in keratinocytes failed to restrict systemic spread of infe

155 By co-culturing decellularized dermis with keratinocytes, fibroblasts and immune cells in the prese

156 ny target cells are present, including basal keratinocytes, fibroblasts, dendritic cells, and lymphoc

157 e small ROS, H(2)O(2), is increased in basal keratinocytes following treatment with paclitaxel.

158 cence (IIF) on human salt-split skin and the keratinocyte footprint assay for anti-laminin 332 antibo

159 hed primary dermal fibroblasts and epidermal keratinocytes from human donors on three biomarkers of c

160 The observation of oxidative stress in keratinocytes from Krt16 null mouse skin, a model for pa

161 Using keratinocyte generated extracellular matrices can enhanc

162 IL-17-dependent gene expression, including keratinocyte genes, improved earlier and more extensivel

163 owever any translational value is limited if keratinocytes get altered by the culture method.

164 Keratinocyte growth factor (KGF) improves cyclophosphami

165 delta-toxin), and cytotoxicity against human keratinocytes (HaCaT).

166 A mammalian cytotoxicity assay with human keratinocytes (HaCaTs) yielded an IC(50) for PGG of 256

167 ycle, in mouse epidermis and human epidermal keratinocytes (HEKs).

168 matrices can enhance infection efficiency in keratinocytes, hepatocytes and neuronal cells.

169 g NIKs and hTERT-MCPyV gene-expressing human keratinocytes (HK) compared to their expression in the c

170 r activated CD4(+) T cell-treated human oral keratinocytes (HOKs).

171 out the genes regulated by DeltaNp63alpha in keratinocytes, how DeltaNp63alpha is regulated is less c

172 , inflammatory skin disease characterized by keratinocyte hyperproliferation and a disease-related in

173 oarray data and RNA sequencing data from SLE keratinocytes identified repression of barrier gene expr

174 dicated that thermal burn injury of the skin keratinocyte in vitro results in the production of the l

175 duces the nuclear translocation of NFATc1 in keratinocytes in an AMPK-dependent manner.

176 nduced differentiation when added to primary keratinocytes in culture.

177 gnaling is strongly induced within epidermal keratinocytes in cutaneous psoriatic lesions, and BMP7 i

178 The ability to grow keratinocytes in vitro allows the study of differentiati

179 dies demonstrate that thermal burn injury to keratinocytes in vitro and human skin explants ex vivo,

180 only resulted in excessive proliferation of keratinocytes in vitro and in vivo but also induced loca

181 sion of these two genes was reduced in tumor keratinocytes in vivo.

182 BJ-5ta (human fibroblasts) and HaCaT (human keratinocytes) in a dose- and time-dependent manner.

183 Knockdown of 11beta-HSD1 in human epidermal keratinocytes increased the production of thymic stromal

184 kin-17 (IL-17) re-programs the urea cycle in keratinocytes increasing polyamines that stabilize RNA-A

185 Consequently, loss of RIPK1 in keratinocytes induces ZBP1-dependent necroptosis and ski

186 When grown as organotypic raft cultures, keratinocytes infected with wild-type but not E7 mutant

187 Keratinocytes infected with Y138F quasiviruses formed st

188 milar inhibitory effect, completely blocking keratinocyte inflammatory mediator expression induced by

189 Therefore, understanding VZV-keratinocyte interactions is important to find new treat

190 suggests that the function of human CIB1 in keratinocytes is limited and involves the restriction of

191 Interestingly, primary keratinocytes isolated and cultured from these cervical

192 pe-2 cytokines (IL-4 and IL-13) that repress keratinocyte (KC) differentiation.

193 Keratinocytes (KCs) have a functional cholinergic mechan

194 (LCs) in the psoriatic epidermis engage with keratinocytes (KCs) in tight physical interactions; more

195 In this study, we demonstrate that keratinocytes (KCs) isolated from two different individu

196 uld rescue the cellular phenotype in patient keratinocytes (KCs).

197 However, keratinocytes lacking Dsg3 or Pkp1 or 3 revealed reduced

198 Here, we show that keratinocytes lacking hemidesmosomal integrin alpha6beta

199 Here, we show that keratinocytes lacking TRPV3 impair the function of prote

200 CRISPR/Cas9 knockout of PTPN14 rescued keratinocyte life span extension in the presence of the

201 is required for high-risk HPV18 E7 to extend keratinocyte life span.

202 ones were generated originating from a human keratinocyte line.

203 In keratinocytes, loss of RHAMM function or expression prom

204 The loss of E5 in keratinocytes maintaining the complete HPV16 genome resu

205 NIPP1-deficient keratinocytes massively expressed proinflammatory chemok

206 The role of keratinocyte metabolism in psoriasis is not fully elucid

207 ibed to accelerate wound healing by enhanced keratinocyte migration and indirect stimulation of fibro

208 hat genetic ablation of IFT20 in vitro slows keratinocyte migration during wound healing.

209 that, unlike in WT mice, in Rhamm-null mice, keratinocyte migration initiates prematurely in the exci

210 motility (RHAMM), coordinates fibroblast and keratinocyte migration speed and ensures appropriate tim

211 ire the coordinated timing of fibroblast and keratinocyte migration.

212 Using a cultured keratinocyte model system, we show that depletion of alp

213 -null mice, indicating that RHAMM suppresses keratinocyte motility but increases fibroblast motility.

214 M partner protein CD44 and thereby increased keratinocyte motility.

215 The DDR limits keratinocyte multiplication upon hyperproliferative stim

216 l lines, including HeLa, HEK 293T, K562, and keratinocytes (N/TERTs).

217 ins K1, K10 and K2 in normal human epidermal keratinocytes (NHEK) and two important cell lines, HaCaT

218 fectively prevented neonatal human epidermal keratinocytes (NHEK) from G2/M phase arrest under high-d

219 profiles in human spontaneously immortalized keratinocytes (NIKs) expressing the early genes from six

220 lasia, involving high proliferation rates of keratinocytes not expressing the transgene.

221 tion factors HES1 in fibroblasts and KLF6 in keratinocytes not only compromised cell proliferation, b

222 outs showed that, relative to controls, skin keratinocytes null for Krt6a/Krt6b or Krt16 exhibit elev

223 ) provides vital structural support in basal keratinocytes of epidermis.

224 Human papillomaviruses (HPVs) infect keratinocytes of stratified epithelia.

225 hesis-free profiling of ACE2 suggests tongue keratinocytes, olfactory epithelial cells, airway club c

226 by mutations in TMC6 or TMC8 originates from keratinocyte or lymphocyte defects.

227 primary fibroblast cells compared to primary keratinocytes (P < .001).

228 ation in primary fibroblasts but not primary keratinocytes (P < .001).

229 th a three-dimensional hierarchy of multiple keratinocyte populations.

230 ed, by laser capture microdissection, MC and keratinocyte precursors from the hair follicle bulge of

231 05 efficiently infected TGM1-deficient human keratinocytes, produced TGM1 protein, and rescued transg

232 Our results demonstrate that keratinocyte-produced SCF is essential to wound closure

233 The basal keratinocyte progenitor cells in cultured epithelial aut

234 tes (CD3+, CD8+, CD11c+, CD163+), markers of keratinocyte proliferation (Ki67+, KRT16), and inflammat

235 GATA6 controls keratinocyte proliferation and differentiation to preven

236 known as p21), which is known to govern both keratinocyte proliferation and differentiation.

237 We show that keratinocyte proliferation is less prominent in galectin

238 PRANCR regulates keratinocyte proliferation, cell cycle progression, and

239 IGF-1 receptor (IGF1R) signaling promotes keratinocyte proliferation, migration, and survival.

240 tion, genes involved in skin barrier repair, keratinocyte proliferation, wound healing, and negative

241 fied nine novel candidate lncRNAs regulating keratinocyte proliferation.

242 sed on these data and our previous findings, keratinocyte purinergic signaling is a modality-conserve

243 Targeting keratinocytes rather than immune cells may be an alterna

244 nflammatory therapies specifically targeting keratinocytes, rather than systemic biologicals, might b

245 the mechanism of IGF1R endocytosis in normal keratinocytes remains unclear.

246 E7 to extend the life span of primary human keratinocytes required PTPN14 binding.

247 expression of S100A9 and S100A8 proteins in keratinocytes, respectively.

248 Keratinocytes respond to environmental signals by elicit

249 promote production of the CXCL1 chemokine by keratinocytes, resulting in neutrophil recruitment.

250 activation and MMP-9 expression, whereas in keratinocytes, RHAMM suppressed these activities.

251 l alarmins S100A8 and S100A9 was measured in keratinocyte RNA extracted from skin tape strips.

252 ic Ca2+ transients could be triggered by two keratinocyte-secreted factors, endothelin and acetylchol

253 s identify alpha3beta1 as a regulator of the keratinocyte secretome and skin tumor microenvironment a

254 eta1 regulates a substantial fraction of the keratinocyte secretome, including fibulin-2 and macropha

255 The discovery of keratinocyte-sensory neuron synaptic-like contacts may c

256 Further, wild-type keratinocytes showed increased levels of Dsg3 oligomers

257 ysis of conditioned medium from immortalized keratinocytes showed that alpha3beta1 regulates a substa

258 o signaling regulated by 14-3-3sigma in skin keratinocytes, shows aberrant subcellular partitioning a

259 ostasis and disease through their effects on keratinocytes, skin barrier integrity, immune activation

260 We found that in epidermal keratinocytes, soy PG inhibited TLR2 and TLR4 activation

261 This suppression is focused on keratinocyte-specific IFN-kappa and is mediated through

262 tion mark 5-hydroxymethylcytosine (5-hmC) in keratinocyte stem cells and transit amplifying cells in

263 rbic acid was accomplished in cultured human keratinocyte stem cells to show similar Ca(++)-induced d

264 c-like contacts: narrow intercellular cleft, keratinocyte synaptic vesicles expressing synaptophysin

265 oteins are less active in regulating CIB1 in keratinocytes than in T cells.

266 integrity and in supporting the survival of keratinocytes that are adhered to them.

267 ve from underlying, transcriptionally active keratinocytes that display filaggrin-containing keratohy

268 bial component-mimicking agents in epidermal keratinocytes that form the physical barrier of the skin

269 ase inhibitor increased viral DNA content in keratinocytes that maintain viral episomes.

270 ered that IkappaBzeta is strongly induced in keratinocytes that sense the fungal glucan zymosan A.

271 this study, we show that in human wound-edge keratinocytes, the expressions of microRNA (miR)-17, miR

272 revealed that CDK4/6 phosphorylated EZH2 in keratinocytes, thereby triggering a methylation-induced

273 t-Ser473 phosphorylation in mTORC2-deficient keratinocytes through expression of constitutive Akt res

274 e they are transferred to adjacent epidermal keratinocytes through pathways that involve microtubule

275 uce inflammation was examined by using human keratinocyte tissue culture and mouse models.

276 ng from exposure of cultured human epidermal keratinocytes to arsenite and antimonite in contrast to

277 dermatosis characterized by the inability of keratinocytes to control cutaneous beta-HPV infection an

278 unrecognized link between TRPV3 and PAR2 in keratinocytes to convey itch information and suggest tha

279 One potential mechanism to allow skin keratinocytes to disperse bioactive substances is via mi

280 hemokines are then secreted from surrounding keratinocytes to further recruit T cells to the skin thr

281 1, and sensory information transmitted from keratinocytes to sensory neurons through SNARE-mediated

282 In Tgammadelta17 cell-deficient mice, basal keratinocyte transcriptome was altered months in advance

283 Thus, during homeostasis, TM keratinocytes transit through a proliferative CP state a

284 cytes, we show that signals from neighboring keratinocytes trigger local compartmentalized Ca2+ trans

285 ormal epidermal states, and a tumor-specific keratinocyte (TSK) population unique to cancer, which lo

286 t of icIL-1Ra1 could be detected in isolated keratinocytes using RNA-sequencing analysis; however, Al

287 ork and attach themselves to the surrounding keratinocytes via homophilic E-cadherin binding.

288 Cutibacterium acnes to induce IL-36gamma in keratinocytes via the combined actions of Kruppel-like f

289 FIH-1 positively regulates DeltaNp63alpha in keratinocytes via variety of signaling partners: (a) Ple

290 Although a culturing technique for skin keratinocytes was developed four decades ago, the xenoge

291 Using human esophageal keratinocytes, we have identified Twist2 as an NFkB-resp

292 ension-induced differentiation and knockdown keratinocytes, we pinpointed candidate bioactive lipid s

293 interaction between melanocyte dendrites and keratinocytes, we show that signals from neighboring ker

294 stem allowing efficient infection of primary keratinocytes, we were able to identify transcriptional

295 transcriptome and genes induced by IL-17 in keratinocytes were evaluated with microarray profiling a

296 the epidermis, is composed predominantly of keratinocytes, which can be stimulated to produce proinf

297 by constitutive high BMP7/BMPR signaling in keratinocytes, which instructs inflammatory DCs to gain

298 as significantly down-regulated in epidermal keratinocytes with age.

299 l that allows efficient infection of primary keratinocytes with HPV16 virions.

300 nsfer of mature melanin granules to adjacent keratinocytes within the basal layer of the epidermis.