ライフサイエンスコーパス: HaCaT cell

1 re compared with immortalized keratinocytes (HaCaT cells).

2 ized but nontumorigenic human keratinocytes (HaCaT cells).

3 dexamethasone (Dex) in human keratinocytes (HaCaT cells).

4 sregulation of phospho-protein expression in HaCaT cells.

5 m all SCC cell lines, but not in medium from HaCaT cells.

6 onsiveness to inflammation in UVB-irradiated HaCaT cells.

7 reduced phosphatidylserine translocation in HaCaT cells.

8 ction was most efficient and reproducible in HaCaT cells.

9 d not affect the attachment of H. ducreyi to HaCaT cells.

10 on in continuous cell lines such as HeLa and HaCaT cells.

11 rees of apoptosis in IEX-HaCaT cells than in HaCaT cells.

12 ificantly activated after UVB irradiation in HaCaT cells.

13 much in the IEX-HaCaT cells when compared to HaCaT cells.

14 was also inhibited by TGF beta in NMuMG and HaCaT cells.

15 ERK in UVB induced cox-2 gene expression in HaCaT cells.

16 ble to inhibit entry of wild-type HSV-1 into HaCaT cells.

17 IEX-HaCaT cells grew faster than HaCaT cells.

18 reater extent in the IEX-HaCaT cells than in HaCaT cells.

19 athway may be involved in stimulating p21 in HaCaT cells.

20 ficient to activate the expression of p21 in HaCaT cells.

21 eby the biologic activity of all-trans RA in HaCaT cells.

22 se reporter gene was stably transfected into HaCaT cells.

23 ion of Bcl-XL in quiescent keratinocytes and HaCaT cells.

24 tive regulatory effects on Smad signaling in HaCaT cells.

25 droxylase in immortalized human keratinocyte HaCaT cells.

26 be induced by TGF-beta in human keratinocyte HaCaT cells.

27 o lack of metabolic inactivation of CD367 in HaCaT cells.

28 rtant role in UVB-induced AP-1 activation in HaCaT cells.

29 te is the p50-p65 heterodimeric NF-kappaB in HaCaT cells.

30 he accumulation of CaN19 mRNA and protein in HaCaT cells.

31 s of E2F1, B-myb, or HsORC1 genes in cycling HaCaT cells.

32 tinocytes, as well as in human keratinocytic HaCaT cells.

33 ree of infectivity found for human epidermal HaCaT cells.

34 in are independent of Ca(i) concentration in HaCaT cells.

35 y responsible for the activity observed with HaCaT cells.

36 cellular matrix and in the culture medium of HaCaT cells.

37 and IL-33 in human primary keratinocytes and HaCaT cells.

38 2(Y689F) was internalized at 37 degrees C by HaCaT cells.

39 caffeine increased UVB-induced apoptosis in HaCaT cells.

40 primary human keratinocytes and immortalized HaCaT cells.

41 ll surface and extracellular matrix (ECM) of HaCaT cells.

42 etic PTHrP peptides on calcium transients in HaCaT cells.

43 gnal transduction in human skin keratinocyte HaCaT cells.

44 overexpressing the NF-kappaB p65 subunit in HaCaT cells.

45 nificantly augmented the invasiveness of the HaCaT cells.

46 d arsenite-induced cell cycle progression in HaCat cells.

47 kinase could translocate into the nucleus of HaCaT cells.

48 ase cleavage was observed in mock-irradiated HaCaT cells.

49 ical roles in the survival of UVA-irradiated HaCaT cells.

50 ignificant, levels of IFN-beta in HEK293 and HaCaT cells.

51 in melanocytes, keratinocytes, melanoma, and HaCat cells.

52 immobilized heparin and human keratinocyte (HaCaT) cells.

53 ted the cellular effects of peroxynitrite in HaCaT cells, a human keratinocyte cell line.

54 s necessary and sufficient for attachment to HaCaT cells, a keratinocyte cell line, but was not requi

55 Using NRP1 promoter constructs in HaCaT cells, a keratinocyte cell line, we could demonstr

56 ect of inhibiting p38 MAPK on UVA-irradiated HaCaT cells, a spontaneously immortalized human keratino

57 Immortalized nontumorigenic keratinocyte (HaCaT) cells abundantly express both Met receptors and C

58 In HaCaT cells, additional characteristic responses were ob

59 In HaCaT cells, adenosine 5'-triphosphate, uridine 5'-triph

60 Isotretinoin reduced Ca2+ entry in HaCaT cells and decreased survival of HaCaT and DD kerat

61 P2Y4, and P2Y6 receptors was demonstrated in HaCaT cells and differentiated and undifferentiated norm

62 ightly increased the basal apoptotic rate of HaCaT cells and dramatically sensitized them to UV or PK

63 In normal proliferating human HaCaT cells and in cells released from serum starvation,

64 , a finding replicated in HeLa, HEK293T, and HaCaT cells and in murine epidermis.

65 In HaCaT cells and in reconstructed human epidermis (RHE),

66 gether our results suggest that treatment of HaCaT cells and mouse skin with delphinidin inhibited UV

67 us, F-US6kan, was found to efficiently enter HaCaT cells and normal human keratinocytes and could spr

68 ch other and colocalize at focal adhesion in HaCaT cells and normal human keratinocytes.

69 ite activates poly(ADP-ribose) polymerase in HaCaT cells and poly(ADP-ribose) polymerase activation c

70 Levels of p53 were highest in HaCat cells and some of the melanoma lines, and barely d

71 actors binding to the canonical Sp1 sites in HaCaT cells and that TGF-beta treatment did not change t

72 o occasional tumors that arose from parental HaCaT cells and vector control cells, which grew slowly

73 d keratinocytes, immortalized keratinocytes (HaCaT cells), and dendritic cells expanded from adult pe

74 pect to the prototype 3a, high NO release in HaCat cells, and ameliorated skin repair in a mouse mode

75 Freshly isolated keratinocytes, HaCaT cells, and cultured keratinocytes all constitutive

76 ormal-skin-derived keratinocytes or cultured HaCat cells, and that caution is necessary for proper in

77 cultured fibroblasts, whereas epidermis and HaCaT cells are negative.

78 yperproliferation, which was evaluated using HaCaT cells as a model, was combined with comparably low

79 obtained further evidence from studies using HaCaT cells as models that this variant disturbed subcel

80 ppress keratinocyte hyperproliferation using HaCaT cells as the primary test system.

81 In HaCaT cells, ASC interacted with p53 at the endogenous l

82 t not CC chemokine receptor 5, expression by HaCaT cells at low cell densities, which was abolished i

83 wo-electron reduction assays as well as in a HaCaT cell-based assay.

84 ypothesis proved to be untrue as eliminating HaCaT cell binding of vitronectin with a monoclonal anti

85 ells; however, LMP2A did not activate Ras in HaCaT cells but did in HSC-39 cells.

86 also show defects in cell-to-cell spread in HaCaT cells, but not in other, nonpolarized cells.

87 ocks S-phase entry in non-synchronized human HaCaT cells by approximately 90% at a 24 microM concentr

88 ariants of human immortalized keratinocytes (HaCaT cells) by expressing MTA1 cDNA in both the sense a

89 UVA irradiation of HaCaT cells caused a rapid rise in GSH efflux across the

90 reyi organisms adherent to but rarely within HaCaT cells cocultured with fibroblasts.

91 On the other hand, HaCaT cells continuously cultivated in low calcium media

92 D receptor, HveC, and entry of F-US6kan into HaCaT cells could also be inhibited with antibodies spec

93 e profiles from cocultures than from HS27 or HaCaT cells cultured separately.

94 Overexpression of NRSF in HaCaT cells decreased NRP1 RNA and protein, whereas a do

95 m of gE and gI in a human keratinocyte line, HaCaT cells, decreased the spread of HSV between cells.

96 , overexpression of TRPC1 or SERCA2-siRNA in HaCaT cells demonstrated resistance to thapsigargin-indu

97 e to abolish the LOXL2-induced inhibition of HaCaT cell differentiation.

98 As in primary cells, IL-31-treated HaCaT cells elicited a differentiation defect in organot

99 e epidermal growth factor receptor (EGFR) in HaCaT cells enhances the level of EGFR-associated PAK1 a

100 F-kappaB signaling pathway and its effect in HaCaT cells exposed to UVB radiation or inflammatory med

101 HaCaT cells expressed high levels of an HSV gD receptor,

102 HaCaT cells expressed TRPC1 in the plasma membrane.

103 the AP-1 family components c-Fos and c-Jun, HaCaT cells expressing estrogen receptor do not.

104 HaCaT cells expressing LMP2A were highly tumorigenic and

105 HaCat cells expressing small interfering RNA to p53 indi

106 n were constitutively expressed in untreated HaCaT cells, expression levels did not increase in respo

107 DNA fragments were measured in IEX-HaCaT or HaCaT cells following UVB irradiation or treatment with

108 Overexpression of Mcl-1 protected HaCaT cells from both UV and PKCdelta-cat-induced apopto

109 rences have been identified that distinguish HaCaT cells from normal human keratinocytes, including d

110 Interference of AhR in human HaCaT cells further supported its role in EMT.

111 We demonstrate that UVB-transformed HaCaT cells gain enhanced proliferation rate, apoptosis-

112 IEX-HaCaT cells grew faster than HaCaT cells.

113 Compared with normal keratinocytes, HaCaT cells have a dysfunctional constitutive NF-kappaB

114 Thus, immortalized HaCaT cells have an abnormal constitutive and dysfunctio

115 regulator of resistance to apoptosis; and 6) HaCaT cells have undetectable p16 protein (hypermethylat

116 In HaCaT cells, high UVB dose caused dramatic increase in p

117 not induced by IFN-gamma and TPA, rendering HaCaT cells highly susceptible to UV-induced apoptosis.

118 Similar to HaCaT cells, highly migratory MDA-MB-231 breast cancer c

119 ificant interleukin 8 (IL-8) expression from HaCaT cell-HS27 cell cocultures.

120 d NF-kappaB activation in human keratinocyte HaCaT cells in early phase (within 6 h) post-UVB.

121 ffects of IEX-1 expression in keratinocytes (HaCaT cells) in the basal state and after the induction

122 Finally, ectopic expression of Bcl-XL in HaCaT cells increased survival after EGFR blockade when

123 se (SERCA)2 small interfering RNA (siRNA) in HaCaT cells increased TRPC1 levels and thapsigargin-stim

124 eatment of immortalized human keratinocytes (HaCaT cells) increased CaN19 mRNA levels by 4.5-fold wit

125 In HaCaT cells incubated with anti-alpha 6 beta 4 antibodie

126 M boundaries was observed in HN12, HN30, and HaCaT cells independent of p53 function, and this effect

127 ulated intracellular calcium mobilization in HaCaT cells, indicating that these sn-2 acetyl-GPC act i

128 rthermore, overexpression of NF-kappaBp65 in HaCaT cells induced colony formation in soft agar and tu

129 We show here that TGF-beta treatment of HaCaT cells induced the formation of E2F4-RB and E2F4-p1

130 s as well as in interferon-gamma-insensitive HaCaT cells, interferon gamma was unable to significantl

131 The AP-1 complex formed in UVB-irradiated HaCaT cells is specifically composed of c-fos and Jun D.

132 ating the TGF-beta-Smad signaling pathway in HaCaT cells is sufficient to prevent TGF-beta-induced gr

133 Human skin reconstitution employing STRA6KD HaCaT cells leads to massive epithelial thickening under

134 The cytotoxicity (MTT assay) on HaCaT cell line demonstrated high cytocompatibilty of th

135 nocytes, the immortalized but nontumorigenic HaCat cell line, and the tumor cell lines SCC-4, SCC-9,

136 On the other hand, a variant of the HaCaT cell line, HC-R1, showed microtubule-disruption-in

137 by the PI 3-kinase signaling pathway in the HaCaT cell line.

138 s a rapid phosphorylation of p38 MAPK in the HaCaT cell line.

139 p in both normal human keratinocytes and the HaCaT cell line.

140 Human keratinocyte (HaCaT) cell line was employed for the bio- and cyto-comp

141 We created inducible p12 antisense HaCaT cell lines [ip12 (-) HaCaT] and showed that select

142 bryonic kidney 293 (HEK293) or keratinocyte (HaCaT) cell lines or human primary dendritic cells or ma

143 h control (HaCaT) and IEX-1-transfected (IEX-HaCaT) cell lines showed no significant differences in t

144 HGF stimulated CD44v5 protein expression and HaCaT cell migration; these events required activation o

145 also show here that matriptase deficiency in HaCaT cells modestly reduces cell proliferation and temp

146 t approximately 13% of H. ducreyi adhered to HaCaT cell monolayers, while only a small proportion (0.

147 In HaCaT cells, neither COX-1 mRNA nor protein was detectab

148 phosphatase mRNA was not detected in either HaCaT cells or human skin, both of which exhibited signi

149 HEK-HPV, whereas PMA did not induce Glis1 in HaCaT cells or in several squamous cell carcinoma cell l

150 CXCL12 blocked IL-22-mediated HaCaT cell proliferation in vitro and synergized with IL

151 In HaCaT cells, reinstatement of p16 pathway restored cell-

152 oculation into the nude mice, while parental HaCaT cells remain non-tumorigenic.

153 on of the constitutive NF-kappaB activity in HaCaT cells resulted in alterations in NF-kappaB signali

154 EGF, which induces MMP-I production by HaCaT cells, resulted in the ability of these cells to m

155 anotypic 3D skin models using stable STRA6KD HaCaT cells showed a significantly thicker epidermis and

156 Spontaneously proliferating HaCaT cells, showing several similarities to basal epide

157 irradiation increased c-fos transcription in HaCaT cells stably transfected with a plasmid containing

158 letion of FADD or TRADD in Sharpin-deficient HaCaT cells suppressed TNF-induced apoptosis, indicating

159 so found that ectopic expression of Pirh2 in HaCaT cells suppresses cell proliferation.

160 Cleavage occurred on both the HaCaT cell surface and extracellular matrix (ECM).

161 n induced higher degrees of apoptosis in IEX-HaCaT cells than in HaCaT cells.

162 ity increased to a greater extent in the IEX-HaCaT cells than in HaCaT cells.

163 g immortalized human epidermal keratinocyte (HaCaT) cells through repetitive exposure to UVB radiatio

164 We have used HPV16 pseudovirus infection of HaCaT cells to analyze how several neutralizing monoclon

165 observed that exposure of human keratinocyte HaCat cells to arsenite resulted in the promotion of cel

166 lly less susceptible than melanoma lines and HaCat cells to etoposide, cisplatin, and staurosporine.

167 s associated with the failure of neighboring HaCaT cells to induce differentiation and cell cycle wit

168 in extrapolating the biological responses of HaCaT cells to those of normal human keratinocytes in th

169 liferating, senescent, and immortalized KCs (HaCaT cells) to antiproliferative agents followed by UV

170 e) polymerase was observed in UVA-irradiated HaCaT cells treated with SB202190 or in cells expressing

171 HaCaT cells treated with sodium lauryl sulfate (SLS), a

172 hat expression of the active PKCdelta-cat in HaCaT cells triggers a reduction in the anti-apoptotic p

173 These data indicate that KCs (but not HaCaT cells) undergoing abruptly induced cell cycle arre

174 t 100 fold less potent than PLTX in reducing HaCaT cells viability (EC50 = 1.1 x 10(-9) M vs 1.8 x 10

175 NF-kappaB activity present in HaCaT cells was not affected by TGF-beta treatment as ju

176 No growth inhibition of HaCaT cells was observed with Scutellaria baicalensis.

177 ssion of EGFR in immortalized keratinocytes (HaCaT cells) was associated with enhanced EGFR activatio

178 ceptors in immortalized human keratinocytes (HaCat cells) was examined.

179 The LMP2A-expressing HaCaT cells were able to grow anchorage independently an

180 damage was much less than that observed when HaCaT cells were cocultured with strain 35000.

181 To address function, HaCaT cells were exposed to two NRP1 ligands, VEGF165 an

182 Finally, both alleles of the DEC1 locus in HaCaT cells were inactivated through targeted homologous

183 HaCaT cells were permissive for clonal expansion of II-4

184 A431 and HaCaT cells were strongly resistant to H2O2-induced S100

185 Metabolomics analyses of human plasma and HaCaT cells were used to compare the above three operati

186 lulose suspension, apoptosis was detected in HaCat cells when at least 5% of the cell population was

187 caspase 3 activity twice as much in the IEX-HaCaT cells when compared to HaCaT cells.

188 d an abnormal localization to the nucleus of HaCaT cells, which was unaffected by MSH/ACTH peptides.

189 An adhesion assay shows that HaCaT cells with calcium-independent desmosomes are more

190 Furthermore, we found that pretreatment of HaCaT cells with delphinidin inhibited UVB-mediated (i)

191 HaCaT cells with down-regulated Mcl-1 had higher activat

192 ot sheath keratinocytes, and H4R-transfected HaCaT cells with histamine and H4R agonist resulted in a

193 Pretreatment of HaCaT cells with platelet-activating factor receptor ant

194 PK activation prevents REGgamma elevation in HaCaT cells with TPA treatment.

195 a transition mutation within the P53 gene of HaCaT cells with verification by direct sequencing of th

196 approximately 2-3 log better killing than by HaCaT cells within 1 hour.

197 f p21 at the mRNA level in the p53-deficient HaCaT cells without increase in the p21 mRNA half-life,