ライフサイエンスコーパス: UVB

1 UVB (290-320 nm wavelengths) exposure before induction o

2 UVB has no effect on the global tri-methylation level of

3 UVB irradiation (290-320 nm) is used to treat skin disea

4 UVB irradiation alone and UVB with heat rekindling are t

5 UVB irradiation significantly increased vitamin D levels

6 UVB irradiation significantly upregulated the expression

7 UVB is a component of solar radiation primarily responsi

8 UVB light is considered the major environmental inducer

9 UVB radiation caused, independently of genotype, a dose-

10 UVB stimulated beta-endorphin expression was higher in D

11 UVB stimulated CRH gene and protein expression in the br

12 UVB stimulated plasma levels of CRH, Ucn, beta-END, ACTH

13 UVB wavelengths of light induce the formation of photopr

14 UVB-induced DNA damage has a critical role in the develo

15 UVB-induced inflammation was less pronounced in shaved h

16 R4(+/+)) mice were subjected to 90 mJ cm(-2) UVB radiation locally, DNA damage in the form of cyclobu

17 of simulated sunlight exposure (5100 J/m(2) UVB and 1.2 x 10(5) J/m(2) UVA), neither MALDI-TOF-MS no

18 increases in 25(OH)D concentrations after 4 UVB treatments and largest decreases in 25(OH)D concentr

19 -filtered FS-40 sun lamps (approximately 60% UVB and 40% UVA).

20 6-formylindolo[3,2-b] carbazole (FICZ), is a UVB photoproduct of tryptophan and a powerful UVA chromo

21 Hypophysectomy abolished UVB stimulation of plasma, but not of skin CORT levels,

22 anoyl-phorbol-13-acetate treatment and acute UVB exposure.

23 ermal cyclopyrimidine dimers following acute UVB exposure are equivalent in the presence or absence o

24 After UVB treatments, rs10741657 in CYP2R1 and rs4588 in GC pr

25 ylating agent, 5-aza-2'-deoxycytidine, after UVB exposure.

26 role of Dsg1 in aiding differentiation after UVB damage was tested.

27 cyclobutane pyrimidine dimers 24 hours after UVB radiation.

28 as nuclear translocation of NF-kappaB after UVB radiation.

29 analysis of the skin of IL1r(-/-) mice after UVB exposure showed decreased gene expression of proinfl

30 of TLR4(+/+) mice than TLR4(-/-) mice after UVB exposure.

31 regulates skin tissue injury and pain after UVB overexposure, it is discussed whether TRPV4 downregu

32 he pro-death activity of peroxynitrite after UVB radiation.

33 ucing a signal for cellular protection after UVB carcinogenesis provocation.

34 ht to test whether skin barrier repair after UVB damage is dependent on the activation of TLR3.

35 levels were compared in these strains after UVB exposure, BMDCs from UV-irradiated TLR4(-/-) mice pr

36 lied DHA potentiate cellular defense against UVB-induced skin inflammation and photocarcinogenesis th

37 excellent protectors of melanocytes against UVB-induced pathology.

38 xygenase-1 in the skin and protected against UVB-induced oxidative stress, inflammation and papilloma

39 tly increased after toll-like receptor 2 and UVB treatment in lupus keratinocytes, and neutralization

40 rix remodeling with both UVA1 (P=5.5e-7) and UVB (P=2.9e-22).

41 ng ultraviolet B (UVB) irradiation alone and UVB irradiation with heat rekindling.

42 UVB irradiation alone and UVB with heat rekindling are translational models of inf

43 l concentrations between oral vitamin D3 and UVB groups (difference in median of oral vitamin D3 minu

44 ow that LITE-1 directly absorbs both UVA and UVB light with an extinction coefficient 10-100 times th

45 peaks of the ZnO-NPs existed in both UVA and UVB region.

46 -simulated UVR (ssUVR), a mixture of UVA and UVB, are not well characterized.

47 t that if the photon fluxes of PAR, UVA, and UVB radiation are separately determined and the waveleng

48 UVA1 and UVB caused different effects on matrix metalloproteinase

49 reduce the transmittance of incident UVC and UVB light by up to 90%, and UVA transmittance by up to 2

50 eak intensities of radiation in both UVC and UVB range while remaining visible-blind, and a high sign

51 s on 25(OH)D concentrations after artificial UVB irradiation and supplementation by vitamin D(3)-fort

52 trations in the same manner after artificial UVB-induced vitamin D and consumption of vitamin D(3)-fo

53 centrations after a given dose of artificial UVB irradiation and 25 single nucleotide polymorphisms l

54 meable TRPV4 has recently been identified as UVB-receptor in skin keratinocytes, where it regulates s

55 clusion, we demonstrated that Rg1 attenuated UVB-induced GC insensitivity.

56 ts were well correlated to the daily average UVB light intensity corrected for light screening incorp

57 Ultraviolet radiation B (UVB) is a skin-specific stressor that can activate this

58 vitamin D in response to ultraviolet type B (UVB) light.We tested the hypothesis that, in vitamin D-d

59 te machinery that responds to ultraviolet B (UVB) and functions critically to convert the keratinocyt

60 idemiological studies suggest ultraviolet B (UVB) component (290-320 nm) of sun light is the most pre

61 The effects of a single ultraviolet B (UVB) exposure on hyaluronan content and molecular mass,

62 s of inflammatory pain, using ultraviolet B (UVB) irradiation alone and UVB irradiation with heat rek

63 In response to sublethal ultraviolet B (UVB) irradiation, human keratinocytes transiently block

64 nflammatory pain that involve ultraviolet B (UVB) irradiation, which can employ peripheral and centra

65 ronmental stresses, including ultraviolet B (UVB) irradiation.

66 Ultraviolet B (UVB) light is the principal aetiological factor associat

67 ming human telomeric DNA with ultraviolet B (UVB) light results in the formation of anti cyclobutane

68 ated secondary to exposure to ultraviolet B (UVB) radiation (whether from the sun or from an artifici

69 cancer development induced by ultraviolet B (UVB) radiation is dependent on its gene dose.

70 duced in the skin by moderate ultraviolet B (UVB) radiation on central nervous system (CNS) autoimmun

71 found that the proportion of ultraviolet B (UVB) radiation-induced C>T transitions differed signific

72 urated fatty acids (PUFAs) on ultraviolet B (UVB)-induced skin inflammation and photocarcinogenesis u

73 sion was reduced with successful narrow band UVB (NB-UVB), etanercept, and anti-IL-17 treatments.

74 d the epidermis of untreated and narrow band UVB (NBUVB)-treated human vitiligo skin.

75 s for vitiligo repigmentation is narrow-band UVB (NBUVB), but how the hair follicle melanocyte precur

76 (n = 60) and those who received narrow-band UVB exposure (n = 58) </=6 mo.There was no difference in

77 ells from 12 patients undergoing narrow-band UVB phototherapy and 12 corresponding healthy controls r

78 pin splitting of the uppermost valence band (UVB) and the lowermost conduction band (LCB) in bulk and

79 ntibodies to BMDCs of TLR4(-/-) mice (before UVB exposure) inhibited repair of CPDs, with a concomita

80 d expression of ATF4 and CHOP protein before UVB irradiation significantly enhanced apoptosis, sugges

81 There were strong associations between UVB exposure and post-holiday levels of T-T dimers and v

82 to chemically induced double strand breaks, UVB and ionizing radiation.

83 gulator of immune responses, is activated by UVB irradiation in the skin.

84 NOX1 is uniquely present and activated by UVB radiation with biphasic expression of the enzyme imm

85 eral sensitisation in both species driven by UVB irradiation, with a clear mechanical and thermal hyp

86 t protection against the effects elicited by UVB radiation; however, there was no efficient protectio

87 fy mechanisms regulating body homeostasis by UVB through activation of the HPA axis that originate in

88 Potentially mutagenic DNA lesions induced by UVB (wavelengths 280-320 nm) are important risk factors

89 xpression of ATF4 or CHOP was not induced by UVB as compared with traditional ISR activators.

90 Loss of eIF2alpha-P induced by UVB diminished G1 arrest, DNA repair, and cellular senes

91 ative stress after corneal damage induced by UVB irradiation.

92 y barrier repair following injury induced by UVB irradiation.

93 vitamin D2 production in dried mushrooms by UVB irradiation.

94 ant response is that ATF4 mRNA is reduced by UVB, and despite its ability to be preferentially transl

95 uction of this systemic immune regulation by UVB radiation, because ablation of Langerhans cells abol

96 melanoma-competent MCSCs upon stimulation by UVB, which induces MCSC activation and translocation via

97 ours is marked and much greater than that by UVB.

98 loped multiple epidermal cysts after chronic UVB exposure.

99 t in the presence or absence of LCs, chronic UVB-induced p53 mutant clonal islands expand more readil

100 skin tumors in female mice with chronically UVB-damaged skin.

101 In culture, UVB causes a direct, TRPV4-dependent Ca(2+) response in

102 In monolayer cultures, UVB increased hyaluronan synthase Has1 mRNA already 4 h

103 In organotypic cultures, UVB treatment also resulted in increased expression of b

104 ir and innate immune response after damaging UVB exposure.

105 t with a TRPV4-selective inhibitor decreases UVB-evoked pain behavior, epidermal tissue damage, and e

106 in we show that LC-intact epidermis develops UVB-induced tumors more readily than LC-deficient epider

107 sphorylated STAT3 after exposure to low dose UVB.

108 n cell proliferation in response to low dose UVB.

109 ppm wt/vol, applied on rabbit corneas during UVB irradiation and healing (UVB doses 1.01 J/cm(2) once

110 The molecular events that occur during UVB-induced skin carcinogenesis are poorly understood la

111 In addition to its panoply of effects, UVB (290-320 nm) radiation can specifically affect vario

112 cyte into a pain-generator cell after excess UVB exposure.

113 n matrix metalloproteinase (MMP) expression: UVB induced MMP1, MMP3, and MMP10 mRNA at 24 hours to a

114 a major cause of premature aging, following UVB exposure to human reconstructed skin tissue.

115 e tumors (57 of 59) that developed following UVB or 7,12-dimethylbenz(a)anthracene/phorbol 12-myrista

116 ression increases in the epidermis following UVB treatment.

117 in TC-PTP-deficient keratinocytes following UVB irradiation.

118 SR is deleterious in keratinocytes following UVB.

119 epithelial cells in wild-type mice following UVB treatment.

120 d inflammatory cytokine production following UVB irradiation.

121 yed a delay in skin barrier repair following UVB damage.

122 the inhibition of DNA replication following UVB irradiation.

123 ir rate, apoptosis, and senescence following UVB exposure, here we used cultured human keratinocytes

124 uate the roles of PTK6 in the skin following UVB-induced damage, we exposed back skin of Ptk6 +/+ and

125 gnificantly reduced cell viability following UVB exposure in comparison with untreated TC-PTP-deficie

126 lational control reduced viability following UVB that was alleviated by cycloheximide (CHX), indicati

127 itamin E as a topical preventative agent for UVB-induced skin cancer have yielded conflicting results

128 n to promote skin carcinogenesis and, as for UVB, this is associated with the acquisition of genomic

129 enterococci and E. coli after correcting for UVB light screening, suggesting that although the exogen

130 on, however, mast cells were dispensable for UVB-induced immune suppression, whereas basophil-derived

131 Our data show that AREG is essential for UVB-induced CHS suppression.

132 n mouse skin, SIRT1 is haploinsufficient for UVB-induced DNA damage repair and expression of xeroderm

133 rea, we have developed an in vitro model for UVB-induced skin cancer using immortalized human epiderm

134 al for use as a chemopreventive strategy for UVB radiation-induced malignancies.

135 te-derived TRPV4 as a therapeutic target for UVB-induced sunburn, in particular pain.

136 ne-thrombocytopenic patients when tested for UVB tolerance.

137 that although NF-kappaB protects cells from UVB-induced death, its pro-survival activity was likely

138 Furthermore, SFN rescued cells from UVB-induced toxicity in dose-dependent fashion, which wa

139 and its metabolites protect melanocytes from UVB-induced DNA damage and oxidative stress through acti

140 e in organotypic skin models recovering from UVB exposure.

141 h a topical antioxidant, without any further UVB exposure.

142 corneas during UVB irradiation and healing (UVB doses 1.01 J/cm(2) once daily for four days).

143 larger bullseyes are associated with higher UVB incidence.

144 hich is responsible for DNA demethylation in UVB-exposed skin.

145 PTK6 activation was detected in UVB-induced tumors, and this correlated with increased a

146 ated the anti-inflammatory effects of Dex in UVB-irradiated mouse skin.

147 d to contribute to the gender differences in UVB-induced vitamin D production and to its reversal of

148 e p38alpha is restricted to the epidermis in UVB-exposed skin, and that p38alpha ablation targeted to

149 An SD increase in UVB exposure at age 14 to 19 years (OR, 0.81; 95% CI, 0.

150 stored Dex responsiveness to inflammation in UVB-irradiated HaCaT cells.

151 prabasilar epidermis, yet the role of LCs in UVB-induced carcinogenesis is largely unknown.

152 data demonstrate that LCs have a key role in UVB-induced cutaneous carcinogenesis and suggest that LC

153 ere we determined whether AREG has a role in UVB-induced, Treg cell-mediated suppression of CHS react

154 r Hmga2 in the skin plays a critical role in UVB-mediated melanomagenesis.

155 m intakes are low with little seasonality in UVB-exposure.

156 s consistent with the dual roles of SIRT1 in UVB-induced skin tumorigenesis.

157 ntion of oxidative and nitrosative stress in UVB irradiated corneas, which may represent a novel prop

158 g inhibition of chromosomal DNA synthesis in UVB-irradiated keratinocytes.

159 ither photoaction spectra or total, incident UVB irradiance.

160 on from different damaging factors including UVB.

161 Increased UVB exposure was associated with reduced myopia, particu

162 how that honokiol has the ability to inhibit UVB-induced immunosuppression in preclinical model and,

163 Honokiol application also inhibited UVB-induced DNA hypermethylation and its elevation of th

164 in gaining valuable mechanistic insight into UVB-induced skin carcinogenesis, identification of novel

165 As a likely UVB photoproduct of intracellular tryptophan, FICZ repre

166 Local UVB radiation of the skin influences systemic immune rea

167 nd immunotherapeutic approaches for managing UVB-induced cutaneous DNA damage and skin cancer.

168 chanism to minimize the risk of mutagenesis, UVB-irradiated cells also activate a checkpoint signalin

169 nhibits the removal of potentially mutagenic UVB-induced DNA photolesions by nucleotide excision repa

170 ng-remitting MS were treated with narrowband UVB phototherapy.

171 e common and effective therapies, narrowband-UVB treatment and long-term biologic treatment systemica

172 reduced with successful narrow band UVB (NB-UVB), etanercept, and anti-IL-17 treatments.

173 pectrally pure UVA1 (50 J cm(-2)) and 300 nm UVB (30 mJ cm(-2)).

174 different spectral regions (UVC, 100-280 nm; UVB, 280-320 nm; and UVA, 320-400 nm) on the lipids and

175 ach highlights the genetic evolution and non-UVB mutational signatures associated with melanoma devel

176 ownregulation can also be found in other non-UVB-exposed cancers.

177 UV (UVA or UVB) and found that UVA, but not UVB, induces progerin expression and HGPS-like abnormal

178 Notably, UVB treatment of human psoriatic lesions reduced skin-in

179 Together, these novel, UVB-transformed progression model cell lines can be very

180 C57BL/6 mice was exposed to 400 mJ cm(-2) of UVB or was sham irradiated.

181 Direct DNA absorption of UVB photons in a spectral range of 290-320 nm of terrest

182 o persist and expand long after cessation of UVB irradiation.

183 ate immunity in promoting the development of UVB-induced p53 mutations, immune suppression, and skin

184 Development of UVB-induced skin carcinoma is a multistep and complex pr

185 Ptk6 -/- SENCAR mice to incremental doses of UVB for 30 weeks.

186 ubrious effects of suberythemogenic doses of UVB irradiation for the skin barrier.

187 tin mRNA was up-regulated after all doses of UVB with a maximum level at 50 mJ/cm(2) after 12h for D2

188 Effects of UVB light were analyzed in a murine model of CNS autoimm

189 Little is known about the efficiency of UVB emitting LEDs tuned to different wavelengths for pro

190 Formation of UVB-induced lesions is not random, and conformational fe

191 nt difference in the levels of inhibition of UVB-induced immunosuppression amongst mice that were tre

192 anical and thermal stimulation in a model of UVB irradiation and in a model of UVB irradiation with h

193 a model of UVB irradiation and in a model of UVB irradiation with heat rekindling.

194 Odds ratios (ORs) of UVB, serum vitamin D3 concentrations, vitamin D single-n

195 own, South Africa, has a seasonal pattern of UVB radiation and a predominantly dark-skinned urban pop

196 er increased its activity in the presence of UVB.

197 novel potential target for the prevention of UVB-induced skin cancer.

198 ion and thermoregulation, increased rates of UVB-induced epidermal apoptosis and caused a severe path

199 oteome and thereby preventing the removal of UVB-induced DNA lesions.

200 his study was to determine whether repair of UVB-induced DNA damage is regulated by Toll-like recepto

201 In contrast, the skins of UVB-irradiated invariant NKT cell-knockout (Jalpha18(-/-

202 implications for predicting the hot spots of UVB-induced lesions in nucleic acids.

203 e in median of oral vitamin D3 minus that of UVB: 1.5 mg/dL; 95% CI: -5.0, 7.0 mg/dL).

204 Treatment of UVB-exposed monolayer or organotypic cultures with trich

205 After acute inflammation from 10 weeks of UVB irradiation subsides, small areas of focal hyperemia

206 loped >12 tumors per mouse after 32 weeks of UVB therapy, whereas haired mice developed fewer than th

207 tein A, and we find that its accumulation on UVB-damaged chromatin is partially attenuated in cells w

208 A simple linear regression model based on UVB light intensity appears to be a useful tool for pred

209 ot of skin CORT levels, and had no effect on UVB stimulation of CRH and Ucn levels in the plasma, dem

210 area) had a significant preventive effect on UVB-induced suppression of the CHS response.

211 al found in plants of the genus Magnolia, on UVB-induced immunosuppression using contact hypersensiti

212 ailure to properly suppress DNA synthesis on UVB-damaged DNA templates.

213 D deficiency with either oral vitamin D3 or UVB does not improve the lipid profile.

214 ere sensitized to apoptosis induced by SS or UVB.

215 ependent film irradiation with either UVA or UVB dosages upwards of 80 J/cm(2) both reduce UV transmi

216 er different conditions (white light, UVA or UVB for 12 or 24h a day at 18 or 25 degrees C) to maximi

217 ed doses of longwave or shortwave UV (UVA or UVB) and found that UVA, but not UVB, induces progerin e

218 steroids, phototherapy (psoralen with UVA or UVB), topical chemotherapy, topical bexarotene, and radi

219 nal diary entries, and recording of personal UVB exposure doses with electronic dosimeters.

220 HaCaT cells in early phase (within 6 h) post-UVB.

221 l-NAME in partial restore IkappaB level post-UVB.

222 0741657 in CYP2R1 and rs4588 in GC predicted UVB-induced 25(OH)D concentrations as previously shown i

223 ific heterozygous deletion of SIRT1 promotes UVB-induced skin tumorigenesis, whereas homozygous delet

224 tify an essential role for CD1d in promoting UVB-induced cutaneous tissue injury and inflammation.

225 tion of myopia with ultraviolet B radiation (UVB; directly associated with time outdoors and sunlight

226 Loss of TC-PTP also reduced UVB-induced apoptosis.

227 um C (XPC), a protein critical for repairing UVB-induced DNA damage.

228 Mechanistically, Rg1 rescued UVB-induced HDAC2 degradation.

229 d that CD1d knockout (CD1d(-/-)) mice resist UVB-induced cutaneous tissue injury and inflammation com

230 (OH)D) synthesis are both initiated by solar UVB.

231 eous adverse and beneficial effects of solar UVB exposure in holidaymakers.

232 In both species, UVB irradiation produces peripheral sensitisation measur

233 In both species, UVB with heat rekindling produces central sensitisation.

234 the major determinants of vitamin D status (UVB exposure, diet, pigmentation, and genetics).

235 We then discuss how the lack of sufficient UVB exposure could have contributed to the rapid increas

236 Here we show that sunscreen (UVA superior, UVB sun protection factor (SPF) 50) delayed the onset of

237 helial compartment is sufficient to suppress UVB-induced inflammation.

238 tumors per mouse after 44 weeks of long-term UVB irradiation.

239 We conclude that UVB-induced vitamin D synthesis is associated with consi

240 We demonstrate that UVB-transformed HaCaT cells gain enhanced proliferation

241 We demonstrated that UVB exposure exacerbated inflammation and reduced both t

242 We determined that UVB irradiation is a potent inducer of eIF2-P in keratin

243 We previously found that UVB irradiation of the cornea caused the imbalance betwe

244 To test the hypothesis that UVB can activate the hypothalamic-pituitary-adrenal (HPA

245 Combined, our results indicate that UVB-mediated activation of TC-PTP plays an important rol

246 A luciferase reporter assay indicates that UVB-induced NF-kappaB activation is totally diminished i

247 Here, we report that UVB exposure triggers phosphatase and tensin homolog (PT

248 0 years from when it was first reported that UVB radiation exposure would modulate immune signaling,

249 Here we show that UVB radiation induces Sesn2 expression in normal human k

250 The UVB-induced reduction in both Dsg1 transcript and protei

251 e ablation of Langerhans cells abolished the UVB-induced phenotype.

252 ng of Has2 and especially Has3 decreased the UVB-induced accumulation of hyaluronan.

253 COX-2) expression and PGE2 production in the UVB-exposed skin.

254 The spin splittings of the UVB and the LCB near the Gamma-point in the Brillouin zo

255 Dsg1 in keratinocyte monolayers rescued the UVB-induced differentiation defect.

256 in UVA exposed skin and its response to the UVB spectrum of the solar UV flux remains unexplored.

257 ) have been shown to be responsible for this UVB-induced suppression of CHS.

258 t selected mammalian 14-3-3 proteins bind to UVB-induced phosphorylated histone H3 (Ser10 and Ser28).

259 acil-induced apoptosis and melanoma cells to UVB- and vemurafenib-induced apoptosis.

260 rmal differentiation, it also contributes to UVB-induced injury and tumorigenesis in vivo.

261 target Noxa, and sensitizes the epidermis to UVB-induced apoptosis in vivo, while heterozygous SIRT1

262 ced the DNA repair in melanocytes exposed to UVB and stimulated expression of p53 phosphorylated at S

263 contrast, female mice chronically exposed to UVB and treated topically with vitamin E alone showed a

264 opose a novel mechanism by which exposure to UVB activates a local HPA axis in skin, which in turn ac

265 N/TERT human keratinocytes upon exposure to UVB and the DNA-alkylating chemicals such as methyl meth

266 Exposure to UVB estimated by combining meteorological and questionna

267 Cutaneous exposure to UVB irradiation is an important source of vitamin D.

268 Upon exposure to UVB irradiation, fat-1 transgenic mice exhibited a signi

269 n keratinocytes was increased by exposure to UVB light through activation of the AKT pathway.

270 (HaCaT) cells through repetitive exposure to UVB radiation.

271 receptor 2, 3, or 4 agonists or exposure to UVB radiation.

272 Exposure of thrombocytopenic mice to UVB light provokes cutaneous petechial bleeding.

273 d from IL1r(-/-) mice were more resistant to UVB-triggered cell death compared with wild-type cells,

274 eIF2alpha-P is cytoprotective in response to UVB by a mechanism featuring translation of a specific s

275 ntral regulator for melanocytes' response to UVB exposure and reveal the molecular basis underlying t

276 the skin-draining lymph nodes in response to UVB exposure, connect the cutaneous immune response to C

277 or eIF2alpha-P cytoprotection in response to UVB in human keratinocytes.

278 is stimulated during the initial response to UVB irradiation, which leads to suppression of keratinoc

279 s AKT activation and survival in response to UVB stress and chemotherapeutics and suggest that Sesn2

280 ver, in male mice, the vitamin D response to UVB was attenuated and mineral and skeletal abnormalitie

281 Sunburn, an acute inflammatory response to UVB-induced cutaneous tissue injury, represents a clinic

282 by defects in multiple cellular responses to UVB-induced DNA damage, including through a failure to p

283 Wild-type mice were more sensitive to UVB and exhibited increased inflammation and greater act

284 e Rev3L deletion were much more sensitive to UVB radiation than mice defective in other DNA repair ge

285 d no effect upon apoptotic susceptibility to UVB or SS.

286 als, HF disruption altered susceptibility to UVB-induced BCCs.

287 In the mouse skin and skin tumors, UVB radiation downregulates E-cadherin.

288 d mushrooms can produce ergocalciferol under UVB irradiation.

289 Inflammation is a key mechanism underlying UVB's various detrimental effects.

290 rate that TC-PTP activity was increased upon UVB exposure, and overexpression of TC-PTP in keratinocy

291 inhibitors could reduce IKKalpha level upon UVB radiation.

292 ed electron transfer using longer wavelength UVB radiation.

293 trying to understand the mechanisms by which UVB initiates inflammatory responses and modulates immun

294 his study delineates the mechanisms by which UVB regulates protein synthesis in human keratinocytes a

295 iduals in summer, was highly correlated with UVB exposure, and was associated with greater HIV-1 repl

296 adults, the replenishment of vitamin D with UVB exposure would lower LDL-cholesterol concentrations

297 tamin D3 but significant downregulation with UVB.Correcting vitamin D deficiency with either oral vit

298 radiation of cultured human melanocytes with UVB stimulated ROS production, which was reduced in cell

299 tion of elastase activity did not occur with UVB.

300 MS patients treated with UVB phototherapy showed an increase in induced Tregs and