ライフサイエンスコーパス: hairless

1 vate the transcription factor, Suppressor of Hairless.

2 e recessive mcub allele, cub/cub mice appear hairless.

3 ly thought to be caused only by mutations in HAIRLESS.

4 activated transcription factor Suppressor of Hairless.

5 ess, decapentaplegic and Notch/Suppressor of Hairless.

6 epressor complexes, including the antagonist Hairless.

7 g site for the Notch effector, Suppressor of Hairless.

8 tream transcriptional effector Suppressor of Hairless.

9 t Insv can antagonize Notch independently of Hairless.

10 ) in concert with its Drosophila corepressor Hairless.

11 HYP7 encodes the RHL1 (ROOT HAIRLESS 1) protein, and sequence analysis reveals that

12 h and the transcription factor Suppressor of Hairless [3] [4] [5].

13 The levels of Suppressor of Hairless, a key transcriptional effector of Notch requir

14 In contrast, overexpression of Hairless, a negative regulator of the Notch pathway, and

15 appa, the mammalian homolog of Suppressor of Hairless, a protein that associates physically with Notc

16 h pathway transcription factor Suppressor of Hairless activates its own expression, specifically in t

17 nes fringe, Delta, Serrate and Suppressor of Hairless, also participate in Notch function during leg

18 taneous anthrax model have demonstrated that hairless and haired HRS/J mice are extremely resistant t

19 SKH-1 hairless and immunocompetent mice (n = 180) were fed AIN

20 L2 functioned as a CSL (CBF-1, suppressor of hairless and Lag-1)-dependent transcriptional co-activat

21 led a likely evolutionary connection between Hairless and Metastasis-associated (MTA) protein, a comp

22 ctivity that is independent of Suppressor of Hairless and might be used to link Notch activity to tha

23 As both are able to bind Hairless and Notch proteins, Su(H)(S269D) and Su(H)(R266

24 Both hairless and rhino mice have a number of skin and nail a

25 sed on the structure, we designed mutants in Hairless and Su(H) that affect binding, but do not affec

26 define crucial roles for the adaptor protein Hairless and the co-repressors Groucho and CtBP in confe

27 y genes Notch, presenilin, and Suppressor of Hairless and the Enhancer of split complex.

28 h the absolute requirement for Suppressor of Hairless and the Enhancer of split-Complex for cone cell

29 called CSL (CBF-1/RBP-J kappa, Suppressor of Hairless, and Lag-1) and a coactivator of the Mastermind

30 both endogenous CSL (for CBF1, Suppressor of Hairless, and Lag-1) and Mastermind-Like-1 (Maml).

31 lso known as RBP-Jkappa, CBF1, Suppressor of Hairless, and Lag-1) and recruits Mastermind-like transc

32 it associates with the CBF-1, Suppressor of Hairless, and Lag-2 (CSL) and Mastermind-Like (MAML) pro

33 ct to hair, knockout mice for vitA receptor, hairless, and vitamin D genes have similar phenotypes, a

34 The hairless AQP3 null mice had normal perinatal survival, g

35 onserved microsynteny suggest that S-CAP and Hairless arose from a tandem duplication of an ancestral

36 n the pathway, Notch, mastermind, Delta, and Hairless, as well as two novel mutations.

37 rmis in both resistant B6 and sensitive SKH1 hairless backgrounds, we show that the role of SIRT1 in

38 Roots of hairless barley (Hordeum vulgare L. cv Optic) mutant (NR

39 Hairless binding produces a large conformational change

40 Hairless binds the VDR in the presence of ligand through

41 e evidence that whether or not Suppressor-of-Hairless can become a transcriptional activator is the k

42 t finding that Drosophila CSL (Suppressor of Hairless) can also mediate transcriptional activation in

43 ferentially expressed in the differentiating hairless cells (atrichoblasts) during a period in which

44 ngle cortical cell differentiate into mature hairless cells (N cells; atrichoblasts).

45 of this aerial mycelium and grow as smooth, hairless colonies.

46 How did Hairless come to replace this ancestral paradigm?

47 e determine the X-ray structure of the Su(H)-Hairless complex bound to DNA.

48 The hairless cub/cub mcub/mcub mice show normal contact sens

49 teral inhibition mediated by a Suppressor of Hairless-dependent Notch signaling pathway, in which X-D

50 In Drosophila, the antagonist Hairless directly binds Su(H) (the fly CSL ortholog) to

51 ng a dominant negative form of Suppressor of Hairless (dn-Su(H)) results in reduced levels of spgcm m

52 Hairless dog breeds show a form of ectodermal dysplasia

53 t in a historical museum sample of pedigreed hairless dog skulls by using ancient DNA extraction and

54 Unlike in the coated wild type dogs, the hairless dogs were characterised in both the mandibular

55 cells via CSL (CBF-1, mammals; suppressor of hairless, Drosophila melanogaster; Lag-1, Caenorhabditis

56 -1 act7-4 and act8-2 act7-4) or totally root-hairless (e.g., act2-1 act8-2).

57 Human hairless encodes a putative single zinc finger transcrip

58 n inflammation and photocarcinogenesis using hairless fat-1 transgenic mice harboring omega-3 desatur

59 clinical features include a well-demarcated hairless fatty nevus on the scalp, benign ocular tumors,

60 ene, identified in mouse frizzy (fr) and rat hairless (fr(CR)) animals, respectively, have been propo

61 resent the genomic organization of the human hairless gene (HGMW-approved symbol HR), which spans ove

62 Mutations in the hairless gene (HR) cause this phenotype in both mouse an

63 ly, we cloned the human homolog of the mouse hairless gene and identified pathogenic mutations in sev

64 ody of evidence implicating mutations in the hairless gene as an underlying cause of congenital atric

65 chia with papules in a patient with a normal HAIRLESS gene but with mutations in both alleles of the

66 The human hairless gene encodes a putative single zinc-finger tran

67 f a 22-bp deletion mutation in exon 3 of the hairless gene in a large consanguineous Arab Palestinian

68 se mutation in the zinc-finger domain of the hairless gene in a large inbred family of Irish Travelle

69 irless mice carrying homozygous mutations in hairless gene manifest rudimentary hair follicles (HFs),

70 -activated transcription factor, whereas the hairless gene product (Hr) acts as a corepressor of both

71 The hr (hairless) gene encodes a putative transcription factor w

72 ed SC water content in AQP3 null mice in the hairless genetic background (165 +/- 10 versus 269 +/- 1

73 low-cell geometry and in vivo on the skin of hairless guinea pig (HGP).

74 Here we identify Hairless (H) as a Runt-interacting molecule that functio

75 Although Hairless (H) is the canonical nuclear Notch pathway inhi

76 Hairless (H), a novel Drosophila protein, binds to Su(H)

77 overed multiple alleles of groucho (gro) and Hairless (H).

78 motif similar to the Su(H)-binding domain in Hairless has revealed a likely evolutionary connection b

79 hat MTGR1 is in a complex with Suppressor of Hairless Homolog, a key Notch effector, and represses No

80 Near-naked hairless (Hr(N)) is a semi-dominant, spontaneous mutatio

81 The hairless (hr) and rhino (hrrh) mutations are autosomal r

82 al hair loss disorder caused by mutations in hairless (HR) and vitamin D receptor (VDR) genes, respec

83 The Hairless (Hr) gene encodes a nuclear receptor corepresso

84 The mammalian hairless (hr) gene plays a critical role in the maintena

85 Although mutations in the mammalian hairless (Hr) gene result in congenital hair loss disord

86 Both the vitamin D receptor (VDR) and hairless (hr) genes play a role in the mammalian hair cy

87 The frip gene maps to the hairless (hr) locus on mouse chromosome 14.

88 The hairless (HR) protein contains a Jumonji C (JmjC) domain

89 by allelism testing to be allelic with mouse Hairless (Hr).

90 In this study, we injected hairless immune competent mice with purified immunoglobu

91 ents' sera and then injected them into adult hairless immunocompetent mice.

92 hich some cells grow hairs and others remain hairless in a position-dependent manner, has become an e

93 Hairless is present only in the Pancrustacea, raising th

94 rave from the island of Malo (n = 9) and the hairless Kapia from the island of Tanna (n = 9), as well

95 y C promoter binding factor-1, suppressor of hairless, Lag-1 (CSL).

96 lar domain to a CSL (for CBF1, Suppressor of Hairless, LAG-1) protein.

97 ption factor CSL (CBF1/RBP-Jk, Suppressor of Hairless, Lag-1).

98 cy C-promoter binding factor-1/suppressor of hairless/lag-1 (CSL) and induces transcription of Notch

99 o repress all canonical [CBF-1/Suppressor of hairless/LAG-1 (CSL)-dependent] Notch signaling exclusiv

100 n factor called CSL (for CBF-1/Suppressor of Hairless/Lag-1) to induce expression of target genes.

101 binding protein CSL (for CBF-1/Suppressor of Hairless/Lag-1) to regulate target gene expression.

102 CSL (CBF1/Suppressor of Hairless/LAG-1), a core component of the Notch signaling

103 the DNA-binding protein CBF-1/suppressor of hairless/Lag1 (CSL) bound the VEGFR-3 promoter and trans

104 DNA-binding protein CSL (CBF1/Suppressor of Hairless/Lag1) and activate transcription of Notch-CSL t

105 Researchers studying evolution of 'naked' (hairless) larval cuticle in Drosophila sechellia have di

106 suggest a model in which Notch/Suppressor of Hairless levels are insufficient to activate rhomboid ex

107 determine how MC1R photoprotects, an in vivo hairless MC1R model containing Mc1r(-/-) albino, MC1R(+)

108 Hairless mice (SKH1-hrBR) are used as a model for human

109 In vivo experiments performed using SKH1 hairless mice also confirmed increased dermal penetratio

110 pharmacokinetic studies performed using SKH1 hairless mice also confirmed the efficacy of SP50 in der

111 Here, 9-10 challenges with oxazolone (Ox) to hairless mice also produced a chronic Th2-like HR.

112 ion of imiquimod or S-28463 to the flanks of hairless mice and rats leads to increases in local conce

113 l was topically applied on the skin of SKH-1 hairless mice at a dose of 10 micromol/mouse (in 0.2 ml

114 Hairless mice carrying homozygous mutations in hairless

115 ess mice, PKCepsilon overexpression in SKH-1 hairless mice decreased the latency (12 weeks), whereas

116 Overall, 100% of hairless mice developed >12 tumors per mouse after 32 we

117 ocol, the nontransgenic littermates or SKH-1 hairless mice did not develop tumors or pigmented cysts

118 y and restoration of the calcium gradient in hairless mice exposed to 4 degrees C external temperatur

119 T, but not OHBT, when applied to the skin of hairless mice following acute barrier disruption by tape

120 e was developed and compared to control SKH1 hairless mice in terms of skin tumor induction and extra

121 In this study, we used SKH-1 hairless mice in which COX-1 was selectively deleted to

122 Here, we generated Keap1(flox/flox) SKH-1 hairless mice in which Nrf2 is disrupted (Keap1(flox/flo

123 a representative omega-3 PUFA, in wild type hairless mice induced expression of the Nrf2 target prot

124 SKH-1 hairless mice lacking the EP2 receptor were therefore st

125 rified anti-CMP EBA antibodies injected into hairless mice produced the clinical, histological, immun

126 CFU of either acapsular or SLS- strains into hairless mice resulted in lesions approximately 70% smal

127 Our use of hairless mice revealed this response to be largely indep

128 Hairless mice should facilitate comparison of various ta

129 o application of siRNA formulation to SKH-1E hairless mice significantly suppressed GAPDH expression

130 PKCepsilon FVB/N transgenic mice with SKH-1 hairless mice to generate PKCepsilon-overexpressing SKH-

131 We exposed hairless mice to low-dose UV radiation over a period of

132 n hydrophilic antioxidants, we exposed SKH-1 hairless mice to O3 concentrations of 0, 0.8, 1, and 10

133 Tumor onset in hairless mice was 10 weeks earlier than in haired litter

134 SKH-1 hairless mice were exposed to a ultraviolet (UV) source

135 SKH-1 hairless mice were exposed to UVB alone for 15 weeks, an

136 Several groups of hairless mice were followed over a period of 18 mo to do

137 Hairless mice were injected with PAF or serotonin recept

138 f mtDNA mutations in UV-induced skin tumors, hairless mice were irradiated to produce tumors, and the

139 SKH-1 hairless mice were irradiated with ultraviolet B (UVB) t

140 SKH-1 hairless mice were irradiated with UVB and the skin remo

141 Tumors in hairless mice were more aggressive than in haired litter

142 Anesthetized hairless mice were scanned by using a 2.5-MHz transducer

143 Male SKH-1 hairless mice were subjected to full-thickness thermal i

144 SKH-1 hairless mice were topically treated with GTP (5 mg/0.2

145 Female SKH1 (hr/hr) albino hairless mice were treated 5 d per wk for 12 wk.

146 Hairless mice were treated topically with activators of

147 Hairless mice were treated with cyclophosphamide (100 mg

148 Topical treatment of normal hairless mice with 22(R)-hydroxycholesterol or 24(S),25-

149 reaction, initiated by treating the skin of hairless mice with a solution of dihydroxyacetone in buf

150 Moreover, topical treatment of hairless mice with ciglitazone or troglitazone increases

151 We treated Skh-1 hairless mice with daily doses of suberythemal UVB for 4

152 Hairless mice with Ercc1-deficient skin were hypersensit

153 Treatment of SKH-1 hairless mice with ultraviolet B light (UVB; 30 mJ/cm(2)

154 Treatment of SKH-1 hairless mice with UVB (30 mJ/cm(2)) twice a week for 20

155 efect is brittle hair resulting in alopecia (hairless mice).

156 of SC tocopherols to solar simulated UVR in hairless mice, (ii) the baseline levels and distribution

157 dothelial growth factor-A (VEGF-A) in normal hairless mice, a specific response to permeability barri

158 lopment, we bred Ptch(+/-)/C57BL6 with SKH-1 hairless mice, followed by brother-sister cross to get F

159 PARalpha, on hyperproliferative epidermis in hairless mice, induced either by repeated barrier abroga

160 In hairless mice, inflammatory infiltrate was found around

161 rneum, by acetone application on the skin of hairless mice, led to a marked accumulation of HA in the

162 As compared with the wild-type hairless mice, PKCepsilon overexpression in SKH-1 hairle

163 uced squamous papillomas in SENCAR and SKH-1 hairless mice, respectively, to Pc4-PDT, and assessed it

164 However, in SKH-1 hairless mice, the most common and highly sensitive mode

165 KH1 (nonpigmented) versus SKH2/J (pigmented) hairless mice, we evaluated how a pigment-dependent redu

166 ed in drinking water (0.2%, wt/vol) to SKH-1 hairless mice, which were then exposed to multiple doses

167 ments with three separate mouse lines (SKH-1 hairless mice, wild-type FVB, and protein kinase C epsil

168 to generate PKCepsilon-overexpressing SKH-1 hairless mice.

169 d associated mechanisms of silibinin in SKH1 hairless mice.

170 on UVB-induced skin carcinogenesis in SKH-1 hairless mice.

171 e development of UVB-induced tumors in SKH-1 hairless mice.

172 e topical application of HI-TOPK-032 in SKH1 hairless mice.

173 sis and c-Jun phosphorylation levels in SKH1 hairless mice.

174 was less pronounced in shaved haired than in hairless mice.

175 ependent depletion by solar simulated UVR in hairless mice; (ii) a gradient distribution within untre

176 We used the outbred, immune-competent Skh-1 hairless mouse model of UVB-induced inflammation and non

177 citation spectra (emission at 380 nm) of SKH hairless mouse model skin are characterized by two bands

178 Using a hairless mouse model, we have demonstrated that testoste

179 findings to the in vivo situations in SKH-1 hairless mouse model, which is regarded to have relevanc

180 ion-mediated skin tumorigenesis in the SKH-1 hairless mouse model.

181 les and a solar ultraviolet radiation-driven Hairless mouse model.

182 UVB-mediated skin carcinogenesis in an SKH-1 hairless mouse model.

183 The molecular basis of the hairless mouse phenotype was previously found to be the

184 .5 uM EGFR siRNA (50 nM SNA-NCs) for 3 wk to hairless mouse skin almost completely abolishes EGFR exp

185 -7-ene, in propylene glycol:ethanol (7:3) to hairless mouse skin and assessed whether discrete pH cha

186 Changes in hairless mouse skin as a function of age and chronic UVB

187 elphinidin (1 mg/0.1 ml DMSO/mouse) to SKH-1 hairless mouse skin inhibited UVB-mediated apoptosis and

188 e polymer Nafion) and a biological membrane (hairless mouse skin) recorded during diffusive and ionto

189 In hairless mouse skin, immunohistochemical analysis and fl

190 n immortalized HaCaT keratinocytes and SKH-1 hairless mouse skin.

191 MMP-3 (63%), MMP-7 (62%), and MMP-9 (60%) in hairless mouse skin.

192 days x 7 exposures) radiations in the SKH-1 hairless mouse skin.

193 studied the role of acid-sphingomyelinase in hairless mouse skin.

194 nsdermally delivered by iontophoresis across hairless mouse skin.

195 enzoyl peroxide produces skin changes in the hairless mouse that qualitatively resemble those produce

196 During chronologic aging in the hairless mouse, baseline epidermal DNA synthesis rates r

197 follicles, and the defects engendered by the hairless mutation, in live skin tissue.

198 Similar to individuals with HAIRLESS mutations, her skin showed an absence of normal

199 severe thymic developmental defects and the hairless (nude) phenotype.

200 sv fully rescued sensory organ precursors in Hairless null clones, indicating that Insv can antagoniz

201 er-sister cross to get F2 homozygous mutant (hairless) or wild-type (haired) mice.

202 ding of Drosophila CSL (called Suppressor of Hairless, or Su(H)) to the intracellular domain of Droso

203 nhanced cholangiocarcinoma growth in vivo in hairless outbred mice with severe combined immunodeficie

204 eam Element; combinations of a Suppressor of Hairless Paired Site (SPS) and a specific proneural prot

205 thway activation induced de novo HFs also in hairless paw skin, divorced from confounding effects of

206 fied proteomic changes that explain the root hairless phenotype and the altered immune response obser

207 em of generating an inducible and reversible hairless phenotype by anti-hedgehog monoclonal antibody

208 7 mutants and moderately suppressed the root-hairless phenotype of act2 act8 mutants.

209 The root hairless phenotype of sos4 mutants was complemented by t

210 The hairless phenotype was reversible upon suspension of mon

211 ntary hair follicles (HFs), epidermal cysts, hairless phenotype, and enhanced susceptibility to squam

212 cyanide in cys-c1 mutants as well as a root hairless phenotype.

213 ssive activities of TGF-alpha/EGFR result in hairless phenotypes and skin cancers.

214 he Notch pathway in Drosophila, utilizes the Hairless protein to recruit two co-repressors, Groucho (

215 sion requires a lower level of Suppressor of Hairless protein, and, consequently, a lower level of No

216 we inserted hollow, glass microneedles into hairless rat skin in vivo and human cadaver skin in vitr

217 Hairless rats additionally had dehydration defects in sk

218 In vivo experiments on hairless rats with leuprolide acetate confirmed the pote

219 Pharmacokinetic analysis in hairless rats yielded LNG delivery rates that maintained

220 pharmacokinetic studies were carried out on hairless rats, and DHE plasma levels were determined by

221 ow can be either the mammalian Suppressor of Hairless (RBP-J) or its paralogue, RBP-L.

222 Recombining binding protein suppressor of hairless (RBPJ) is considered a central transcriptional

223 nduce de novo hair follicles in a variety of hairless recipient skin sites.

224 uxin restored the root hair phenotype of the hairless root hair defective 6 (rhd6) mutant.

225 orph axes developed largely unbranched, root-hairless rootlets, here we report that stigmarian rootle

226 ak1 and Pak1 levels are high in UV-B-exposed hairless SKH mouse model skin samples as compared with u

227 UV carcinogenesis was performed in hairless SKH-1 mice by three protocols: dietary cyclospo

228 Female hairless SKh-1 mice receiving 0.4% and 0.04% lutein plus

229 Hairless SKH-1 mice were exposed once to UVB light (180

230 Hairless skh-1 mice were irradiated with UVB (three time

231 is and inhibit UVB-induced carcinogenesis in hairless SKH-1 mice.

232 nase C epsilon (PKCepsilon)expression in the hairless SKH-1 mouse strain commonly used in UV carcinog

233 llowing acute ultraviolet irradiation in the hairless SKH-1 mouse.

234 hrough disruption of Fas/Fas-L interactions, hairless SKH-hr1 mice were exposed to chronic UV irradia

235 We have previously shown that in hairless SKH-hr1 mice, UVB-induced p53 mutations arise v

236 isappearance of p53 mutations in the skin of hairless SKH-hr1 mice.

237 wild-type and AQP3 null mice generated in a hairless SKH1 genetic background.

238 ry, and wound healing in AQP3 null mice in a hairless (SKH1) genetic background and investigate the c

239 In hairless (SKH1) mice with the lambdasupFG1 transgene, in

240 cubated for 24 h under a cotton patch on the hairless skin of newborn mice and using scanning electro

241 e primaries arose on non-ultraviolet-exposed hairless skin of the extremities (3 and 14 per megabase

242 In contrast, the hairless skin of the naked mole-rats had an exceptional

243 irs that are widely spaced over an otherwise hairless skin.

244 mily are expressed in touch receptors in rat hairless skin.

245 A hairless SPARC-null mouse was developed and compared to

246 Therefore, novel hairless strains exhibiting comparable immunodeficiency

247 own of the Notch effecter gene Suppressor of Hairless Su(H) similarly results in a loss of cnidocyte

248 emented by the nuclear protein Suppressor of Hairless (Su(H)) and is triggered by the ligand Delta.

249 y with the DNA-binding protein Suppressor of hairless (Su(H)) in flies, or recombination signal bindi

250 Suppressor of Hairless (Su(H)) is a DNA-binding protein component of t

251 or for the DNA-binding protein Suppressor of Hairless (Su(H)) to mediate myriad cell fate decisions.

252 , Twist (Twi), Snail (Sna) and Suppressor of Hairless (Su(H)), and encode the threshold variable in t

253 nizing a repressor function of Suppressor of Hairless (Su(H)).

254 rget of Notch nuclear effector Suppressor of Hairless (Su(H)).

255 The Suppressor of Hairless (Su[H]) protein of the Notch pathway is require

256 e N-signal-dependent activator Suppressor of Hairless [Su(H)] and by the proneural bHLH proteins acha

257 the pathway are encoded by the suppressor of hairless [Su(H)] and deltex (dx) genes.

258 regulated transcription factor Suppressor of Hairless [Su(H)] and found that the fly genome contains

259 nisms, one that the depends on Suppressor of Hairless [Su(H)] and the other on Deltex1 (DTX1).

260 We show that Suppressor of Hairless [Su(H)] and the POU-domain factor Ventral veins

261 on in niche cells, whereas the Suppressor of Hairless [Su(H)] and U-shaped (Ush) transcriptional regu

262 hows that A2BP1 is part of the Suppressor of Hairless [Su(H)] complex in the presence and absence of

263 ression of a dominant-negative Suppressor of Hairless [Su(H)] construct, confirming that Notch active

264 the Notch signaling pathway TF Suppressor of Hairless [Su(H)] discriminates PC from CC enhancer activ

265 on gene expression through the Suppressor of Hairless [Su(H)] DNA-binding protein.

266 A-binding transcription factor Suppressor of Hairless [Su(H)] functions as an activator during Notch

267 nvolves a DNA binding protein, Suppressor of Hairless [Su(H)] in Drosophila and CBF1 in mammals, and

268 anscription factor CSL, called Suppressor of Hairless [Su(H)] in Drosophila.

269 Suppressor of Hairless [Su(H)] is predominantly associated with solubl

270 e or active forms of the RBP-J/Suppressor of Hairless [Su(H)] transcription factor indicated that act

271 homology in a binding site for Suppressor of Hairless [Su(H)], a transcriptional mediator of Notch si

272 ed by overexpression of Notch, Suppressor of Hairless [Su(H)], and Enhancer of split m7.

273 N pathway transcription factor Suppressor of Hairless [Su(H)], and their activation is generally high

274 sed repressors, Runt (Run) and Suppressor of Hairless [Su(H)], in patterning the Drosophila embryo.

275 ammalian homolog of Drosophila Suppressor of Hairless [Su(H)], switches from a transcriptional repres

276 Suppressor of Hairless [Su(H)], the transcription factor at the end of

277 During Drosophila development Suppressor of Hairless [Su(H)]-dependent Notch activation upregulates

278 g effector of Notch signaling, Suppressor of Hairless [Su(H)].

279 the Notch transcription factor Suppressor of Hairless [Su(H)].

280 Suppressor of Hairless [Su(H)]/Lag-1/RBP-Jkappa/CBF1 is the only known

281 e inhibits Notch-mediated CBF1/Suppressor of Hairless [(Su(H)]/Lag-1-dependent transcription and indu

282 that the transcription factor Suppressor of Hairless, Su(H), helps define dorsal boundaries for many

283 activated transcription factor Suppressor of Hairless, suggesting that all are directly regulated by

284 either Notch signaling through Suppressor of Hairless (SuH) nor deltaD is necessary for the wild-type

285 Different amounts of Suppressor of Hairless (SuH)-dependent Notch (N) signaling is often us

286 discover an initial sluggish response of the hairless tail epidermis to wounding that is rapidly comp

287 ncidence of BCCs was significantly higher in hairless than in haired animals; however, the magnitude

288 t cluster of binding sites for Suppressor of Hairless, the transducing transcription factor for the p

289 Although nude mice are not truly hairless, they demonstrate abnormal hair structure and g

290 with the transcription factor Suppressor of Hairless to regulate gene expression.

291 luate the susceptibility of PKCepsilon SKH-1 hairless transgenic mice to UVR carcinogenesis, the mice

292 The SKH hairless transgenic mice were observed to be as sensitiv

293 anscriptional repressor Yan or Suppressor of Hairless, two previously identified targets of Spen.

294 The human homolog of a murine gene, hairless, was localized in this interval by radiation hy

295 h (recombining binding protein suppressor of hairless) we observed excessive sprouting of segmental a

296 SC hydration in hairless wild-type and AQP3 null mice was reduced to com

297 tion with RBPJ, the vertebrate Suppressor of Hairless, within a stable trimeric DNA-binding complex (

298 reduces photocarcinogenesis in UV-irradiated hairless WT repair-proficient and Xpc(+/-) heterozygous

299 fects of Polypodium leucotomos extract (PL), hairless Xpc(+/-) mice were fed for 10 days with PL (300

300 aneous flaps 2 x 10 cm2 were raised in white hairless Yucatan miniature pigs and were treated with a