ライフサイエンスコーパス: hairless

1 epressor complexes, including the antagonist Hairless.

2 vate the transcription factor, Suppressor of Hairless.

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

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

5 activated transcription factor Suppressor of Hairless.

6 ess, decapentaplegic and Notch/Suppressor of Hairless.

7 cooperation with Suppressor of Hairless and Hairless.

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

9 tream transcriptional effector Suppressor of Hairless.

10 t Insv can antagonize Notch independently of Hairless.

11 ) in concert with its Drosophila corepressor Hairless.

12 esent a molecular analysis of the RHL1 (ROOT HAIRLESS 1) gene that, if mutated, prevents the formatio

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

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

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

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

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

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

19 stasis analysis indicates that Suppressor of Hairless acts downstream of numb, and results from in vi

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

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

22 ions in close cooperation with Suppressor of Hairless and Hairless.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

40 Hairless binding produces a large conformational change

41 Hairless binds the VDR in the presence of ligand through

42 ligule (ectopic ligule), auricle-like, macro-hairless blade and wild-type blade.

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

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

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

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

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

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

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

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

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

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

53 Hairless dog breeds show a form of ectodermal dysplasia

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

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

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

57 -1 act7-4 and act8-2 act7-4) or totally root-hairless (e.g., act2-1 act8-2).

58 Human hairless encodes a putative single zinc finger transcrip

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

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

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

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

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

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

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

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

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

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

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

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

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

72 Recently, a mutation in the human hairless gene was implicated in the pathogenesis of cong

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

74 ementation groups corresponding to the 'root hairless' genes RHL1, RHL2 and RHL3 and the 'ectopic roo

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

76 Delta (Dl) and Hairless (H) are two chromosome 3 candidate neurogenic l

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

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

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

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

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

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

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

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

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

86 Transcription of the rat hairless (hr) gene is highly up-regulated by thyroid hor

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

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

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

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

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

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

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

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

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

96 present evidence that a Ciona Suppressor of Hairless inverted question markCi-Su(H) inverted questio

97 These studies reveal that Suppressor of Hairless is required for only a subset of the asymmetric

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

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

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

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

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

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

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

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

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

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

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

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

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

111 hat the genetic interaction between numb and Hairless may occur through direct protein-protein intera

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

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

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

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

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

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

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

119 Hairless mice carrying homozygous mutations in hairless

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

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

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

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

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

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

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

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

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

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

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

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

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

133 Hairless mice should facilitate comparison of various ta

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

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

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

137 To test this hypothesis, SKH-1 hairless mice were anesthetized and exposed for 2 h to O

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

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

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

141 Hairless mice were injected with PAF or serotonin recept

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

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

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

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

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

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

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

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

150 Hairless mice were treated topically with activators of

151 Hairless mice were treated with cyclophosphamide (100 mg

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

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

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

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

156 Hairless mice with Ercc1-deficient skin were hypersensit

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

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

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

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

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

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

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

164 In hairless mice, inflammatory infiltrate was found around

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

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

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

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

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

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

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

172 d associated mechanisms of silibinin in SKH1 hairless mice.

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

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

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

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

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

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

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

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

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

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

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

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

185 .5 uM EGFR siRNA (50 nM SNA-NCs) for 3 wk to hairless mouse skin almost completely abolishes EGFR exp

186 -7-ene, in propylene glycol:ethanol (7:3) to hairless mouse skin and assessed whether discrete pH cha

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

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

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

190 In hairless mouse skin, immunohistochemical analysis and fl

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

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

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

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

195 nsdermally delivered by iontophoresis across hairless mouse skin.

196 is factor in cultures of cells isolated from hairless mouse skin.

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

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

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

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

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

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

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

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

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

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

207 7 mutants and moderately suppressed the root-hairless phenotype of act2 act8 mutants.

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

209 The hairless phenotype was reversible upon suspension of mon

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

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

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

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

214 Hairless rats additionally had dehydration defects in sk

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

242 Therefore, novel hairless strains exhibiting comparable immunodeficiency

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

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

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

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

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

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

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

250 f the pathway: Deltex (Dx) and Suppressor of Hairless (Su(H)).

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

287 l to the murine homolog of the suppressor of hairless transcription factor, also known as recombinati

288 he recognition sequence of the Suppressor of Hairless transcription factor, thereby raising the possi

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

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

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

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

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

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

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

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

297 forms of X-Delta-2 and Xenopus Suppressor of Hairless (X-Su(H)) into embryos, and assayed the effects

298 solated the Xenopus homolog of Suppressor of Hairless (X-Su(H)), a component of the Notch signaling p

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