ライフサイエンスコーパス: xeroderma

1 by a report demonstrating a low level of the xeroderma pigmentosa group A (XPA) protein and induction

2 ), a protein implicated in the human disease xeroderma pigmentosa.

3 The R273H mutant of p48 identified from a xeroderma pigmentosium (group E) patient is not subjecte

4 is mutated in the repair-deficiency disease xeroderma pigmentosum (Group E).

5 suffering from the repair deficiency disease xeroderma pigmentosum (group E).

6 tients, aged 1-61 years, were diagnosed with xeroderma pigmentosum (n = 77) or xeroderma pigmentosum/

7 Imiquimod enhanced the expression of xeroderma pigmentosum (XP) A and other DNA repair genes

8 nd CSA, leads to hereditary diseases such as xeroderma pigmentosum (XP) and Cockayne syndrome (CS).

9 two rare genetic disorders, the cancer-prone xeroderma pigmentosum (XP) and the cancer-free, multisys

10 linical entities, including the cancer-prone xeroderma pigmentosum (XP) and the multisystem disorder

11 Xeroderma pigmentosum (XP) and trichothiodystrophy (TTD)

12 he diverse clinical features associated with xeroderma pigmentosum (XP) and trichothiodystrophy (TTD)

13 ry cancer-prone DNA repair-defective disease xeroderma pigmentosum (XP) are highly predisposed to UV

14 Cockayne syndrome (CS) and xeroderma pigmentosum (XP) are human photosensitive dise

15 ted mutations of the TFIIH helicase subunits xeroderma pigmentosum (XP) B or XPD yield overlapping DN

16 Mutations of the involved proteins cause the xeroderma pigmentosum (XP) cancer predisposition syndrom

17 The use of xeroderma pigmentosum (XP) cells, which are deficient in

18 Xeroderma pigmentosum (XP) complementation group A (XPA)

19 Xeroderma pigmentosum (XP) complementation group E gene

20 t from cell strains derived from a subset of Xeroderma Pigmentosum (XP) complementation group E indiv

21 ction and mutational defects associated with xeroderma pigmentosum (XP) disease, a series of stable b

22 ines derived from Cockayne syndrome (CS) and Xeroderma pigmentosum (XP) group C patients, that are de

23 Individuals with the genetic disease xeroderma pigmentosum (XP) have impaired nucleotide exci

24 XPC DNA repair gene in 74% of families with xeroderma pigmentosum (XP) in the Maghreb region (Algeri

25 Xeroderma pigmentosum (XP) is a heritable human disorder

26 Xeroderma pigmentosum (XP) is a human disorder which is

27 Xeroderma pigmentosum (XP) is a human genetic disease wh

28 Xeroderma pigmentosum (XP) is a rare autosomal recessive

29 Xeroderma pigmentosum (XP) is a rare DNA repair disorder

30 Xeroderma pigmentosum (XP) is a rare, autosomal recessiv

31 Xeroderma pigmentosum (XP) is a skin cancer-prone autoso

32 ene can result in the cancer-prone disorders xeroderma pigmentosum (XP) or the XP-Cockayne syndrome c

33 Xeroderma pigmentosum (XP) patients are highly sensitive

34 Xeroderma pigmentosum (XP) patients have 1,000-fold high

35 in cutaneous melanoma induction, we studied xeroderma pigmentosum (XP) patients who have defective D

36 compound heterozygous skin fibroblasts from xeroderma pigmentosum (XP) patients with different PTCs

37 Xeroderma pigmentosum (XP) patients with inherited defec

38 mary human fibroblasts from individuals with Xeroderma Pigmentosum (XP) that harbor mutations in the

39 The xeroderma pigmentosum (XP) variant (XPV) is a form of XP

40 is past UV photoproducts and is deficient in xeroderma pigmentosum (XP) variants.

41 h normal human fibroblasts and NER-defective xeroderma pigmentosum (XP) XPA and XPG cells.

42 dividuals initially classified as group E of xeroderma pigmentosum (XP), a hereditary, photosensitive

43 Xeroderma pigmentosum (XP), a UV-sensitivity syndrome ch

44 NA partially complementing UV sensitivity in xeroderma pigmentosum (XP), but this was not explored fu

45 In humans, a deficiency in NER causes xeroderma pigmentosum (XP), characterized by extreme sen

46 e neurodegenerative and progeroid disorders (xeroderma pigmentosum (XP), Cockayne syndrome (CS) and t

47 ause three distinct phenotypes: cancer-prone xeroderma pigmentosum (XP), or aging disorders Cockayne

48 To document the ocular manifestations of xeroderma pigmentosum (XP), presenting via the United Ki

49 Using repair-deficient xeroderma pigmentosum (XP)-A cells that stably express p

50 be involved in the repair of psoralen ICLs [xeroderma pigmentosum (XP)-A, XP-C, XP-F, Cockayne's syn

51 milies with the autosomal recessive disorder xeroderma pigmentosum (XP).

52 on result in the skin cancer-prone disorder, xeroderma pigmentosum (XP).

53 e clinical features of another NER syndrome, xeroderma pigmentosum (XP).

54 in the UV-induced skin cancer-prone disease xeroderma pigmentosum (XP).

55 nes encoding NER factors are associated with xeroderma pigmentosum (XP).

56 transcription factor IIH result in combined xeroderma pigmentosum (XP)/Cockayne syndrome (CS), a sev

57 e human DDB2 gene generate the E subgroup of xeroderma pigmentosum (XP-E).

58 DNA polymerase eta (pol eta), encoded by the xeroderma pigmentosum (XP-V) gene, plays an essential ro

59 counterpart, POLH, cause the variant form of xeroderma pigmentosum (XP-V), and XP-V individuals suffe

60 he gene implicated in the hereditary disease xeroderma pigmentosum (XPG, also known as Ercc5).

61 The variant form of the human syndrome xeroderma pigmentosum (XPV) is caused by a deficiency in

62 e cancer prone syndrome, the variant form of xeroderma pigmentosum (XPV).

63 s POLH) in humans causes the variant form of xeroderma pigmentosum (XPV).

64 ed ATR's interaction with the key NER factor xeroderma pigmentosum A (XPA) and facilitated recruitmen

65 ated complex with the key DNA repair protein xeroderma pigmentosum A (XPA).

66 in part by the circadian oscillation of the xeroderma pigmentosum A DNA damage recognition protein.

67 The XPA (Xeroderma pigmentosum A) protein is one of the six core

68 We have assessed the ability of xeroderma pigmentosum and normal keratinocytes grown out

69 molecular understanding of mutations causing xeroderma pigmentosum and trichothiodystrophy in humans.

70 tructural basis for defects in patients with xeroderma pigmentosum and trichothiodystrophy, with muta

71 ns for understanding the differences between xeroderma pigmentosum and TTD and illustrate the value o

72 sts of a core that includes the DNA helicase Xeroderma pigmentosum B (XPB) and a kinase subcomplex.

73 The xeroderma pigmentosum C (XPC) complex initiates nucleoti

74 s that abrogation of NER, by deletion of the xeroderma pigmentosum C (Xpc) gene, will heighten melano

75 tion of ubiquitinated proteins and decreased xeroderma pigmentosum C (XPC) levels in mice, indicative

76 environmental sources are recognized by the xeroderma pigmentosum C (XPC) nucleotide excision repair

77 The xeroderma pigmentosum C (XPC) protein has a central role

78 Xeroderma pigmentosum C (XPC) protein initiates the glob

79 The xeroderma pigmentosum C (XPC) protein is essential for i

80 pressed expression of the key GG-NER protein xeroderma pigmentosum C (XPC) through the AKT/p38 signal

81 air through suppressing the transcription of xeroderma pigmentosum C (XPC), a factor essential for in

82 -induced DNA damage repair and expression of xeroderma pigmentosum C (XPC), a protein critical for re

83 o deficient in global genomic repair [Csb-/-/xeroderma pigmentosum C (Xpc)-/-] are more profoundly af

84 e recently identified the DNA-repair complex xeroderma pigmentosum C (XPC)-RAD23B-CETN2 as a stem cel

85 the intrinsic genomic instability arising in xeroderma pigmentosum C (XPC).

86 1 promoted ubiquitylation of SUMOylated XPC (xeroderma pigmentosum C) protein, a central DNA damage r

87 Xeroderma pigmentosum cells deficient in the NER genes X

88 rigin-based shuttle vector and replicated in xeroderma pigmentosum complementation group A (XPA) cell

89 is greater than that previously measured in Xeroderma pigmentosum complementation group A (XPA) mice

90 Xeroderma pigmentosum complementation group A (XPA) prot

91 which actively recruits the key NER protein xeroderma pigmentosum complementation group A (XPA) to s

92 1, telomeric repeat binding factor 1 (TRF1), xeroderma pigmentosum complementation group A (XPA), pyg

93 e damage-binding proteins of excision repair xeroderma pigmentosum complementation group A and C prot

94 Xeroderma pigmentosum complementation group A protein (X

95 the nucleotide excision repair factor, XPA (xeroderma pigmentosum complementation group A protein).

96 Expression of DNA repair gene XPA (xeroderma pigmentosum complementation group A) was signi

97 5-HT receptor antagonists into UV-irradiated Xeroderma pigmentosum complementation group A-deficient

98 at includes two DNA helicases encoded by the Xeroderma pigmentosum complementation group B (XPB) and

99 ompared cells expressing only a mutated p89 (xeroderma pigmentosum complementation group B [XPB]), th

100 ough positively regulating the expression of xeroderma pigmentosum complementation group C (XPC) and

101 The Xeroderma pigmentosum complementation group C (XPC) comp

102 e excision repair (NER) via deubiquitinating xeroderma pigmentosum complementation group C (XPC) prot

103 iated domains (UBA1 and UBA2) separated by a xeroderma pigmentosum complementation group C binding (X

104 ytoplasm and accumulates in the nucleus in a xeroderma pigmentosum complementation group C protein (X

105 The xeroderma pigmentosum complementation group E (XP-E) gen

106 repair cross-complementing protein 1 (ERCC1)/xeroderma pigmentosum complementation group F (XPF) nucl

107 pair cross-complementation group 1) and XPF (xeroderma pigmentosum complementation group F), leads to

108 urrent model and argue that the endonuclease xeroderma pigmentosum complementation group F-excision r

109 ned all three fibroblast strains to the rare xeroderma pigmentosum complementation group G (only 10 o

110 ) that showed residual ability to complement xeroderma pigmentosum complementation group G cells.

111 We studied three newly diagnosed xeroderma pigmentosum complementation group G patients w

112 Keratinocytes have been studied from xeroderma pigmentosum complementation groups A (three bi

113 ulation of proteins involved in NER, such as xeroderma pigmentosum complimentation group A (XPA).

114 s associated with various conditions such as xeroderma pigmentosum continue to be uncovered, the lite

115 Xeroderma pigmentosum factor D (XPD) is a 5'-3' superfam

116 the disruption of CSA, CSB, or some types of xeroderma pigmentosum genes.

117 Here, we report that TC-NER-deficient cells [xeroderma pigmentosum group A (XP-A), XP-D, XP-F, XP-G,

118 Xeroderma pigmentosum group A (XPA) is a core nucleotide

119 Xeroderma pigmentosum Group A (XPA) is a crucial factor

120 Human xeroderma pigmentosum group A (XPA) is an essential prot

121 ate-limiting subunit of excision repair, the xeroderma pigmentosum group A (XPA) protein, and the exc

122 idence showing that the cellular function of xeroderma pigmentosum group A (XPA), a major nucleotide

123 We identify mitochondrial dysfunction in xeroderma pigmentosum group A (XPA), a nucleotide excisi

124 se progeroid cells exhibited nuclear foci of xeroderma pigmentosum group A (XPA), a unique nucleotide

125 ncluding TFIID, TFIIH, RNA polymerase II and xeroderma pigmentosum group A (XPA), in the triplex-medi

126 te cyclase activity, which in turn activated Xeroderma pigmentosum group A (XPA)-binding protein 1 an

127 ATR physically interacts with the NER factor Xeroderma pigmentosum group A (XPA).

128 The three xeroderma pigmentosum group A and the xeroderma pigmento

129 is activated in Cockayne's syndrome but not Xeroderma pigmentosum group A cells providing evidence t

130 The xeroderma pigmentosum group A complementing protein (XPA

131 JW cells and cells with defective Artemis or xeroderma pigmentosum group A genes.

132 on of the nuclear foci formed with RecQ4 and xeroderma pigmentosum group A in human cells.

133 Bioassays were conducted in xeroderma pigmentosum group A knockout mice and diethyln

134 eased gamma-OHPdG levels in the liver DNA of xeroderma pigmentosum group A knockout mice and remarkab

135 asts deficient in DNA repair (derived from a xeroderma pigmentosum group A patient) failed to augment

136 Two proteins, xeroderma pigmentosum group A protein (XPA) and replicat

137 of most NER proteins, but low levels of the xeroderma pigmentosum group A protein (XPA) and the ERCC

138 A direct interaction between RPA and the xeroderma pigmentosum group A protein (XPA) facilitates

139 ing protein that can form a complex with the xeroderma pigmentosum group A protein (XPA).

140 that of the damage recognition protein XPA (xeroderma pigmentosum group A protein).

141 omparable decreases in zinc content for XPA (xeroderma pigmentosum group A) protein (CCCC zinc finger

142 we showed that the essential NER factor XPA (xeroderma pigmentosum group A) underwent nuclear accumul

143 istently, RecQ4 could directly interact with xeroderma pigmentosum group A, and this interaction was

144 The human xeroderma pigmentosum group B (XPB) helicase is essentia

145 of UVB damage to DNA, is lost or mutated in xeroderma pigmentosum group C (XP-C), a rare inherited d

146 V-induced interaction of DDB2 with PARP-1 or xeroderma pigmentosum group C (XPC) and also decreases l

147 te that the mRNA and protein products of the xeroderma pigmentosum group C (XPC) gene are UV-inducibl

148 We investigated the contribution of the xeroderma pigmentosum group C (XPC) gene to DNA repair.

149 Recognition of DNA lesions by xeroderma pigmentosum group C (XPC) protein in chromatin

150 The Xeroderma Pigmentosum group C (XPC) protein is indispens

151 The xeroderma pigmentosum group C (XPC)-Rad23B complex is in

152 HR23B complex mimics the interaction between xeroderma pigmentosum group C and HR23B, thereby providi

153 glycanase catalytic core in complex with the xeroderma pigmentosum group C binding domain from HR23B.

154 The different interaction interfaces of the xeroderma pigmentosum group C binding domains in yeast a

155 e process of cellular transformation of this xeroderma pigmentosum group C cell strain involves the p

156 s associated with the transformation of this xeroderma pigmentosum group C cell strain, we examined t

157 Cells from humans with xeroderma pigmentosum group C do not perform NER in the

158 5), isolated from normal appearing skin of a xeroderma pigmentosum group C patient that repeatedly un

159 oaded full-length centrin-2 complexed with a xeroderma pigmentosum group C peptide.

160 Two xeroderma pigmentosum group C peptides both bound to cen

161 f molecular interactions between centrin and xeroderma pigmentosum group C protein, we characterized

162 nucleotide excision repair by binding to the xeroderma pigmentosum group C protein.

163 le in damage recognition in complex with the xeroderma pigmentosum group C protein.

164 Xeroderma pigmentosum group C samples proved heterogeneo

165 the DNA repair factor Rad4 (termed XPC, for xeroderma pigmentosum group C, in humans).

166 hich are implicated in Cockayne syndrome and xeroderma pigmentosum group C, respectively, modulates c

167 lutamine-encoding allele at codon 751 of the xeroderma pigmentosum group D (XPD) DNA repair gene were

168 The xeroderma pigmentosum group D (XPD) gene encodes a DNA h

169 The xeroderma pigmentosum group D (XPD) helicase is a compon

170 Xeroderma pigmentosum group D (XPD) helicase is a compon

171 The xeroderma pigmentosum group D (XPD) helicase is a subuni

172 The xeroderma pigmentosum group D (XPD) protein is a subunit

173 The Xeroderma pigmentosum group D (XPD) protein is an essent

174 hether polymorphisms in the DNA repair gene, Xeroderma pigmentosum group D (XPD), modified the risk.

175 In a subset of 55 patients, the xeroderma pigmentosum group D (XPD)-751, x-ray cross-com

176 Xeroderma pigmentosum group D (XPD/ERCC2) encodes an ATP

177 The archaeal Rad3 (xeroderma pigmentosum group D protein (XPD)) helicase is

178 The archaeal Rad3 helicase XPD (xeroderma pigmentosum group D protein) from Ferroplasma

179 three xeroderma pigmentosum group A and the xeroderma pigmentosum group D samples were at least six

180 s been proposed that the 5'-3' helicase XPD (xeroderma pigmentosum group D) protein plays a decisive

181 The xeroderma pigmentosum group E (XP-E) causing K244E mutan

182 tions in DDB2 cause a cancer prone syndrome, xeroderma pigmentosum group E (XP-E).

183 Here, we show that the xeroderma pigmentosum group E (XPE) gene product, damage

184 is absent from cells of a subset (Ddb(-)) of xeroderma pigmentosum Group E (XPE) patients.

185 g histone H2A at UV-damaged DNA sites in the xeroderma pigmentosum group E cells contributes to the f

186 DNA damaged by UV, is absent in a subset of xeroderma pigmentosum group E cells, and is required for

187 The xeroderma pigmentosum group E gene product DDB2, a prote

188 Cell strains derived from xeroderma pigmentosum group E individuals also have enha

189 nding activity (UV-DDB) is deficient in some xeroderma pigmentosum group E individuals due to mutatio

190 and DDB2, the latter of which is mutated in xeroderma pigmentosum group E patients, is a substrate-r

191 r-proficient IMR-90 and two repair-deficient xeroderma pigmentosum group E strains (XP95TO and XP3RO)

192 utations in the human DDB2 gene give rise to xeroderma pigmentosum group E, a disease characterized b

193 Mutations in DDB2 are responsible for xeroderma pigmentosum group E, a disorder with defects i

194 Mutations in DDB2 are responsible for Xeroderma Pigmentosum group E, but no mutants of mammali

195 The DDB2 gene, which is mutated in xeroderma pigmentosum group E, enhances global genomic r

196 been correlated with the hereditary disease xeroderma pigmentosum group E.

197 is missing in partially purified extracts of xeroderma pigmentosum group-D fibroblasts.

198 ome sample showed the high susceptibility of xeroderma pigmentosum groups A and D only at a higher fl

199 ry photosensitive disorders, including other xeroderma pigmentosum groups, Cockayne syndrome, and a n

200 nd tumor necrosis factor-alpha from cultured xeroderma pigmentosum keratinocytes tended to occur at l

201 enzymes to sun-damaged skin of patients with xeroderma pigmentosum lowered the rate of development of

202 ion synthesis: DNA polymerase eta, the yeast Xeroderma pigmentosum ortholog, and Rev1, a deoxycytidyl

203 kage is exacerbated in Cockayne Syndrome and xeroderma pigmentosum patient-derived lymphoblastoid and

204 role in the etiology of neurodegeneration in xeroderma pigmentosum patients.

205 excision repair (NER) pathway can cause the xeroderma pigmentosum skin cancer predisposition syndrom

206 In patients with xeroderma pigmentosum the frequency of all forms of skin

207 ith the deficiency of the DNA repair protein xeroderma pigmentosum type A (XPA).

208 s, and all 17 were in complementation groups xeroderma pigmentosum type A or type D and reported acut

209 opsies), C (three biopsies), D (one biopsy), xeroderma pigmentosum variant (two biopsies), and Cockay

210 ed variable regions from three patients with xeroderma pigmentosum variant (XP-V) disease, who lack p

211 DNA from lymphocytes of patients with xeroderma pigmentosum variant (XP-V) disease, whose poly

212 Human polymerase eta, a product of the xeroderma pigmentosum variant (XP-V) gene, catalyzed the

213 dent pathway and, as a consequence, protects xeroderma pigmentosum variant (XP-V) patient cells from

214 cific DNA polymerase POLH gene is mutated in xeroderma pigmentosum variant (XP-V) patients who exhibi

215 leta), which is defective in humans with the Xeroderma pigmentosum variant (XP-V) phenotype, little i

216 UV-induced replication arrest in the xeroderma pigmentosum variant (XPV) but not in normal ce

217 ging agents, have been evaluated in HeLa and xeroderma pigmentosum variant (XPV) cell extracts.

218 human fibroblasts (NHF1) were compared with xeroderma pigmentosum variant (XPV) cells (polymerase et

219 polymerase eta (PolH) is the product of the xeroderma pigmentosum variant (XPV) gene and a well-char

220 NA polymerase eta (Pol(eta)), encoded by the Xeroderma pigmentosum variant (XPV) gene, is known for i

221 The xeroderma pigmentosum variant (XPV) is a genetic disease

222 Xeroderma pigmentosum variant (XPV) patients have normal

223 A synthesis, and PolH deficiency predisposes xeroderma pigmentosum variant (XPV) patients to cancer.

224 Xeroderma pigmentosum variant (XPV) patients with mutati

225 The inherited cancer-propensity syndrome xeroderma pigmentosum variant (XPV) results from error-p

226 t of malignant skin cancers in patients with xeroderma pigmentosum variant (XPV), an autosomal recess

227 blished ultraviolet-sensitive syndrome, only xeroderma pigmentosum variant cells exhibited normal uns

228 DNAs containing gamma-HOPdG in wild type and xeroderma pigmentosum variant cells revealed a somewhat

229 Experiments with xeroderma pigmentosum variant cells, which lack pol eta,

230 d a somewhat decreased mutation frequency in xeroderma pigmentosum variant cells.

231 ral blood lymphocytes of three patients with xeroderma pigmentosum variant disease, whose polymerase

232 tion repair after ultraviolet irradiation in xeroderma pigmentosum variant fibroblasts, and is involv

233 These results suggest that xeroderma pigmentosum variant heterozygotes can be ident

234 ne are responsible for the genetic defect in xeroderma pigmentosum variant patients.

235 and shown to be defective in humans with the Xeroderma pigmentosum variant phenotype.

236 The xeroderma pigmentosum variant samples showed intermediat

237 Patients with xeroderma pigmentosum variant show clinical photosensiti

238 ernative, simple method for the diagnosis of xeroderma pigmentosum variant that measures by autoradio

239 roductive rearrangements from a patient with xeroderma pigmentosum variant with a defect in pol eta w

240 -proficient but not in Poleta-deficient XPV (Xeroderma pigmentosum variant) cells, suggesting that US

241 DNA polymerase eta (Pol(eta), xeroderma pigmentosum variant, or Rad30) plays an import

242 lication of damaged DNA in the human disease xeroderma pigmentosum variant.

243 tosensitive patients that were identified as xeroderma pigmentosum variant.

244 lymerase eta (poleta), which is defective in xeroderma pigmentosum variants, there is little informat

245 lymerase eta (poleta), which is defective in xeroderma pigmentosum variants, there is little informat

246 rticularly in individuals with NER-defective xeroderma pigmentosum who accumulate dimers, errors made

247 ssues from patients with the genetic disease xeroderma pigmentosum who are unable to carry out nucleo

248 irteen corneal specimens of 11 patients with xeroderma pigmentosum who underwent keratoplasty (lamell

249 ignificant hearing loss in the patients with xeroderma pigmentosum with xeroderma pigmentosum-type ne

250 splants, or hereditary disease (albinism and xeroderma pigmentosum), prior to the start date, conduct

251 sorders of DNA repair (Cockayne syndrome and xeroderma pigmentosum).

252 ding pol eta are implicated in nearly 20% of xeroderma pigmentosum, a human disease characterized by

253 repair (NER) pathway by mutations can cause xeroderma pigmentosum, a syndrome predisposing affected

254 In patients with xeroderma pigmentosum, aged 4-30 years, a four-frequency

255 cause the genetic complementation group E of xeroderma pigmentosum, an autosomal recessive disease ma

256 ng Cockayne syndrome, UV-sensitive syndrome, xeroderma pigmentosum, and trichothiodystrophy, result f

257 nd cancer propensity in the genetic diseases xeroderma pigmentosum, Cockayne syndrome, and trichothio

258 Disease states, such as xeroderma pigmentosum, Cockayne's syndrome, Bloom's synd

259 was little repair of 8-MOP-ICLs and -MAs in xeroderma pigmentosum, complementation group A-deficient

260 n together, our results establish a role for xeroderma pigmentosum, complementation group C (XPC) in

261 We also analyzed the role of the xeroderma pigmentosum, complementation group G (XPG) pro

262 -ray repair cross-complementing 1 and 3, and Xeroderma pigmentosum, group D (XRCC1-Arg399Gln, XRCC3-T

263 models for the human NER deficiency disease, xeroderma pigmentosum, leading to speculation that the r

264 In addition to xeroderma pigmentosum, mutations in the human XPG gene c

265 e is the target of mutation in patients with xeroderma pigmentosum, trichothiodystrophy, and Cockayne

266 cause cancer-prone human disorders, such as xeroderma pigmentosum, which are also characterized by s

267 on minimal sun exposure in all patients with xeroderma pigmentosum, who had at least one complete aud

268 oral bone histology in a patient with severe xeroderma pigmentosum-type neurological degeneration rev

269 cute burning on minimal sun exposure without xeroderma pigmentosum-type neurological degeneration was

270 the patients with xeroderma pigmentosum with xeroderma pigmentosum-type neurological degeneration was

271 Of the 17 patients with xeroderma pigmentosum-type neurological degeneration, 13

272 allels neurological decline in patients with xeroderma pigmentosum-type neurological degeneration.

273 39-fold increased risk (P = 0.002) of having xeroderma pigmentosum-type neurological degeneration.

274 xposure and age were important predictors of xeroderma pigmentosum-type neurological degeneration.

275 Xeroderma pigmentosum-variant (XP-V) patients have sun s

276 (pol eta) causes the UV-sensitivity syndrome xeroderma pigmentosum-variant (XP-V) which is linked to

277 langiectasia, Rothmund-Thomson syndrome, and xeroderma pigmentosum.

278 disorders such as ataxia telangiectasia and xeroderma pigmentosum.

279 ncluding Cockayne syndrome and some forms of xeroderma pigmentosum.

280 tations cause the skin cancer-prone syndrome xeroderma pigmentosum.

281 e cancer-prone syndrome, the variant form of xeroderma pigmentosum.

282 utations result in the cancer-prone disorder xeroderma pigmentosum.

283 of the heritable, skin cancer-prone disorder xeroderma pigmentosum.

284 e cancer-prone syndrome, the variant form of xeroderma pigmentosum.

285 e cancer-prone syndrome, the variant form of xeroderma pigmentosum.

286 he rate of new skin cancers in patients with xeroderma pigmentosum.

287 model for the human NER deficiency disorder, xeroderma pigmentosum.

288 e excision repair and the hereditary disease xeroderma pigmentosum.

289 e cancer-prone syndrome, the variant form of xeroderma pigmentosum.

290 e cancer prone syndrome, the variant form of xeroderma pigmentosum.

291 rted in skin tumors from human patients with xeroderma pigmentosum.

292 e cancer-prone syndrome, the variant form of xeroderma pigmentosum.

293 been linked to the repair deficiency disease xeroderma pigmentosum.

294 trated by the devastating inherited syndrome xeroderma pigmentosum.

295 clinical phenotypes of the genetic disorder Xeroderma pigmentosum.

296 nosed with xeroderma pigmentosum (n = 77) or xeroderma pigmentosum/Cockayne syndrome (n = 2).

297 ) had severe abnormalities suggestive of the xeroderma pigmentosum/Cockayne syndrome complex includin

298 in both alleles, were associated with severe xeroderma pigmentosum/Cockayne syndrome neurologic sympt

299 (telomere metabolism), genetically linked to xeroderma pigmentosum/Cockayne syndrome, Warsaw breakage

300 morigenesis when tested in the cancer-prone, xeroderma-pigmentosum-complementation-group-C-deficient