ライフサイエンスコーパス: xeroderma pigmentosum

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

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

3 disorders such as ataxia telangiectasia and xeroderma pigmentosum.

4 ncluding Cockayne syndrome and some forms of xeroderma pigmentosum.

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

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

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

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

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

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

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

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

13 e excision repair and the hereditary disease xeroderma pigmentosum.

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

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

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

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

18 been linked to the repair deficiency disease xeroderma pigmentosum.

19 lial melanoma/dysplastic nevus syndrome, and xeroderma pigmentosum.

20 trated by the devastating inherited syndrome xeroderma pigmentosum.

21 clinical phenotypes of the genetic disorder Xeroderma pigmentosum.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

36 The xeroderma pigmentosum C (XPC) complex initiates nucleoti

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

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

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

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

41 Xeroderma pigmentosum C (XPC) protein initiates the glob

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

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

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

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

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

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

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

49 1 promoted ubiquitylation of SUMOylated XPC (xeroderma pigmentosum C) protein, a central DNA damage r

50 Xeroderma pigmentosum cells deficient in the NER genes X

51 tional activator of the collagenase gene, to xeroderma pigmentosum cells did not detectably alter the

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

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

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

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

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

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

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

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

60 Xeroderma pigmentosum complementation group A (XPA) prot

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

62 1, telomeric repeat binding factor 1 (TRF1), xeroderma pigmentosum complementation group A (XPA), pyg

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

64 Xeroderma pigmentosum complementation group A protein (X

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

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

67 5-HT receptor antagonists into UV-irradiated Xeroderma pigmentosum complementation group A-deficient

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

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

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

71 The Xeroderma pigmentosum complementation group C (XPC) comp

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

102 The three xeroderma pigmentosum group A and the xeroderma pigmento

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

104 The xeroderma pigmentosum group A complementing protein (XPA

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

134 Two xeroderma pigmentosum group C peptides both bound to cen

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

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

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

138 Xeroderma pigmentosum group C samples proved heterogeneo

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

196 39-fold increased risk (P = 0.002) of having xeroderma pigmentosum-type neurological degeneration.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

211 Xeroderma pigmentosum variant (XPV) patients have normal

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

213 Xeroderma pigmentosum variant (XPV) patients with mutati

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

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

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

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

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

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

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

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

222 ult in the sunlight-sensitive, cancer-prone, Xeroderma pigmentosum variant group phenotype.

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

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

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

226 The xeroderma pigmentosum variant samples showed intermediat

227 Patients with xeroderma pigmentosum variant show clinical photosensiti

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

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

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

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

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

233 tosensitive patients that were identified as xeroderma pigmentosum variant.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

248 Xeroderma pigmentosum (XP) and trichothiodystrophy (TTD)

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

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

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

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

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

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

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

256 Xeroderma pigmentosum (XP) complementation group E gene

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

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

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

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

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

262 Xeroderma pigmentosum (XP) is a heritable human disorder

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

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

265 Xeroderma pigmentosum (XP) is a rare autosomal recessive

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

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

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

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

270 Xeroderma pigmentosum (XP) patients are highly sensitive

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

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

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

274 Xeroderma pigmentosum (XP) patients with inherited defec

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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