ライフサイエンスコーパス: XPD

1 but not expression of the 5' --> 3' helicase XPD.

2 terface between the Arch and 4FeS domains in XPD.

3 sms in 3 DNA repair genes: XRCC1, XRCC3, and XPD.

4 as detected to be physically interacted with XPD.

5 activating a latent 'processivity switch' in XPD.

6 depend on two translocase subunits, XPB and XPD.

7 f extramitochondrial Fe-S proteins including XPD.

8 ing the DNA-binding and ATP-binding sites of XPD.

9 an cells deficient in FANCJ but not DDX11 or XPD.

10 r per 1-unit increase in severity score) and XPD (0.60 points/year per 1-unit increase), and in ADL t

11 scores significantly increased over time in XPD (0.91 points/year, 95% confidence interval: 0.61, 1.

12 d for developmental apoptosis in C. elegans, XPD-1 only activates stress-responsive functions of casp

13 Using C. elegans, we show XPD-1-dependent activation of CED-3 caspase promotes sur

14 patients, the xeroderma pigmentosum group D (XPD)-751, x-ray cross-complementing group 3 (XRCC3) and

15 XPD, a 5'-3' helicase involved in nucleotide excision re

16 lectrodes, we show DNA-mediated signaling by XPD, a helicase that contains a [4Fe-4S] cluster and is

17 Polymorphisms in XPD, a member of the nucleotide excision repair pathway,

18 rocess occurs in a stepwise fashion in which XPD acquires a Fe-S cluster from the CIA targeting compl

19 l regulatory mechanism that switches XPB and XPD activities making them mutually exclusive between NE

20 eukaryotic helicases that includes mammalian XPD, an enzyme involved in transcription-coupled nucleot

21 When XPD and EndoIII are mixed together, they coordinate in r

22 evidence for DNA-mediated signaling between XPD and Endonuclease III (EndoIII), a base excision repa

23 factor TFIIH, containing the helicases XPB, XPD and five 'structural' subunits, p62, p44, p34, p52 a

24 ential assembly process for Fe-S assembly on XPD and highlight the existence of quality control mecha

25 l the ATP-driven translocation mechanisms of XPD and its bacterial homolog DinG, revealing all on-pat

26 ation in the Walker A box in both alleles of XPD and lacks DNA helicase activity.

27 ovide further support to the hypothesis that XPD and p53 can functionally interact in a p53-mediated

28 tanding disease consequences of mutations in XPD and related 4Fe-4S helicases including FancJ.

29 t also impairs the DNA unwinding activity of XPD and the nucleotide excision repair activity of TFIIH

30 used to identify interacting factor(s) with XPD and TUFM, a mitochondrial Tu translation elongation

31 me genes, namely ERCC2/XPD or ERCC3/XPB Both XPD and XPB proteins belong to the 10-subunit complex tr

32 with the localization of the TFIIH helicases XPD and XPB, support a DNA translocation model of XPB an

33 eurological symptoms, especially in the XPA, XPD and XPG groups, with early-onset and late-onset form

34 Gene activation was undiminished in XPA, XPD and XPG human cell lines, indicating that activation

35 XPA, XPD and XPG patients showed higher SARA scores compared

36 ve impairment were frequent findings in XPA, XPD and XPG.

37 Gli1, c-jun, and the upregulation of ERCC1, XPD and XRCC1 in cisplatin-resistant human ovarian cance

38 Genetic polymorphisms in XPD and XRCC1 may be important prognostic factors in pla

39 as well as the polymorphic DNA repair genes XPD and XRCC1, in influencing response to chemotherapy a

40 isplatin treatment, including: c-jun, ERCC1, XPD and XRCC1.

41 uence similarity to the human (Homo sapiens) XPD and yeast (Saccharomyces cerevisiae) RAD3 genes requ

42 Mutations in XPDS and MRXSH alter binding sites for different splicin

43 tion of three genes essential to NER (ERCC1, XPD) and base excision repair (XRCC1).

44 but is devoid of detectable levels of ERCC2 (XPD) and CAK.

45 which are partially defective in the ERCC2 (XPD) and ERCC3 (XPB) helicase activities shared between

46 ng high-resolution X-ray powder diffraction (XPD) and rotation electron diffraction (RED) techniques.

47 to complement extracts prepared from ERCC2 (XPD)- and ERCC3 (XPB)-deficient cells, respectively, in

48 ests a function for p62 in the regulation of XPD, and allows the mapping of previously unresolved hum

49 DNA helicase superfamily that includes XPB, XPD, and BLM.

50 nducted a similar analysis in XPA, XPB, XPC, XPD, and CSB fibroblasts.

51 CAK complex), the two helicases Xpb/Hay and Xpd, and p34, p44, p52 and p62.

52 Mutations in the TFIIH subunits XPB, XPD, and p8 lead to severe premature ageing and cancer p

53 ree nucleotide excision repair genes (ERCC1, XPD, and XPF), a gene involved in double-strand break re

54 Defects in the XPB, XPD, and XPG genes can result in three different syndrom

55 isms in DNA repair genes APE1, XRCC1, ERCC1, XPD, and XRCC3 in predicting therapeutic outcomes of old

56 scopy analyses, we demonstrate that UvrB and XPD are able to load onto DNA and pursue lesion verifica

57 ypothesized that TFIIH DNA helicases XPB and XPD are members of the p53-mediated apoptotic pathway.

58 TFIIH DNA helicases, XPB and XPD, are also components in this apoptotic pathway.

59 her, our results identify the ARCH domain of XPD as a platform for the recruitment of CAK and as a po

60 Here, we use XPD as a prototypical Fe-S protein to further characteri

61 Individually, only XPD Asp312Asn, RAG1 Lys820Arg, and a p53 intronic SNP ex

62 ism to evaluate genetic polymorphisms of the XPD (Asp312Asn) and XRCC1 (Arg399Gln) DNA repair genes i

63 , our findings shed light on the etiology of XPD-associated genetic syndromes.

64 tailed structures of its constituent XPB and XPD ATPases, and how the core and kinase subcomplexes of

65 Structural studies have shown XPD bound to its single-stranded DNA substrate, but mole

66 d extensive all-atom MD simulations of human XPD bound to undamaged and damaged ssDNA, containing a m

67 ls and decreased level of ATP6AP2 protein in XPDS brain may compromise V-ATPase function, as seen wit

68 match, which is not a specific substrate for XPD but, like a lesion, inhibits CT.

69 d in a number of DNA repair genes, including XPD, but the effect of these polymorphisms on DNA repair

70 Second, disrupting Fe-S cluster assembly on XPD by either 1) depleting cellular iron levels or 2) ut

71 of CSB, CSA, or the TFIIH helicases XPB and XPD can also cause defective TCR and CS.

72 nt with a role in NER, we show that archaeal XPD can initiate unwinding from a DNA bubble structure,

73 ses, we determined crystal structures of the XPD catalytic core from Sulfolobus acidocaldarius and me

74 Expressed wild-type XPC or XPD cDNAs in these cells restored the survival to UVC ra

75 XPC and TTD/XPD cell lines were complemented using retroviral transf

76 Both XBP and XPD cells were deficient in repair of nontranscribed DNA

77 repair rate, in the complemented XPC and TTD/XPD cells, almost all of the CPDs at "hotspots" for muta

78 V cDNA appeared more stable in mutant XPB or XPD cells.

79 ction of the full-size ATP6AP2 transcript in XPDS cells and decreased level of ATP6AP2 protein in XPD

80 These data suggest that the XPD codon 751 glutamine variant protects against myeloid

81 Furthermore, homozygosity for the XPD codon 751 glutamine variant was associated with a si

82 927 patients with AML, we show here that the XPD codon 751 glutamine-encoding variant significantly a

83 ession analysis, the Gln/Gln genotype in the XPD codon 751 showed the strongest association with both

84 lar matrix (ECM), in TTD patients mutated in XPD compared with their healthy parents.

85 In both XPC and TTD/XPD complemented lines, CPD repair on the non-transcribe

86 The DNA helicases XPB and XPD, components of transcription factor TFIIH, have been

87 nd XPC bind damaged DNA and are required for XPD cross-linking to the psoralen-adducted base, neither

88 and space group symmetry were found from the XPD data, and were essential for the initial analysis of

89 Similar to the findings in XPD-deficient cells, mitochondrial common deletion and o

90 ppressed human osteosarcoma (U2OS) cells and XPD-deficient human fibroblasts.

91 found to stimulate the signaling pathway of XPD-dependent apoptosis.

92 We identify the XPD(DinG) global domain motions that modulate the streng

93 its repair functions and harbors the XPB and XPD DNA-dependent ATPase/helicase subunits, which are af

94 By sequentially coordinating the XPB and XPD DNA-unwinding activities, the switch ensures precise

95 on 751 of the xeroderma pigmentosum group D (XPD) DNA repair gene were significantly more likely to h

96 Whereas XPD does not share significant sequence identity with Uv

97 s known to regulate the helicase activity of XPD during NER, p62 is thought to be purely structural.

98 e nucleotide excision repair genes ERCC1 and XPD (Ercc1(d/-) and Xpd(TTD) mice), we explored age-depe

99 human TFIIH complex proteins XPB (ERCC3) and XPD (ERCC2) play a principal role in the degradation of

100 re carriers of at least one minor allele for XPD/ERCC2 at D312N (OR, 2.78; 95% CI, 1.28-6.04) or D711

101 or alleles in DNA repair genes XPF/ERCC4 and XPD/ERCC2 were associated with altered risk for pancreat

102 Xeroderma pigmentosum group D (XPD/ERCC2) encodes an ATP-dependent helicase that plays

103 ncies for 16 SNPs in DNA repair genes ERCC1, XPD/ERCC2, XPC, XPF/ERCC4, OGG1, and XRCC1 were compared

104 pair of nuclear DNA, however, whether or not XPD exerts similar functions in mitochondria remains elu

105 ren treated for de novo AML was performed at XPD exon 23.

106 RPA1 competed with XPD for ssDNA access.

107 h and pull the lesion-containing strand into XPD for verification.

108 A crystal structure of XPD from Sulfolobus acidocaldiarius that lacks helicase

109 ative helicases: PcrA from superfamily 1 and XPD from superfamily 2.

110 The 2.25 A crystal structure of XPD from the crenarchaeon Sulfolobus tokodaii, presented

111 dence that three common polymorphisms of the XPD gene (C156A, Asp312Asn, and Lys751Gln) may be associ

112 patients with characterized mutations in the XPD gene have the haematological features of beta-thalas

113 Here we report the first involvement of the XPD gene in a new case of UV-sensitive COFS syndrome, wi

114 rescued by transferring the wild-type XPB or XPD gene into the corresponding mutant cells.

115 The xpd gene is the target of mutation in patients with xero

116 studies have identified polymorphisms in the XPD gene that are associated with increased risk of brai

117 The polymorphisms C156A and Asp312Asn of the XPD gene were not associated with response to 5-fluorour

118 complex disorder caused by mutations in the XPD gene which affect both DNA repair and transcription.

119 r and have germ-line mutations in the XPB or XPD gene, but not in the XPA or XPC gene, have a deficie

120 t of TTD or XP cases with mutations in ERCC2/XPD gene, we identify the expression alterations specifi

121 s of genotype-phenotype relationships in the XPD gene.

122 We previously mapped the XPDS gene to a 28 Mb region on Xp11.2-X13.3.

123 The xeroderma pigmentosum group D (XPD) gene encodes a DNA helicase that functions in nucle

124 entosum complementation group B (XPB) and D (XPD) genes and a cyclin-dependent protein kinase encoded

125 the only data in pediatric AML, suggest that XPD genotype does not affect the etiology or outcome of

126 other toxicities were also found for variant XPD genotypes/haplotypes.

127 Patients with XPD Gln751C/Asp312G ('D') haplotype were more likely to

128 XPD has a 5' to 3' polarity and the helicase activity is

129 , we show that Xeroderma pigmentosum protein XPD has a conserved function in activating the expressio

130 nit of the TFIIH complex, the 5'-3' helicase XPD, has been identified in archaea.

131 ent study puts to rest the debate of whether XPD helicase 'verifies' the appropriateness of the DNA d

132 The XPD helicase (Rad3 in Saccharomyces cerevisiae) is a com

133 n-adducted oligonucleotide was observed, and XPD helicase activity was readily inhibited by both sing

134 ructural and dynamic molecular depictions of XPD helicase activity with unmodified DNA and its inhibi

135 strate the role of CAK in downregulating the XPD helicase activity within TFIIH.

136 issue, Honda et al. report that the archaeal XPD helicase can bypass a single-stranded DNA-binding pr

137 Mutations in the XPD helicase component of TFIIH can result in the divers

138 Here, DNA binding by the archaeal XPD helicase from Thermoplasma acidophilum has been inve

139 ements of the unwinding activity of a single XPD helicase in the presence of RPA2 reveal a mechanism

140 bp) resolution, we analyzed DNA unwinding by XPD helicase, a Superfamily 2 (SF2) DNA helicase involve

141 Mutations in XPD helicase, required for nucleotide excision repair (N

142 lyzed the substrate specificity of the Rad3 (XPD) helicase from Ferroplasma acidarmanus (FacRad3) and

143 The xeroderma pigmentosum group D (XPD) helicase is a component of the transcription factor

144 Xeroderma pigmentosum group D (XPD) helicase is a component of the transcription factor

145 The xeroderma pigmentosum group D (XPD) helicase is a subunit of transcription/DNA repair f

146 a acidarmanus xeroderma pigmentosum group D (XPD) helicase serves as a model for understanding the mo

147 Rad3 (xeroderma pigmentosum group D protein (XPD)) helicase is a prototypical member of the Rad3 fami

148 iption factor IIH complex, including XPB and XPD helicases involved in promoter melting and open comp

149 nition pathways converge and how the XPB and XPD helicases of Core7 move the DNA lesion for verificat

150 in the FeS domain of human Bach1 (FancJ) and XPD helicases that result in distinct disease phenotypes

151 phoblastoid cell lines (LCLs), but not in an XPD heterozygote LCL, after exposure to doxorubicin, a D

152 By combining X-ray powder diffraction (XPD), high-resolution transmission electron microscopy (

153 d by mutating two highly conserved residues (XPD, His-237 and Asp-609; UvrB, H341A and D510A).

154 ein levels of the core TFIIH component Rad3 (XPD homologue) and Ssl2 (XPB homologue) were significant

155 iochemical studies of the monomeric archaeal XPD homologues have aided a mechanistic understanding of

156 in understanding the molecular mechanism of XPD human disease causing mutations.

157 et oxygen, (2) the formation of a stable L(2)XPd(I)OOH triplet species, (3) a spin transition resulti

158 a spin transition resulting in a stable L(2)XPd(II)OOH singlet species, and (4) the loss of H(2)O(2)

159 cate the nuclear DNA repair proteins XPB and XPD in a cellular defense against retroviral infection.

160 XPD in contrast is shown to be a rigid protein with almo

161 Pase and helicase activities of both XPB and XPD in Core7 to promote NER, whereas non-genuine NER sub

162 ved to be achieved by the helicases UvrB and XPD in the prokaryotic and eukaryotic processes, respect

163 sion and deliver the damaged strand to Rad3 (XPD) in an open form suitable for subsequent lesion scan

164 ng blocks Fe-S cluster assembly and prevents XPD incorporation into TFIIH.

165 , and that gene complementation with XPA and XPD increases resistance to cisplatin.

166 show that triplexes are capable of inducing XPD-independent double strand breaks, which result in th

167 presence of RPA2 reveal a mechanism in which XPD interconverts between two states with different proc

168 ive stress showed an enhanced recruitment of XPD into mitochondrial compartment.

169 XPD is a 5' to 3' helicase with an essential iron-sulfur

170 XPD is a key nucleotide excision repair (NER) protein wh

171 Archaeal XPD is closely related in sequence to the eukaryal enzym

172 Apart from two canonical helicase domains, XPD is composed of a 4Fe-S cluster domain involved in DN

173 Moreover, Xpd is downregulated at the beginning of mitosis when Cd

174 ponent of transcription factor II H (TFIIH), XPD is involved in DNA unwinding during nucleotide excis

175 is study, we provide the first evidence that XPD is localized in the inner membrane of mitochondria,

176 though iron-sulfur (Fe-S) cluster binding by XPD is required for activity, the process mediating Fe-S

177 Xeroderma pigmentosum factor D (XPD) is a 5'-3' superfamily 2 helicase and the founding

178 XPA, which binds between XPB and XPD, kinks the DNA duplex and shifts XPC and the DNA les

179 5, bcl-2 and bax were observed in normal and XPD LCLs after treatment with doxorubicin, indicating th

180 PARP cleavage was not delayed in XPD LCLs in response to anti-Fas (CD95) antibody-mediate

181 at apoptosis is reduced and delayed in three XPD lymphoblastoid cell lines (LCLs), but not in an XPD

182 nd no differences in the distribution of the XPD Lys751Gln or XRCC1 Arg194Trp genotypes.

183 We conclude that XPD Lys751Gln polymorphism may be an important marker in

184 We hypothesized that XPD Lys751Gln polymorphism may play a role in causation

185 Furthermore, the XPD Lys751Gln polymorphism was a significant modifier of

186 , group D (XRCC1-Arg399Gln, XRCC3-Thr241Met, XPD-Lys751Gln).

187 Simultaneously, the downregulation of Xpd might be a major mechanism of mitotic silencing of b

188 The value of this XPD model demonstrates the generalized approach for the

189 UvrB as a template for the development of an XPD model was tested by mimicking human disease-causing

190 repair gene, Xeroderma pigmentosum group D (XPD), modified the risk.

191 DNA repair-deficient XPB and XPD mutant cell lines exhibited an increase in transduct

192 virus viral production was greater in XPB or XPD mutant cells but not XPA mutant cells.

193 grated provirus, and 2LTR circles in XPB and XPD mutant cells.

194 pleting cellular iron levels or 2) utilizing XPD mutants defective in either Fe-S cluster or CIA targ

195 Here, XPB and XPD mutations are shown to block transcription activatio

196 case activity and explains the phenotypes of xpd mutations in humans.

197 previously suggested links between specific XPD mutations in the fetal genome and the risk of placen

198 mental and physical developmental delay, has XPD mutations not previously reported, and barely detect

199 TFIIH from cells with XPB or XPD mutations was defective in supporting repair, wherea

200 we show that the Drosophila TFIIH component Xpd negatively regulates the cell cycle function of Cdk7

201 es important for genomic stability including XPD (nucleotide excision repair), DDX11 (sister chromati

202 Moreover, the TFIIH factor, XPD, occupies a central role in triggering apoptosis in

203 FM studies, we observe the redistribution of XPD onto kilobase DNA strands containing a single base m

204 om mutations in the same genes, namely ERCC2/XPD or ERCC3/XPB Both XPD and XPB proteins belong to the

205 harbor mutations in the TFIIH DNA helicases XPD or XPB.

206 m cells deficient in the NER genes XPG, XPA, XPD or XPF were resistant to Et743, and sensitivity was

207 Increasing numbers of either XPD or XRCC1 variant alleles were associated with shorte

208 with CS symptoms have mutations in the XPB, XPD, or XPG genes, which result in UV hypersensitivity a

209 Our analyses demonstrate that the XPB, XPD, p44, and p62 proteins interact with each other.

210 r is TFIIH, which has a 6-subunit core (XPB, XPD, p44, p34, p52, p62) and a 3-subunit kinase (CAK).

211 xploited the availability of the cloned XPB, XPD, p62, p44, and p34 genes (all of which encode polype

212 en-subunit TFIIH core complex formed by XPB, XPD, p62, p52, p44, p34, and p8 is competent for DNA rep

213 of apoptotic levels in cells from WS, XPB or XPD patients was attained only by overexpression of the

214 d to the DRC phenotype were defined in ERCC2/XPD, PHACTR2, and DUSP1.

215 Our findings clearly demonstrate that XPD plays crucial role(s) in protecting mitochondrial ge

216 We therefore examined XPD polymorphisms at Lys751Gln and Asp312Asn in 341 whit

217 These results suggest that the two XPD polymorphisms have a modulating effect on DRC, espec

218 pyrimidone UV photoproduct (6-4PP), near the XPD pore entrance.

219 X-linked parkinsonism with spasticity (XPDS) presents either as typical adult onset Parkinson's

220 The xeroderma pigmentosum group D (XPD) protein is a subunit of transcription factor TFIIH

221 The Xeroderma pigmentosum group D (XPD) protein is an essential participant in nucleotide e

222 yclin H, and p36/MAT1) as well as the ERCC2 (XPD) protein.

223 The XPB and XPD proteins are subunits of RNA polymerase II (RNAP II)

224 -damaged sites; (iii) recruitment of XPB and XPD proteins to UV DNA damage sites; and (iv) increased

225 least two of the subunits of TFIIH (XPB and XPD proteins) are implicated in the disease xeroderma pi

226 s share high homology with the human XPB and XPD proteins.

227 y mimicking human disease-causing mutations (XPD: R112H, D234N, R601L) in UvrB (E110R, D338N, R506A)

228 The XPD(R658H) TTD protein, like XPD(T46I/R658H), is codomin

229 g by the iron-sulfur cluster of the archaeal XPD (Rad3) helicase was used as a calibrated proximity s

230 edicted to be an iron-sulfur helicase in the XPD/Rad3 helicase family based on sequence analysis, the

231 ctly interacts with the DNA helicase subunit XPD/Rad3 in native TFIIH and is required for the integri

232 We characterize how XPD responds to the presence of the DNA lesion, delineat

233 defects and lethality, whereas a decrease in Xpd results in increased CAK activity and cell prolifera

234 olecule imaging of p44/p62 complexes without XPD reveals they bind to and randomly diffuse on DNA, ho

235 at a complex containing p44 and p62 enhances XPD's affinity for dsDNA 3-fold over p44 alone.

236 nsive contacts with p44 and in part occupies XPD's DNA binding site.

237 Remarkably, XPG caps XPD's DNA-binding groove and bridges both junctions of t

238 (NER), the xeroderma pigmentosum D helicase (XPD) scans DNA searching for bulky lesions, stalls when

239 During NER, XPD serves as a 5'-3' single-strand DNA translocase that

240 mutation at a regulatory DNA binding site on XPD similarly activates this switch.

241 HRTEM and XPD simulations show that stacking faults do occur, but

242 In contrast, RPA2 did not interfere with XPD-ssDNA binding but markedly slowed down XPD transloca

243 idate how the lesion is verified by inducing XPD stalling.

244 Quantifying the sequence dependence of XPD stepping dynamics with near base pair resolution, we

245 The XPD structural model can be employed in understanding th

246 sate for the T46I mutation by perturbing the XPD structure in a way that counteracts the effect of th

247 aFold predicts that STK19 interacts with the XPD subunit of TFIIH, and disrupting this interface impa

248 s with mutations in ERCC2, which encodes the XPD subunit of TFIIH, but not in XP cells with ERCC2 mut

249 NA: these proteins are RPA70, RPA32, and the XPD subunit of TFIIH.

250 Mutations in the XPD subunit of the DNA repair/transcription factor TFIIH

251 Specific mutations in the XPD subunit of transcription factor IIH result in combin

252 t, a 5' --> 3' DNA helicase catalyzed by its XPD subunit, and a carboxyl-terminal domain (CTD) kinase

253 erface between the p62 Anchor region and the XPD subunit.

254 repair of mtDNA was markedly reduced in both XPD-suppressed human osteosarcoma (U2OS) cells and XPD-d

255 st restore helicase activity to the inactive XPD(T46I) protein.

256 The XPD(R658H) TTD protein, like XPD(T46I/R658H), is codominant when overexpressed in V-H

257 rnary CAK kinase complex associated with the XPD TFIIH subunit) are used as model systems to validate

258 Mutations in XPD that affect DNA repair but not transcription result

259 ithin preincision complexes, it is RPA32 and XPD that are in close contact with the lesion.

260 Here we show that the specific mutations in XPD that cause TTD result in reduced expression of the b

261 In contrast, cells lacking either XPD, the 3'-helicase, or the 3'-endonuclease XPG were eq

262 formation and find that mutations in XPB or XPD, the DNA helicase subunits of the transcription and

263 Downregulation of Xpd thus seems to contribute to the upregulation of mito

264 Excess Xpd titrates CAK activity, resulting in decreased Cdk T-

265 olecular and dynamic characterization of how XPD translocates on undamaged DNA and how it stalls to v

266 repaired by NER may not present a barrier to XPD translocation in vivo, in contrast to some predictio

267 h XPD-ssDNA binding but markedly slowed down XPD translocation.

268 oteins RPA1 and RPA2 differentially affected XPD translocation.

269 thelium-dependent vasodilator dysfunction in Xpd(TTD) animals was increased.

270 n repair genes ERCC1 and XPD (Ercc1(d/-) and Xpd(TTD) mice), we explored age-dependent vascular funct

271 nsity, and renal function in both fast aging Xpd(TTD/TTD) and naturally aged mice.

272 We show that monomeric XPD unwinds duplex DNA in 1-bp steps, yet exhibits frequ

273 e microscopy reveals for the first time that XPD utilizes different recognition strategies to verify

274 We have cloned the XPD variants Lys751Gln, Asp312Asn, and Lys751Gln-Asp312A

275 First, XPD was found to associate in a mutually exclusive fashi

276 XPD was not stalled by substrates containing extrahelica

277 XPD was subsequently recruited to the triplex-induced do

278 he human nucleotide excision repair protein, XPD, was developed based on the structural and functiona

279 osum complementation groups B and D (XPB and XPD) which are partially defective in the ERCC2 (XPD) an

280 XPB and XPD, which track the lesion-containing strand but transl

281 p62 rigging interlaces p34, p44 and XPD while capping the DNA-binding and ATP-binding sites

282 ion studies indicate that the association of XPD with the CIA targeting complex occurs in the cytopla

283 The archaeal Rad3 helicase XPD (xeroderma pigmentosum group D protein) from Ferropl

284 It has been proposed that the 5'-3' helicase XPD (xeroderma pigmentosum group D) protein plays a deci

285 mutations in DNA repair/transcription genes XPD, XPB or TTDA, and in TTDN1, a gene of unknown functi

286 XPA rigging interlaces XPF/ERCC1 with RPA, XPD, XPB, and 5' ssDNA, exposing XPA's crucial role in l

287 ng eight different genotypes (XPA, XPB, XPC, XPD, XPE, XPF, XPG and XP variant or XPV).

288 e nucleotide excision repair apparatus (XPB, XPD, XPG and CSB), cells defective for the ERCC1-XPF str

289 Mutations in CSA (ERCC8), CSB (ERCC6), XPB, XPD, XPG, XPF (ERCC4) and ERCC1 can give rise to clinica

290 nd/or protein levels included: c-jun, ERCC1, XPD, XRCC1, Gli1, Gli2, SHH, IHH, GAPDH and alpha-tubuli

291 ase subunits xeroderma pigmentosum (XP) B or XPD yield overlapping DNA repair and transcription syndr