ライフサイエンスコーパス: XPD

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

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

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

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

5 XPD was not stalled by substrates containing extrahelica

6 XPD was subsequently recruited to the triplex-induced do

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

8 oteins RPA1 and RPA2 differentially affected XPD translocation.

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

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

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

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

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

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

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

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

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

18 5, bcl-2 and bax were observed in normal and XPD LCLs after treatment with doxorubicin, indicating th

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

49 depend on two translocase subunits, XPB and XPD.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

129 activating a latent 'processivity switch' in XPD.

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

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

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

133 f extramitochondrial Fe-S proteins including XPD.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

201 The XPD structural model can be employed in understanding th

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

230 927 patients with AML, we show here that the XPD codon 751 glutamine-encoding variant significantly a

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

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

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

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

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

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

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

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

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

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

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

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

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

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

245 Whereas XPD does not share significant sequence identity with Uv

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

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

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

249 RPA1 competed with XPD for ssDNA access.

250 as detected to be physically interacted with XPD.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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