ライフサイエンスコーパス: XPA

1 XPA and RPA, once forming a complex at the damage site,

2 XPA can be acetylated at lysines 63 and 67.

3 XPA is a unique and essential protein required for the n

4 XPA is an essential protein in eukaryotic NER, although

5 XPA is an essential protein in the nucleotide excision r

6 XPA protein levels are also approximately 3-fold lower i

7 XPA requires RASSF1A to exert full repair activity, and

8 XPA serves as a scaffold for NER, interacting with sever

9 XPA, another key factor in NER, interacts with ERCC1 and

10 XPA-deficient cells complemented with XPA containing a p

11 XPA-deficient cells show defective mitophagy with excess

12 t of the human XPA protein, residues 98-219 (XPA-MBD).

13 ry complex could form between hRPA70(1-326), XPA-MBD and ssDNA, a (1)H-(15)N correlation spectrum was

14 roderma pigmentosum complementation group A (XPA) cells.

15 Xeroderma pigmentosum group A (XPA) is a core nucleotide excision repair (NER) factor e

16 Xeroderma pigmentosum Group A (XPA) is a crucial factor in mammalian nucleotide excisio

17 Human xeroderma pigmentosum group A (XPA) is an essential protein for nucleotide excision rep

18 ma pigmentosum (XP) complementation group A (XPA) is an essential scaffolding protein in the multipro

19 roderma pigmentosum complementation group A (XPA) mice that are deficient in nucleotide excision repa

20 roderma pigmentosum complementation group A (XPA) protein plays a critical role in the repair of DNA

21 n repair, the xeroderma pigmentosum group A (XPA) protein, and the excision repair rate exhibit daily

22 roderma pigmentosum complementation group A (XPA) to sites of nuclear UV photodamage, accelerating cl

23 r function of xeroderma pigmentosum group A (XPA), a major nucleotide excision repair (NER) factor, c

24 ysfunction in xeroderma pigmentosum group A (XPA), a nucleotide excision DNA repair disorder with sev

25 clear foci of xeroderma pigmentosum group A (XPA), a unique nucleotide excision repair protein.

26 roderma pigmentosum complementation group A (XPA), pygopus homolog 2 (PYGO2), protein phosphatase 2A

27 n in NHSFs; and, XP complementation group A (XPA), XP complementation group C, and XP complementation

28 urn activated Xeroderma pigmentosum group A (XPA)-binding protein 1 and induced nuclear translocation

29 he NER factor Xeroderma pigmentosum group A (XPA).

30 roderma pigmentosum complimentation group A (XPA).

31 the key NER factor xeroderma pigmentosum A (XPA) and facilitated recruitment of an XPA-ATR-pS435 com

32 DNA repair protein xeroderma pigmentosum A (XPA).

33 repair protein xeroderma pigmentosum type A (XPA).

34 Additionally, XPA-deficient human brain and mouse liver as well as var

35 omer, while at the higher concentrations, an XPA dimer was involved in the specific binding.

36 PDs in a dose-dependent manner but not in an XPA-deficient cells, indicating that the nucleotide exci

37 um A (XPA) and facilitated recruitment of an XPA-ATR-pS435 complex to sites of cisplatin DNA damage.

38 ents necessary for the rational design of an XPA-based, ERCC1-specific inhibitor.

39 The structure of ERCC1 in complex with an XPA peptide shows that only a small region of XPA intera

40 sure promotes association between PARP-1 and XPA, a central protein in NER.

41 evented cAMP-mediated enhancement of ATR and XPA's associations with cisplatin-damaged DNA, indicatin

42 deficient cell lines, we found that DDB2 and XPA are required for UV-induced XPC modifications.

43 ifications require the functions of DDB2 and XPA, as well as the ubiquitin-proteasome system.

44 Since XPC-hHR23B and XPA-RPA participate in the recognition and verification

45 XPC-hHR23B and XPA-RPA protein complexes were also observed to bind pso

46 iRNA-peptide nanoplexes co-targeting MK2 and XPA to pre-existing p53-deficient tumors in a highly agg

47 trate to establish kinetics of ATR-pS435 and XPA's associations with cisplatin-damaged DNA.

48 s that any complex formation between RPA and XPA that involves the interaction between XPA-MBD and hR

49 amaged DNA by the combined action of RPA and XPA.

50 fication mechanism involving XPC, TFIIH, and XPA for efficient NER.

51 ts reveal that damage recognition by XPC and XPA is critical to maintaining replication fork integrit

52 cision repair (NER) factors, such as XPC and XPA.

53 ated in other studies (MTNR1B, ZNF259/APOA5, XPA/FOXE1 (TTF-2), DARC, CCR3, ABO); 2) localized novel

54 basis for malfunction of disease-associated XPA missense mutations, and contribute to understanding

55 A-mediated ATR phosphorylation, disrupts ATR-XPA binding, delays recruitment of XPA to UV-damaged DNA

56 point mutation of XPA that disrupts the ATR-XPA interaction inhibits the nuclear import of XPA after

57 n together, our results suggest that the ATR-XPA interaction mediated by the helix-turn-helix motif o

58 and differences in substrate binding between XPA and Rad14.

59 nd XPA that involves the interaction between XPA-MBD and hRPA70(1-326) may be modulated by ssDNA.

60 uorescence microscopy reveals that DNA-bound XPA exhibits multiple modes of linear diffusion between

61 ogerin-induced apoptosis could be rescued by XPA, suggesting that XPA-replication fork binding may pr

62 lated kinase family kinases whereas in cells XPA was phosphorylated in an ATR-dependent manner and st

63 ide excision repair (NER) protein complexes, XPA-RPA and XPC-RAD23B, recognized ICLs in vitro, and th

64 At relatively low-protein concentrations, XPA formed a complex with DNA adduct as a monomer, while

65 In contrast, depletion of DDB2, XPA, or XPC does not cause activation of DNA damage chec

66 SIRT1 deacetylates XPA both in vitro and in cells.

67 agonist to TLR4(+/+) BMDC cultures decreased XPA expression and inhibited CPD repair.

68 morphism (SNP) variant exhibits differential XPA binding and inhibits DNA repair.

69 demonstrated that both monomeric and dimeric XPA bound to the DNA adduct of N-acetyl-2-aminofluorene

70 structure of a short motif in the disordered XPA N-terminus bound to the RPA32C domain.

71 contact between the XPA DNA-binding domain (XPA DBD) and the RPA70AB tandem ssDNA-binding domains, w

72 egative regulatory element in the endogenous XPA gene promoter.

73 alpha-MSH) or ACTH induce ATR-pS435, enhance XPA's association with UV-damaged DNA and optimize melan

74 uclear localization of the DNA repair enzyme XPA.

75 tural determinants responsible for the ERCC1/XPA(6)(7)(-)(8)(0) complex stability.

76 Here we showed that the essential NER factor XPA (xeroderma pigmentosum group A) underwent nuclear ac

77 Moreover, the NER factor XPA activates unwinding of normal DNA by Core7, but inhi

78 acilitates the recruitment of the NER factor XPA.

79 reduced interactions with the repair factor XPA and no stimulation of XPF-ERCC1 endonuclease activit

80 sically interacts with the DNA repair factor XPA, establishing the first functional role for XPC-N.

81 essential nucleotide excision repair factor XPA.

82 nt on the nucleotide excision repair factor, XPA.

83 progerin may shift the equilibrium to favor XPA binding.

84 have been reported, the structural basis for XPA's DNA-binding activity remains unknown.

85 ved comparable decreases in zinc content for XPA (xeroderma pigmentosum group A) protein (CCCC zinc f

86 ds-ssDNA junctions at replication forks for XPA binding.

87 r results suggest that the dominant form for XPA to efficiently bind to DNA damage is the XPA dimer.

88 AB1), previously proposed to be required for XPA nuclear import, showed no effect on the nuclear impo

89 A requirement for XPA protein indicates the mechanism of telomeric photopr

90 und 1 analogs exhibited good specificity for XPA over RPA (replication protein A), another DNA-bindin

91 These results suggest that for XPA mutants exhibiting altered DNA-binding properties, a

92 otide excision repair (NER) components (e.g. XPA-1 and XPF-1) imparted extreme sensitivity to TMP/UVA

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

94 ivided into the seven complementation groups XPA through XPG.

95 In contrast, the GTPase XPA binding protein 1 (XAB1), previously proposed to be

96 We have also demonstrated that the hOGG1, XPA, CSB and UVSSA proteins, as well as actively elongat

97 Using the homogeneous XPA protein purified from baculovirus-infected Sf21 inse

98 ehensive docking and refinement revealed how XPA DBD and RPA70AB orient on model NER DNA substrates.

99 However, XPA cells complemented with XPA protein restored repair

100 Human XPA recognizes the lesion comparably to the C8-dG acetyl

101 ures of the central globular domain of human XPA and data on binding of DNA substrates have been repo

102 understand the DNA-binding activity of human XPA in NER, we used NMR to investigate the interaction o

103 studies demonstrate that treatment of human XPA-deficient fibroblasts with the pro-oxidative stresso

104 to examine the DNA binding activity of human XPA.

105 residue 219 yielded a stable, soluble human XPA(98-239) construct that binds to a Y-shaped ssDNA-dsD

106 atomic force microscopy, we show that human XPA binds and bends DNA by ~60 degrees as a monomer.

107 (hRPA70(1-326)), and a fragment of the human XPA protein, residues 98-219 (XPA-MBD).

108 by mouse monoclonal antibody (5F12) to human XPA or in XPC(-/-) fibroblast cell extracts.

109 ith XPA-K6367Q, which mimics hyperacetylated XPA, display significantly higher UV sensitivity compare

110 ge transport adaptor importin-alpha4 imports XPA into the nucleus in an ATR-dependent manner, while X

111 tion-induced ATR signaling is compromised in XPA-deficient human cells during S phase, as shown by de

112 pair of CPDs, with a concomitant decrease in XPA expression.

113 In contrast, HMGB1 depletion in XPA-deficient human cells significantly altered the ICL-

114 d ODD induces a higher mutation frequency in XPA cells than in NHSFs.

115 UV damage or HNE-dG adducts did not occur in XPA cell nuclear extracts that lack the capacity for NER

116 xidants (p = 7.6E-08); a block of 23 SNPs in XPA/FOXE1 (TTF-2) associated with serum TSH (p = 5.5E-08

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

118 cells from MyD88(-/-) mice did not increase XPA gene expression and did not enhance the survival of

119 revious report of a dependence of UV-induced XPA nuclear import on ataxia telangiectasia and Rad3-rel

120 RNA targeting ATR compromised the UV-induced XPA nuclear translocation.

121 at HMGA1 proteins are involved in inhibiting XPA expression, resulting in increased UV sensitivity in

122 ndicate a 2.6-fold decrease in intracellular XPA mRNA in transgenic MCF-7 cells overexpressing HMGA1

123 PAF-R-stimulating activity in UVB-irradiated XPA-deficient fibroblasts using mass spectrometry reveal

124 ere developed to quantify ATR-pS435, measure XPA-photodamage interactions, and assess NER function.

125 Furthermore, SIRT1-mediated XPA deacetylation enhances its interaction with RPA32.

126 tent with a working model in which monomeric XPA bends DNA, displays episodic phases of linear diffus

127 complex of nucleotide excision repair (NER), XPA-RPA, recognizes DNA ICLs.

128 s greater in XPB or XPD mutant cells but not XPA mutant cells.

129 Furthermore, we observe XPA specificity for the helix-distorting base adduct N-(

130 In the absence of XPA or XPC, deleterious consequences of triplex-induced

131 on, which was replaced by combined action of XPA and RPA.

132 derate effect on the DNA-binding activity of XPA.

133 hase, knockdown of ATR reduced the amount of XPA interacting with importin-alpha4.

134 lable structural insight into the binding of XPA to ERCC1 derives from the solution NMR structure of

135 lyses indicated that the specific binding of XPA to the adduct was significantly facilitated and stab

136 more, a titration analysis of the binding of XPA to the human RPA indicated that it was the XPA2 that

137 e apparent interaction and colocalization of XPA with ATR in response to UV irradiation.

138 Importantly, SIRT1-mediated deacetylation of XPA is required for optimal NER pathway since XPA-defici

139 Depletion of XPA or progerin each significantly restored PCNA at repl

140 The structural model enabled design of XPA mutations that inhibit the interaction with RPA70AB.

141 r, our data suggest that the dimerization of XPA may play an important role in the DNA damage recogni

142 x motif in the minimal DNA-binding domain of XPA where an ATR phosphorylation site (serine 196) is lo

143 Conversely, downregulation of XPA by siRNA reduces excision repair activity in proport

144 though Acr does not change the expression of XPA, XPC, hOGG1, PMS2 or MLH1 genes, it causes a reducti

145 or the UV-induced nuclear focus formation of XPA.

146 However, what oligomeric forms of XPA are involved in DNA damage recognition and how the i

147 that in mouse liver only a small fraction of XPA is acetylated and that downregulation of SIRT1 deace

148 and that the lesion recognition function of XPA may be sufficient.

149 A interaction inhibits the nuclear import of XPA after UV irradiation and, thus, significantly reduce

150 excision repair (NER) and nuclear import of XPA from the cytoplasm for NER is regulated in cellular

151 t, showed no effect on the nuclear import of XPA in our siRNA knockdown analysis.

152 e UV (ultraviolet)-induced nuclear import of XPA.

153 , demonstrating the functional importance of XPA DBD-RPA70AB interaction.

154 The critical importance of XPA is underscored by its association with the most seve

155 after UV exposure, no apparent induction of XPA protein is observed in MCF-7 cells expressing HMGA1.

156 Moreover, whereas a >2-fold induction of XPA proteins is observed in normal MCF-7 cells 30 min af

157 When interaction of XPA and RPA with DNA was studied, even though binding of

158 The interaction of XPA with DNA is a core function of this protein; a numbe

159 The interaction of XPA with other components of the repair complex, such as

160 MR was used to map the binding interfaces of XPA DBD and RPA70AB.

161 UVB irradiation of XPA-deficient (Xpa-/-) mice also resulted in increased P

162 RNA interference (RNAi) knockdown of XPA in HGPS cells partially restored DSB repair as evide

163 The level of XPA is controlled at the transcriptional level by the mo

164 epair activity in proportion to the level of XPA.

165 teristic of cells that express low levels of XPA.

166 se that the uncharacteristic localization of XPA to or near DSBs inhibits DSB repair, thereby contrib

167 NER deficiency created by the loss of XPA in fibroblasts or by knockdown of this protein by st

168 dence for an H4K20me2-dependent mechanism of XPA recruitment during lesion recognition in the global-

169 ication fork collapse and mislocalization of XPA in laminopathy-related progeroid syndromes.

170 regulates NER pathway through modulation of XPA acetylation status.

171 on mediated by the helix-turn-helix motif of XPA plays an important role in DNA-damage responses to p

172 In addition, a K188A point mutation of XPA that disrupts the ATR-XPA interaction inhibits the n

173 to the nuclear localization signal (NLS) of XPA, importin-alpha4 or/and importin-alpha7 are required

174 ch is likely to influence the orientation of XPA and RPA on the damaged DNA substrate, remains poorly

175 e, we find that the circadian oscillation of XPA is achieved both by regulation of transcription by t

176 agonistic Ox-GPCs in the pathophysiology of XPA photosensitivity.

177 r activity of NER through phosphorylation of XPA at Ser196 on UV irradiation.

178 ic acid for mimicking the phosphorylation of XPA increased the cell survival to UV irradiation.

179 ts that the ATR-dependent phosphorylation of XPA may promote NER repair of persistent DNA damage.

180 bserved for hRPA70(1-326) in the presence of XPA-MBD and ssDNA as was previously observed in the pres

181 Ubiquitination and proteolysis of XPA are inhibited by DNA damage that promotes tight asso

182 Moreover, the recruitment of XPA and HMGB1 to the ICLs is co-dependent.

183 rupts ATR-XPA binding, delays recruitment of XPA to UV-damaged DNA, and elevates UV-induced mutagenes

184 TR-pS435 accumulation, delays recruitment of XPA to UV-damaged DNA, impairs NER and increases UV-indu

185 PC/HR23B recognition prior to recruitment of XPA.

186 PMS2 or MLH1 genes, it causes a reduction of XPA, XPC, hOGG1, PMS2, and MLH1 proteins; this effect, h

187 PA peptide shows that only a small region of XPA interacts with ERCC1 to form a stable complex exhibi

188 ex may play a role in cellular regulation of XPA activity.

189 ulate NER activity through the regulation of XPA redistribution in human cells upon UV irradiation.

190 esis evidence linking HMGA1 to repression of XPA transcription via binding to a negative regulatory e

191 tion assays, we demonstrate that the role of XPA is in the stabilization of the duplex DNA structure

192 The Ser196 of XPA was identified as a biologically significant residue

193 Stabilization of XPA by downregulation of HERC2 moderately enhances excis

194 Although multiple solution NMR structures of XPA(98-219) have been determined, the molecular basis fo

195 study do not correspond to the substrates of XPA as it functions within the NER machinery.

196 importin-alpha7 in nuclear translocation of XPA in the absence of DNA damage, perhaps with specifici

197 otein 1 and induced nuclear translocation of XPA, a critical factor controlling nucleotide excision r

198 In addition, treatment of XPA-proficient human fibroblast cells with EGCG promoted

199 on-dependent formation of different types of XPA-damaged DNA complex may play a role in cellular regu

200 ontrast, the S196A mutation has no effect on XPA nuclear translocation.

201 Overlapping XPA-MBD- and ssDNA-binding sites on hRPA70(1-326) sugges

202 We show that loss of the DNA repair protein XPA markedly augments the synthetic lethality between MK

203 h the xeroderma pigmentosum group A protein (XPA).

204 R activity and synthesis of the NER proteins XPA, XPC, RAD23B and RPA32.

205 requires nucleotide excision repair proteins XPA and XPC for its association.

206 on recent data showing how the NER proteins, XPA, XPC, XPG, CSA, CSB and UV-DDB, work to stimulate kn

207 ient in the NER damage recognition proteins, XPA and XPC, accumulate more DSBs in response to chromos

208 epair complex consisting of AKAP12-ATR-pS435-XPA at photodamage, which is essential for cAMP-enhanced

209 This complex subsequently recruits XPA to UV DNA damage and enhances 5' strand incision.

210 TTDA recruits XPA through its first 15 amino acids, depleted in some T

211 and its SNP variant differentially regulate XPA protein acetylation, and the SNP variant hyperstabil

212 A-binding assay that the previously reported XPA DBD binds DNA with substantially weaker affinity tha

213 rates cooperative damage recognition by RPA, XPA, and XPC followed by three kinetic proofreading step

214 clude that, in addition to damaged DNA, RPA, XPA, XPC, TFIIH, XPG, XPF-ERCC1, ATR-ATRIP, TopBP1, and

215 ore nucleotide excision repair factors (RPA, XPA, XPC, TFIIH, XPG, and XPF-ERCC1), core DNA damage ch

216 he low-specificity recognition factors, RPA, XPA, and XPC, act in a cooperative manner to locate the

217 nstrate here the formation of a ternary RPA, XPA, and duplex cisplatin-damaged DNA complex as is evid

218 DNA was studied, even though binding of RPA-XPA complex to adducted DNA was observed, the presence o

219 mechanism mediates the formation of the RPA-XPA complex.

220 and stabilized by the presence of the second XPA in a positive cooperative manner.

221 PA is required for optimal NER pathway since XPA-deficient cells complemented with XPA-K6367Q, which

222 wild-type, this study also looks at specific XPA(6)(7)(-)(8)(0) mutants in complex with the ERCC1 cen

223 on of PARP activity decreases UVR-stimulated XPA chromatin association, illustrating that these relat

224 ATR-deficient cells displayed no substantial XPA nuclear translocation while the translocation remain

225 Two-dimensional (15)N-(1)H NMR suggested XPA(98-239) contains the same globular core as XPA98-219

226 nserved binding motif of the XPA N-terminus, XPA(6)(7)(-)(8)(0).

227 on complex (PInC) further composed of TFIIH, XPA, RPA, XPG, and ERCC1-XPF.

228 although PCNA is much more competitive than XPA in binding replication forks, PCNA sequestration by

229 ecognized by XPC-hHR23B alone, but also that XPA-RPA may interact cooperatively with XPC-hHR23B on da

230 rated before checkpoint activation, and that XPA plays a critical role in this activation.

231 hat the XPA DBD should be redefined and that XPA(98-239) is a suitable model to examine the DNA bindi

232 Additional studies demonstrate that XPA contacts both the damaged and undamaged strands of t

233 agreement with a recent report, we find that XPA is post-translationally modified by acetylation.

234 We found that XPA binds different single-stranded/double-stranded junc

235 It is known, that XPA binds kinked DNA structures and that it interacts al

236 It should be noted that XPA-deficient cells are known to have decreased antioxid

237 We have previously reported that XPA forms a homodimer in the absence of DNA.

238 We previously reported that XPA mislocalized to the progerin-induced DNA double-stra

239 Collectively, the data reveal that XPA is a limiting factor in excision repair and that its

240 In this study we show that XPA is a rate-limiting factor in all human cell lines te

241 We showed that XPA was a substrate for in vitro phosphorylation by phos

242 sis could be rescued by XPA, suggesting that XPA-replication fork binding may prevent apoptosis in HG

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

244 The XPA protein functions together with the single-stranded

245 The XPA-deficient cells complemented with XPA-S196A mutant,

246 The XPA-MBD-binding surface showed significant overlap with

247 NA, the MSH2 mismatch repair protein and the XPA nucleotide excision repair (NER) factor are among th

248 However, a second contact between the XPA DNA-binding domain (XPA DBD) and the RPA70AB tandem

249 or/and importin-alpha7 are required for the XPA nuclear import.

250 ion, and the SNP variant hyperstabilizes the XPA-RPA70 complex.

251 erfere with ATR-pS435 generation, impair the XPA-DNA interaction, and reduce DNA repair.

252 esidues (Asn-110 and Tyr-145) located in the XPA-binding site of ERCC1 dramatically affected NER but

253 XPA to efficiently bind to DNA damage is the XPA dimer.

254 to the highly conserved binding motif of the XPA N-terminus, XPA(6)(7)(-)(8)(0).

255 air (NER) by facilitating recruitment of the XPA protein to sites of UV-induced DNA damage.

256 ction of the NER pathway, the binding of the XPA protein to the ERCC1 subunit of the repair endonucle

257 s manifested by XPC-dependent binding of the XPA protein to the nuclear matrix, which was also observ

258 process is well studied, the function of the XPA protein, which is of central importance for successf

259 Moreover, mutation of the XPA residue corresponding to Phe-262 in Rad14, previousl

260 In-depth analysis of the XPA sequence suggested that the original DBD construct l

261 m molecular-dynamics simulation study of the XPA(6)(7)(-)(8)(0) peptide both bound to the ERCC1 centr

262 the first to develop novel inhibitors of the XPA-DNA interaction through structure-guided drug design

263 racted with XPA, but failed to stabilize the XPA-damaged DNA complex.

264 In this study, the XPA mislocalization to DSBs occurred at stalled or colla

265 Together, our results demonstrate that the XPA DBD should be redefined and that XPA(98-239) is a su

266 We find that the XPA protein, which plays an essential role in repair of

267 hese disease-associated mutations map to the XPA(98-219) DNA-binding domain (DBD) first reported ~20

268 ntly higher UV sensitivity compared with the XPA cells complemented with wild-type XPA.

269 ntly higher UV sensitivity compared with the XPA cells complemented with wild-type XPA.

270 Strikingly, these XPA foci colocalized with the DSB sites in the progeroid

271 This XPA-DSB association was further confirmed and found to b

272 However, this XPA peptide is a potent inhibitor of NER activity in a c

273 restingly, the binding of importin-alpha4 to XPA was dependent on UV-irradiation, while the binding o

274 Truncated XPA, lacking the intrinsically disordered N- and C-termi

275 show that restoring expression of wild-type XPA in HMGA1-expressing cells rescues UV resistance comp

276 pared with cells complemented with wild-type XPA, although no effect was observed for repair of (6-4)

277 th the XPA cells complemented with wild-type XPA.

278 th the XPA cells complemented with wild-type XPA.

279 after the simultaneous addition of unlabeled XPA-MBD and ssDNA.

280 RPA70(1-326) after the addition of unlabeled XPA-MBD.

281 sults inform ongoing controversy about where XPA is bound within the NER bubble, provide structural i

282 -ribose) facilitates PARP-1 association with XPA in whole cell extracts, in isolated chromatin comple

283 n cells, HMGB1 functions in association with XPA on ICLs and facilitates the formation of a favorable

284 The ability of ssDNA to compete with XPA-MBD for an overlapping binding site on hRPA70(1-326)

285 XPA-deficient cells complemented with XPA containing a point mutation of S196A displayed a red

286 However, XPA cells complemented with XPA protein restored repair synthesis for both of these

287 since XPA-deficient cells complemented with XPA-K6367Q, which mimics hyperacetylated XPA, display si

288 The XPA-deficient cells complemented with XPA-S196A mutant, in which Ser196 was substituted with a

289 and importin-alpha7 directly interacted with XPA in cells.

290 XPC physically interacted with XPA, but failed to stabilize the XPA-damaged DNA complex

291 d in vivo, and that MutSbeta interacted with XPA-RPA or XPC-RAD23B in recognizing Tdp-ICLs.

292 s that are critical for the interaction with XPA and assessed their importance for NER in vitro and i

293 recruited to DNA lesions by interaction with XPA and incises the DNA 5' to the lesion.

294 o significant effect on the interaction with XPA.

295 SIRT1 interacts with XPA, and the interaction is enhanced after UV irradiatio

296 Interestingly, the interaction of RPA with XPA was not altered by RPA phosphorylation.

297 domain to identify the binding surface with XPA-MBD.

298 and NER-defective xeroderma pigmentosum (XP) XPA and XPG cells.

299 ures of the central globular domain of yeast XPA (Rad14) with lesion-containing DNA duplexes have pro

300 of the DNA binding domain (DBD) of the yeast XPA homolog Rad14 bound to DNA with either a cisplatin l