ライフサイエンスコーパス: XPA

1 XPA and RPA have essential roles in the damage recogniti

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

3 XPA can be acetylated at lysines 63 and 67.

4 XPA formed a dimer (XPA2) in a broad range of XPA and Na

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

6 XPA is an essential protein in the nucleotide excision r

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

8 XPA requires RASSF1A to exert full repair activity, and

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

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

11 XPA, XPC-hHR23B, RPA, and TFIIH all are the damage recog

12 XPA-deficient cells complemented with XPA containing a p

13 XPA-deficient cells show defective mitophagy with excess

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

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

16 roderma pigmentosum complementation group A (XPA) cells.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

32 roderma pigmentosum complimentation group A (XPA).

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

34 DNA repair protein xeroderma pigmentosum A (XPA).

35 repair protein xeroderma pigmentosum type A (XPA).

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

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

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

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

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

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

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

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

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

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

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

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

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

49 these studies demonstrate that both RPA and XPA are in close proximity to the adduct as measured by

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

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

52 Human replication protein A (RPA) and XPA have been reported to interact to form a DNA damage

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

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

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

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

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

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

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

60 and differences in substrate binding between XPA and Rad14.

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

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

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

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

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

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

67 SIRT1 deacetylates XPA both in vitro and in cells.

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

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

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

71 egative regulatory element in the endogenous XPA gene promoter.

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

73 uclear localization of the DNA repair enzyme XPA.

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

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

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

77 acilitates the recruitment of the NER factor XPA.

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

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

80 essential nucleotide excision repair factor XPA.

81 nt on the nucleotide excision repair factor, XPA.

82 n repair is initiated by six repair factors (XPA, RPA, XPC-HR23B, TFIIH, XPF-ERCC1, and XPG) which se

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 However, XPA cells complemented with XPA protein restored repair

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

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

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

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

103 to examine the DNA binding activity of human XPA.

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

105 The human XPA protein purified from baculovirus-infected sf21 inse

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

121 Interestingly, XPA has no effect on the k(on) of RPA for a single-stran

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

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

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

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

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

131 Addition of XPA decreases the nonspecific DNA aggregate formation.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

160 epair activity in proportion to the level of XPA.

161 teristic of cells that express low levels of XPA.

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

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

164 However, the apparent molecular mass of XPA determined by the native gel filtration chromatograp

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

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

167 regulates NER pathway through modulation of XPA acetylation status.

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

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

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

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

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

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

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

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

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

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

178 PA formed a dimer (XPA2) in a broad range of XPA and NaCl concentrations, and the dimerization was no

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

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

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

182 PC/HR23B recognition prior to recruitment of XPA.

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

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

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

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

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

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

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

190 Stabilization of XPA by downregulation of HERC2 moderately enhances excis

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

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

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

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

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

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

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

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

199 the constitutive protein levels of p53, p21, XPA, RPA, ERCC1, and PCNA.

200 eins, xeroderma pigmentosum group A protein (XPA) and replication protein A (RPA), have been implicat

201 d the xeroderma pigmentosum group A protein (XPA) facilitates the assembly of a preincision complex d

202 pigmentosum complementation group A protein (XPA) is an essential component of the repair machinery,

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

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

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

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

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

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

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

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

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

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

216 ctors implicated in damage recognition, RPA, XPA, and XPC, stimulate the remodeling activity of SWI/S

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 icates that the bimolecular k(on) of the RPA-XPA complex is 2.5-fold faster than RPA alone for bindin

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

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

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

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

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

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

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

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

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

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

230 ith greater specificity for damaged DNA than XPA alone.

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

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

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

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

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

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

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

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

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

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

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

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

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

244 matography was about 71 kDa, suggesting that XPA is a dimer.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

267 Here we report that the XPA is a homodimer either in the free state or as a comp

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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 c binding to full-length recombinant Xenopus XPA (xXPA) and/or human RPA.

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

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

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