ライフサイエンスコーパス: XRCC1

1 o NER (ERCC1, XPD) and base excision repair (XRCC1).

2 GSTM3, GSTP1, GSTT1, GSTZ1, MGST1, SOD1, and XRCC1).

3 dinated by X-ray cross-complementing gene 1 (XRCC1).

4 X-ray repair cross-complementing protein 1 (XRCC1).

5 X-ray repair cross-complementing protein 1 (XRCC1).

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

7 distinguish it from its interacting protein Xrcc1.

8 DNA repair pathways with its partner protein Xrcc1.

9 al DNA (mtDNA) maintenance is independent of Xrcc1.

10 ingle-strand breaks, is the scaffold protein XRCC1.

11 atin association of PARP-1, condensin I, and XRCC1.

12 aged bases and single-strand breaks (SSB) is XRCC1.

13 d expression and colocalization of Ref-1 and XRCC1.

14 CC1 heterodimer through its interaction with XRCC1.

15 ent by a mechanism of shortened half-life of XRCC1.

16 o maintain the steady-state protein level of XRCC1.

17 residues between amino acids 166 and 310 of XRCC1.

18 y recruiting the molecular scaffold protein, XRCC1.

19 damage and recruit the DNA repair scaffold, XRCC1.

20 ors interactions between PARylated PARP1 and XRCC1.

21 ote the recruitment of the scaffold protein, XRCC1.

22 ribose) ligand for a stable interaction with XRCC1.

23 In breast cancer, loss of XRCC1 (16%) was associated with high grade (P < 0.0001),

24 enoma (OR, 0.66; 95% CI, 0.44-1.00), and the XRCC1 399Q variant was inversely associated with risk am

25 ed the level of x-ray cross-complementing 1 (XRCC1), a scaffold protein involved in BER.

26 ity depends upon its nuclear binding partner Xrcc1, a critical factor for this DNA repair pathway.

27 Using murine neural-specific inactivation of Xrcc1, a factor that is critical for the repair of DNA s

28 rand breaks and gaps (SSB) is coordinated by XRCC1, a scaffold protein that recruits the DNA polymera

29 h Chinese hamster ovary cells with wild-type XRCC1 (AA8).

30 hosphate-binding pocket is required for EGFP-XRCC1 accumulation at DNA damage induced by UVA laser, H

31 amster ovary cells expressing human forms of XRCC1 after exposure to hydrogen peroxide (H(2)O(2)), me

32 X-ray repair cross-complementing protein 1 (XRCC1), all essential components of the error-prone, alt

33 Loss of Xrcc1 also led to the persistence of DNA strand breaks t

34 switch junctions decreased, suggesting that XRCC1 also participates in alternative nonhomologous end

35 We investigated whether polymorphisms in XRCC1 alter DNA repair capacity and modify breast cancer

36 and HSP90-mediated regulation of Polbeta and XRCC1 alters the DNA repair complex architecture.

37 t failure is more severe in the mice lacking XRCC1, an essential protein for SSB repair, which is res

38 hosphorylation-dependent interaction site in XRCC1 and a forkhead-associated domain in PNKP.

39 ith corresponding increased transcription of XRCC1 and BRCA2 genes, both of which are required for re

40 ions between polymorphisms and haplotypes in XRCC1 and breast cancer risk in a nested case-control st

41 y of the base excision repair (BER) proteins XRCC1 and DNA Pol beta, adding a new level of regulation

42 he mechanism of poly (ADP-ribose) binding by XRCC1 and examined its importance for XRCC1 function.

43 erved Rev1-interacting region (RIR) motif in XRCC1 and included three critical and evolutionarily inv

44 It has been shown that XRCC1 and PARP1 are involved in the repair of base lesio

45 e strength of APE1 interaction with Polbeta, XRCC1 and PARP1 is revealed to be modulated by BER inter

46 rearrangement of the Polbeta complexes with XRCC1 and PARP1, while having no detectable influence on

47 s by a sub-pathway of BER that requires both XRCC1 and PARP1.

48 sis and co-immunoprecipitation indicate that XRCC1 and PCNA are in a complex and likely physically in

49 XRCC1 and PNKP interact via a high-affinity phosphorylat

50 eraction acts as a molecular tether, holding XRCC1 and PNKP together and thereby promoting the low-af

51 at the most stable complex is formed between XRCC1 and Polbeta.

52 ishes the recruitment of the repair proteins XRCC1 and polymerase beta at damaged telomeres, while th

53 ions of four purified BRCT domains, two from XRCC1 and their two partners from DNA ligase IIIalpha an

54 s in the DNA damage response enzymes ATM and XRCC1 and with overexpression of the cell cycle kinase c

55 axin associates with the DNA repair proteins XRCC1 and XRCC4, which are partners of DNA ligase III an

56 orylated FHA domain binding motifs (FBMs) in XRCC1 and XRCC4.

57 ir factor X-ray cross-complementing group 1 (XRCC1) and breast cancer-associated gene 2 (BRCA2), the

58 gen species (ROS) followed by single strand (XRCC1) and double strand (gamma-H2AX) DNA breaks.

59 X-ray repair cross-complementing protein 1 (XRCC1) and tyrosyl-DNA phosphodiesterase 1 (TDP1), using

60 d in four BER genes (APEX1, PARP1, POLB, and XRCC1), and conditional logistic regression was used to

61 Several genes, such as MnSOD, XRCC1, and GST, may modify the association of specific n

62 , 2), nucleolin, DNA ligase III, KU70, KU86, XRCC1, and histones.

63 The cumulative results implicate XRCC1, and more broadly SSBR, in the protection of nondi

64 of PAR, whereas the BRCT domains of Ligase4, XRCC1, and NBS1 recognize ADP-ribose, the basic unit of

65 5 depletion affects the levels of PARP-1 and XRCC1, and our collective results suggest that RECQL5 mo

66 study suggests that polymorphisms in APEX1, XRCC1, and PARP1 may be associated with advanced colorec

67 Other proteins, including histone H1 (HON1), XRCC1, and PARP1, participate in a 'backup' (b)NHEJ proc

68 including PARP-1, hMutSbeta, DNA ligase III, XRCC1, and PNK.

69 s relevant to human cancer and variations in XRCC1, and provide the basis for investigating groups of

70 xic insult also increases binding of APE1 to XRCC1, and this increase is suppressed by NAM or knockdo

71 An anti-XRCC1 antibody inhibits removal of the blocking 3'-phosp

72 Genetic variants in ABCB1, TGFB1, and XRCC1 appear to be associated with susceptibility to HAV

73 ociation between MRN and DNA ligase IIIalpha/XRCC1 are altered in cell lines defective in the major N

74 rp-1, DNA-ligases 1 (Lig1) and 3 (Lig3), and Xrcc1 are implicated in B-NHEJ.

75 DNA ligase 3 (Lig3) and its cofactor XRCC1 are widely considered to be requisite A-EJ factors

76 xcision repair genes, the variant alleles of XRCC1 Arg399Gln were significantly associated with the a

77 nificant differences in the distributions of XRCC1 Arg399Gln, XRCC3 Thr241Met, RAD51 G135C, and P53 A

78 tic polymorphisms of the XPD (Asp312Asn) and XRCC1 (Arg399Gln) DNA repair genes in 103 patients with

79 1 and 3, and Xeroderma pigmentosum, group D (XRCC1-Arg399Gln, XRCC3-Thr241Met, XPD-Lys751Gln).

80 We identified rs1982073-TGFB1 and rs1799782-XRCC1 as target SNPs, whose alleles could modulate gene

81 nally, resveratrol increases APE activity in XRCC1-associated protein complexes, while NAM or knockdo

82 ch is probably a common feature of the known XRCC1-associating end-processing enzymes.

83 n between PNKP and XRCC1 in the retention of XRCC1 at DNA damage sites and in DNA alkylation damage r

84 Furthermore, Xrcc1(+/-) B cells had reduced Igh/c-myc translocations

85 PNK binds to a phosphorylated segment of XRCC1 (between its two C-terminal BRCT domains) via its

86 age and synthesizes ADP-ribose polymers that XRCC1 binds directly.

87 tion of the heterodimer formed from a longer XRCC1 BRCT domain construct, including residues comprisi

88 r proteins that bind to different regions of XRCC1 but also with aprataxin and aprataxin-like factor

89 Repair of pyrimidine base damage may require XRCC1 but does not require PARP1 activity.

90 XRCC1 can also recruit end-processing enzymes, such as P

91 indicating essential DNA repair functions of Xrcc1 can occur in the absence of Lig3.

92 of both proteins to greatly reduce or ablate XRCC1 chromatin binding following H2O2 treatment.

93 required to ablate both ADP-ribosylation and XRCC1 chromatin binding following H2O2 treatment.

94 Furthermore, the XRCC1 co-immunoprecipitate complex (IP) displayed MMEJ a

95 We report here that XRCC1 co-localizes with proliferating cell nuclear antig

96 ancer and smoking dose for participants with XRCC1 codon 194 Arg/Arg (P(trend) = 0.046), 399 Arg/Arg

97 1,137 Whites), to examine associations among XRCC1 codon 194, 280, and 399 genotypes, breast cancer,

98 ent processing) and the human DNA ligase III/XRCC1 complex (general DNA repair) have been shown to be

99 evidence indicates that the ligase IIIalpha-XRCC1 complex binds to DNA nicks in nucleosomes only whe

100 ion between PNKP and the DNA ligase IIIalpha-XRCC1 complex significantly increased the efficiency of

101 fied Bcl2 protein directly disrupts the APE1.XRCC1 complex with suppression of APE1 endonuclease acti

102 e (PARG) to completely disassemble the PARP1-XRCC1 complex without assistance from a mono(ADP-ribose)

103 Bcl2 in cells reduces formation of the APE1.XRCC1 complex, and purified Bcl2 protein directly disrup

104 ell as human DNA ligase I or ligase IIIalpha-XRCC1 complex.

105 g a pSer-pThr dipeptide, and forms a 2:1 PNK:XRCC1 complex.

106 We report the characterization of the new XRCC1 complex.

107 Moreover, ligase IIIalpha-XRCC1 confers specificity onto the reaction in as much a

108 finity to a multiply phosphorylated motif in XRCC1 containing a pSer-pThr dipeptide, and forms a 2:1

109 the loss of cerebellar neurons and ataxia in Xrcc1-defective mice, identifying a molecular mechanism

110 ne-xanthine oxidase as the oxidizing method, XRCC1 deficiency affected both dividing and nondividing

111 results in an aggressive phenotype and that XRCC1 deficiency could also be exploited for a novel syn

112 This is the first study to show that XRCC1 deficiency in breast cancer results in an aggressi

113 e primary biochemical defect associated with XRCC1 deficiency is in the ligation step of BER/SSBR, an

114 Here we demonstrate that XRCC1 deficiency slightly increases the efficiency of CS

115 X-ray repair cross-complementing protein-1 (XRCC1)-deficient cells are sensitive to DNA damaging age

116 rescue the hydrogen peroxide sensitivity of XRCC1- deficient cells.

117 Preclinically, we evaluated XRCC1-deficient and -proficient Chinese hamster and huma

118 incision activity was found to be normal in XRCC1-deficient cell extracts, as were the levels of aba

119 o several DNA-damaging agents that sensitize Xrcc1-deficient cells.

120 Our studies reveal that XRCC1-deficient Chinese hamster ovary WCEs exhibit norma

121 nzopyran-4-one] were synthetically lethal in XRCC1-deficient compared with proficient cells as eviden

122 ogen peroxide between wild-type CHO-9 cells, XRCC1-deficient EM-C11 cells and EM-C11 cells transfecte

123 pocket is required following DNA damage for XRCC1-dependent acceleration of DNA single-strand break

124 Lig3 is to maintain mtDNA integrity and not Xrcc1-dependent DNA repair.

125 blockade of PARP1 enzymatic activity impairs XRCC1-dependent repair of DNA damage and selectively kil

126 sruption of the interaction between PNKP and XRCC1 did not impact their initial recruitment to locali

127 Common to these pathways is the essential XRCC1 DNA repair protein, which interacts with at least

128 required for Iduna ubiquitination of PARP1, XRCC1, DNA ligase III, and KU70.

129 The scaffold protein XRCC1, DNA polymerase beta, and DNA ligase IIIalpha play

130 -DNA ligase IIIalpha heterodimer and mutated XRCC1-DNA ligase IIIalpha complex that does not interact

131 We have isolated wild-type XRCC1-DNA ligase IIIalpha heterodimer and mutated XRCC1-

132 fected the ligation efficiency of the mutant XRCC1-DNA ligase IIIalpha heterodimer in reconstituted B

133 Indeed, homozygous deletion of Xrcc1 does not impair A-EJ of I-SceI-induced DSBs in XRC

134 ever, the rate of repair of damage requiring XRCC1 does reflect the damage complexity.

135 that the BRCT complex between the C-terminal XRCC1 domain and the ligase IIIalpha domain is a heterot

136 More importantly, Lig4 and XRCC1 double-deficient cells switch as efficiently as Li

137 ver, Chinese hamster ovary cells with mutant XRCC1 (EM9) were more sensitive to E2F1-induced apoptosi

138 istone octamer; that the scaffolding protein XRCC1 enhances the ligation; that the ligation occurs wi

139 e of polymorphisms in DNA repair genes APE1, XRCC1, ERCC1, XPD, and XRCC3 in predicting therapeutic o

140 Cells from a patient with mutations in XRCC1 exhibited not only reduced rates of single-strand

141 thanesulfonate-induced DNA damage stimulated XRCC1 expression in E2F1(+/+) but not E2F1(-/-) mouse em

142 We investigated XRCC1 expression in early breast cancers (n = 1,297) and

143 Endogenous XRCC1 expression increased in cells conditionally expres

144 ls, with (AA8 cells) and without (EM9 cells) XRCC1 expression.

145 Moreover, we failed to detect XRCC1 foci in Adprt1-/- MEFs after treatment with H2O2.

146 RTS primary fibroblasts also accumulate more XRCC1 foci than control cells in response to endogenous

147 e in base excision repair, it was found that XRCC1 forms a tight complex with DNA ligase IIIalpha and

148 occurs within a complex that ligase IIIalpha-XRCC1 forms with the host nucleosome; and that the ligas

149 ing by XRCC1 and examined its importance for XRCC1 function.

150 ent at DNA damage sites and is important for XRCC1 function.

151 plasmid vector carrying wild-type or mutant XRCC1 gene and find that the plasmid encoding XRCC1 prot

152 e show that biallelic mutations in the human XRCC1 gene are associated with ocular motor apraxia, axo

153 Polymorphisms in the XRCC1 gene may lead to variation in repair proficiency a

154 26602T, Arg(399)Gln, and Gln(632)Gln) in the XRCC1 gene.

155 protein levels included: c-jun, ERCC1, XPD, XRCC1, Gli1, Gli2, SHH, IHH, GAPDH and alpha-tubulin.

156 Our study indicates that XRCC1 haploinsufficiency in mammals has little effect on

157 XRCC1 has been shown to have a large number of single-nu

158 X-ray cross-complementing 1 (XRCC1) has been suggested to function at nearly every st

159 DNA break (SSB) repair machinery, including XRCC1, have been implicated in A-EJ.

160 te that Pol beta and the DNA ligase IIIalpha-XRCC1 heterodimer are present at equimolar concentration

161 beta (Pol beta) and the DNA ligase IIIalpha-XRCC1 heterodimer efficiently bind/cross-link to the sub

162 motes recruitment of the DNA ligase IIIalpha-XRCC1 heterodimer through its interaction with XRCC1.

163 -linking efficacy of the DNA ligase IIIalpha-XRCC1 heterodimer was decreased about 2-fold in the Pol

164 es not interact with the DNA ligase IIIalpha-XRCC1 heterodimer.

165 of DNA Pol beta with the DNA ligase IIIalpha-XRCC1 heterodimer.

166 nological and biological aging parameters in XRCC1 heterozygous (HZ) mice were examined.

167 Primary XRCC1 heterozygous mouse cerebellar granule cells exhibi

168 -jun, and the upregulation of ERCC1, XPD and XRCC1 in cisplatin-resistant human ovarian cancer cells.

169 al abnormalities given the prominent role of XRCC1 in endoderm and mesoderm formation.

170 and reveal a unique role for ligase IIIalpha-XRCC1 in enhancing the efficiency of the final two steps

171 slocations during CSR, supporting a role for XRCC1 in microhomology-mediated joining.

172 ostatic interactions, supporting the role of XRCC1 in nuclear cotransport of APLF.

173 Moreover, knockdown of XRCC1 in primary human fetal brain neurons leads to enha

174 genes involved in DNA strand breaks, such as XRCC1 in single-strand break repair, XRCC3 and RAD51 in

175 l roles for the interaction between PNKP and XRCC1 in the retention of XRCC1 at DNA damage sites and

176 recapitulate the hallmark features of neural Xrcc1 inactivation such as DNA damage-induced cerebellar

177 Here, we report that Xrcc1 inactivation via conditional gene-targeted deletio

178 1, and the base excision repair (BER) factor XRCC1 increases dramatically upon single-strand break da

179 ells to telomere oxidative damage as well as XRCC1 inhibition.

180 We found that XRCC1 interacts in vitro with ROS1 and ZDP and stimulate

181 Although it has no known enzymatic activity, XRCC1 interacts with multiple DNA repair proteins and is

182 protein X-ray repair cross-complementing 1 (XRCC1) interacts with multiple enzymes involved in DNA b

183 involvement in the recruitment of endogenous XRCC1 into oxidized chromatin we have established 'isoge

184 Our results suggest that XRCC1 is a component of plant base excision repair and f

185 XRCC1 is a critical scaffold protein that orchestrates e

186 XRCC1 is a key component of DNA base excision repair, si

187 XRCC1 is a molecular scaffold protein that assembles mul

188 XRCC1 is an excellent prototype to provide a forum for d

189 ig4-deficient cells, clearly indicating that XRCC1 is dispensable for A-EJ in CH12F3 cells during CSR

190 XRCC1 is important for efficient processing of an AP sit

191 Here we show that XRCC1 is involved in the repair of base lesions and SSBs

192 Our findings firmly demonstrate that XRCC1 is not a requisite factor for A-EJ of chromosomal

193 XRCC1 is phosphorylated in vivo and in vitro by CK2, and

194 inding pocket in the central BRCT1 domain of XRCC1 is required for selective binding to poly (ADP-rib

195 The current evidence suggests a model where XRCC1 is sequestered via its interaction with PCNA to si

196 One of the most important interactions of XRCC1 is that with polynucleotide kinase/phosphatase (PN

197 Of these, ligase IIIalpha-XRCC1 is the most efficient.

198 formed by DNA polymerase beta (Polbeta) and XRCC1 is thought to facilitate repair by recruiting Polb

199 Human X-ray cross-complementing group 1 (XRCC1) is a single-strand DNA break repair protein which

200 X-ray repair cross-complementing protein 1 (XRCC1) is assembled sequentially at the site of damage.

201 X-ray Repair Cross Complementing 1 (XRCC1) is thought to function as a scaffolding protein i

202 demonstrate that DNA ligase IIIalpha, unlike XRCC1, is phosphorylated in a cell cycle-dependent manne

203 strate herein that shRNA lentiviral-mediated XRCC1 knockdown in human SH-SY5Y neuroblastoma cells res

204 LIG3 mutant cells have relatively normal XRCC1 levels but elevated sister chromatid exchange.

205 th damage and proliferative signals increase XRCC1 levels, the mechanisms regulating XRCC1 transcript

206 homologous end joining (alt-NHEJ) components-XRCC1, LIG3, and PARP1-suppresses stress-induced TNR mut

207 I partly compensates for the absence of the XRCC1/ligaseIII during short-patch BER of an AP site whe

208 Genetic polymorphisms in XPD and XRCC1 may be important prognostic factors in platinum-tr

209 In contrast, the stability of the XRCC1 monomer is protected from CHIP-mediated ubiquityla

210 mage sensitivity to DNA alkylation agents of xrcc1 mutant cells.

211 Moreover, XRCC1 mutant EM9 cells possess steady-state levels of en

212 Furthermore, extracts from xrcc1 mutant plants exhibit a reduced capacity to comple

213 One XRCC1 mutant, A482T, that was defective in binding to po

214 SSB repair-defective cell line, EM9 with an XRCC1 mutation, has an increased number of spontaneous g

215 Formation of a complex between the XRCC1 N-terminal domain (NTD) and DNA polymerase beta (P

216 Two crystal forms of XRCC1-NTD complexed with Pol beta have been solved, reve

217 occur distal to the interface, the oxidized XRCC1-NTD forms additional interactions with Pol beta, e

218 ol beta have been solved, revealing that the XRCC1-NTD is able to adopt a redox-dependent alternate f

219 ha2 helix and the betaD and betaE strands of XRCC1-NTD to the energetics of beta-Pol binding.

220 BGDE) and the protruding alpha2 helix of the XRCC1-NTD.

221 is required for the assembly or stability of XRCC1 nuclear foci after oxidative DNA damage and sugges

222 ost nucleosome; and that the ligase IIIalpha-XRCC1-nucleosome complex decays when ligation is complet

223 in vitro by CK2, and CK2 phosphorylation of XRCC1 on S518, T519, and T523 largely determines apratax

224 XRCC1 operates as a scaffold protein in base excision re

225 his difference in repair efficiency involves XRCC1 or other BER proteins, synthetic oligonucleotides

226 cells proficient (AA8) or deficient (EM7) in XRCC1 or purified BER proteins.

227 requencies was detected with atm, atr, lig4, xrcc1, or parp1 mutants.

228 Although the XRCC1-PARP1 complex is relevant to the proposed therapeu

229 Recent studies have shown that XRCC1 participates in S phase-specific DNA repair pathwa

230 related syndrome caused by mutations in the XRCC1 partner protein PNKP and implicates hyperactivatio

231 n of the APLF FHA domain with phosphorylated XRCC1 peptides using crystallographic, NMR, and fluoresc

232 idinic endonuclease, and DNA ligase IIIalpha-XRCC1, performs uracil-initiated base excision repair.

233 gh-resolution crystal structure of a PNK-FHA-XRCC1 phosphopeptide complex reveals the basis for this

234 MMEJ activation was dependent on XRCC1 phosphorylation by casein kinase 2 (CK2), enhancin

235 NKP with lower affinity and independently of XRCC1 phosphorylation.

236 XRCC1 plays a key role in the repair of DNA base damage

237 s in the ligation step of BER/SSBR, and that XRCC1 plays no significant role in endogenous base damag

238 These data suggest an important role for the XRCC1-Pol beta interaction for coordinating the efficien

239 Moreover, studies indicate that XRCC1 possesses discrete G1 and S phase-specific functio

240 To study these upstream mechanisms, the XRCC1 promoter was cloned into a luciferase reporter.

241 an inactive mutant E2F1(132E), activated the XRCC1 promoter-luciferase reporter, and deletion of pred

242 mical data to demonstrate that two preformed XRCC1 protein complexes exist in cycling HeLa cells.

243 vely, these data establish the importance of XRCC1 protein complexes for normal neurological function

244 Similar results were observed for PNKP; an XRCC1 protein partner important for repair of oxidative

245 pulation variants had little or no effect on XRCC1 protein stability or the interactions with POLbeta

246 We find that a point mutation in the XRCC1 protein which disrupts functional interaction with

247 RCC1 gene and find that the plasmid encoding XRCC1 protein, that does not interact with Pol beta has

248 Studies using recombinant XRCC1 proteins revealed that: a C389Y substitution, resp

249 The RecQ1 A159C, RAD54L C157T, XRCC1 R194W, and ATM T77C genotypes had a significant ef

250 is that poly (ADP-ribose) synthesis promotes XRCC1 recruitment at DNA damage sites and is important f

251 ARP1 or PARP2 are sufficient for near-normal XRCC1 recruitment at oxidative single-strand breaks (SSB

252 , suggesting that poly (ADP-ribose) promotes XRCC1 recruitment both at single-strand breaks globally

253 by either PARP1 or PARP2, are sufficient for XRCC1 recruitment following oxidative stress.

254 XRCC1 recruitment is promoted by PARP1, an enzyme that i

255 ved in translocation formation and show that Xrcc1 reinforces the function of Lig3 in the process wit

256 X-ray repair cross-complementing protein 1 (XRCC1), relevant to neurodegeneration following kainic a

257 All four genes except XRCC1 remained as independent predictors of survival in

258 tion by itself is a high affinity ligand for XRCC1, requiring a minimum chain length of 7 ADP-ribose

259 including tyrosyl-DNA phosphodiesterase-1 or XRCC1, resulted in increased Top1cc formation and excess

260 805389 [ LIG4], rs8079544 [ TP53], rs25489 [ XRCC1], rs1673041 [ POLD1], and rs11615 [ ERCC1]) and su

261 or false discovery rate [FDR-P] = 0.017) and XRCC1 rs1799782 (OR, 1.57; 95% CI, 1.27-1.94; FDR-P = 0.

262 ssociation for one of the associated SNPs in XRCC1 (rs25487) was replicated in two independent data s

263 rylation by casein kinase 2 (CK2), enhancing XRCC1's interaction with the end resection enzymes MRE11

264 Mice heterozygous for XRCC1 showed a significant increase in the frequencies o

265 es (rs2079147, Pinteraction=0.0033), whereas XRCC1 SNPs had similar effects in mutation-positive and

266 Although the frequency of CSR was normal in Xrcc1(+/-) splenic B cells, the length of microhomology

267 e-nucleotide gap filling was not affected by XRCC1 status, a significant approximately 2-4-fold reduc

268 MRN interacts with DNA ligase IIIalpha/XRCC1, stimulating intermolecular ligation, and together

269 genetic assay to identify mutant versions of XRCC1 that are selectively defective in interacting with

270 approaches a second PNKP interaction site in XRCC1 that binds PNKP with lower affinity and independen

271 he rapid recruitment of the scaffold protein XRCC1 that interacts with, stabilizes and stimulates mul

272 a stable complex with the DNA repair protein XRCC1 that is also found only in higher eukaryotes.

273 11/hRad50/Nbs1 (MRN) and DNA ligase IIIalpha/XRCC1, that have been linked with alt-NHEJ.

274 a complex with PARP1 and its binding partner XRCC1, this interaction acts as a backup attempt to inte

275 T523 largely determines aprataxin binding to XRCC1 though its FHA domain.

276 stitutively bound to the scaffolding protein XRCC1 through interactions between the C-terminal BRCT d

277 reated dictates the specific contribution of XRCC1 to cellular resistance.

278 To further define the contribution of XRCC1 to DNA metabolism, we determined the in vivo local

279 tematically the quantitative contribution of XRCC1 to specific biochemical steps of BER and single-st

280 ease XRCC1 levels, the mechanisms regulating XRCC1 transcription remain unclear.

281 (ABCC2, ABCG2, ERCC1, ERCC2, GSTP1, MPO, and XRCC1) using polymerase chain reaction and Pyrosequencin

282 Increasing numbers of either XPD or XRCC1 variant alleles were associated with shorter overa

283 When expressed in HeLa cells, the XRCC1 variants-excluding E98K, which was largely nucleol

284 Ligase IIIalpha-XRCC1 was also able to bind and disrupt nucleosomes cont

285 Loss of XRCC1 was associated with a two-fold increase in risk of

286 To determine its role in A-EJ and CSR, Xrcc1 was deleted by targeted mutation in the CSR profic

287 ation efficiency by T4 ligase and ligase III/XRCC1 was largely unaffected by the nucleotide analogues

288 ERCC1, XPD/ERCC2, XPC, XPF/ERCC4, OGG1, and XRCC1 were compared after adjusting for age, sex, and sm

289 genes, CDK6 (cyclin-dependent kinase 6) and XRCC1, were significantly associated with DN after Bonfe

290 X-ray repair cross-complementing protein 1 (XRCC1), which completes the fourth and final step in (sh

291 In contrast, DNA ligase IIIalpha-XRCC1, which completes BER, was appreciably active only

292 the BER protein X-ray cross-complementing-1 (XRCC1), while inhibition of SIRT1 with nicotinamide (NAM

293 The FHA domain-dependent interaction of XRCC1 with APLF joins repair scaffolds that support sing

294 Recent data has found an association of XRCC1 with proteins causally linked to human spinocerebe

295 A structural model for a XRCC1 x DNA ligase IIIalpha heterotetramer is proposed a

296 on stabilizes TDP1, induces the formation of XRCC1 (X-ray cross-complementing group 1)-TDP1 complexes

297 work, we examined the possible role of plant XRCC1 (x-ray cross-complementing group protein 1) in DNA

298 XRCC1 (X-ray repair cross-complementing gene 1) deficien

299 XRCC1 (x-ray repair cross-complementing group 1) protein

300 the hypothesis that genetic polymorphisms in XRCC1, XRCC3, RAD51, XRCC7, and p53 were associated with