ライフサイエンスコーパス: BER

1 BER counters the mutagenic and cytotoxic effects of dama

2 BER gap-filling polymerase activity was partially inhibi

3 BER gene expression levels and IFN treatment responses w

4 BER genes NEIL3 was down-regulated in IFN-treated patien

5 BER genes were assessed by quantitative RT-PCR.

6 BER is a major pathway that copes with DNA damage induce

7 In some instances the binding of a BER factor to one nucleosomal lesion appeared to facilit

8 We hypothesize that aberrant BER, resulting from mutations in BER genes, can lead to

9 n oxidized dNTPs pool together with aberrant BER processing contribute to TNR expansion in non-replic

10 led to provide excision of the 5'-adenylated BER intermediate in mitochondrial extracts.

11 While folate depletion did not affect BER activity of the mothers, BER increased in the offspr

12 Therefore, although BER of simple lesions occurs rapidly, pathway choice and

13 We conclude that multiple interactions among BER proteins lead to large complexes, which are critical

14 APOBEC3 and BER gene expression at treatment endpoints partially cor

15 ng active roles for oxidative DNA damage and BER in TNR instability.

16 results provide direct evidence that MMR and BER, operating together, form a novel hybrid pathway tha

17 trioxsalen plus UVA, implying that NEIL1 and BER may interfere with normal cellular processing of int

18 These studies suggest that both NER and BER pathways mediate repair of a diverse set of hydantoi

19 evaluate the relative processing by NER and BER.

20 ads to concurrent relocalization of NPM1 and BER components from nucleoli to the nucleoplasm, and cel

21 l mechanistic switch between replication and BER.

22 Here we show that NPM1 stimulates APE1 BER activity in cells.

23 This attempted BER accounts for many of the potentially lethal or mutag

24 identified a novel mechanistic role of both BER and MMR pathways in mediating cellular responses to

25 Gh lesions are excellent substrates of both BER and NER.

26 Targeting both BER and MMR pathways resulted in no additional resistanc

27 cient in repair of endogenous DNA lesions by BER.

28 CC1 and PARP1 is revealed to be modulated by BER intermediates to different extents, depending on the

29 t nucleosomes control the patch size used by BER.

30 athways, mechanisms regulating BER capacity, BER responses to DNA damage and their links to checkpoin

31 portant contributors in controlling cellular BER protein levels, enzymatic activities, protein-protei

32 itro Subsequent restoration of the chaperone-BER complex in cell, presumably after completion of repa

33 BER product ratios may depend on competitive BER and NER protein binding to these lesions.

34 filling DNA polymerase activity and complete BER.

35 lacking the CTD, not only inhibits complete BER in vitro but also prevents its chromatin association

36 zed base and a ribonucleotide can compromise BER and RER in repeated sequences.

37 ic relocalization of APE1 and the consequent BER deficiency.

38 ocessing of the 5'-adenylated dRP-containing BER intermediate.

39 In contrast, BER activity is affected by the presence of a ribonucleo

40 r of the whole BER pathway by 1) controlling BER protein levels, 2) regulating total BER capacity, an

41 ow that the LigC complex interacts with core BER enzymes in vivo and demonstrate that together these

42 ngs on NEIL2's role in transcription-coupled BER.

43 (i) regulating the expression of a critical BER enzyme (Mag1), (ii) supporting efficient DNA damage

44 le selectively knocking out or down critical BER proteins to identify the impact on luciferase expres

45 and high-fat feeding from weaning, decreased BER activity significantly in the cortex, cerebellum, hi

46 The levels of the detected BER intermediates are 1 and 2 orders of magnitude lower

47 polymerase (PARP) inhibitors, which disrupt BER, markedly sensitize ovarian cancer cells to FdUrd, s

48 viously unidentified role of OGG1-driven DNA BER in the generation of endogenous signals for inflamma

49 e of its slow polymerization activity during BER in vivo.

50 ion forks collide with SSBs generated during BER.

51 ease responsible for the DNA incision during BER.

52 nd stimulatory effect on DNA ligation during BER in a hairpin loop.

53 requirement for the gap-filling step during BER.

54 We demonstrate that during BER of 8-oxoguanine (8-oxodG) in TNR sequences, DNA poly

55 complexes, which are critical for efficient BER in mammalian cells, and the CTD interaction could be

56 in the nuclear genome via the base excision (BER) and SSB repair (SSBR) pathways, respectively, is we

57 In summary, in human cell extracts, BER and NER activities co-exist and excise Gh and Sp DNA

58 fidence interval [CI], .22-.70) and a faster BER from the TTP model (OR, 0.71; 95% CI, .55-.94).

59 In the case of mouse embryonic fibroblasts, BER of the Sp lesion is strongly reduced in NEIL1(-/-) r

60 BER pathway, our data suggest a function for BER proteins in the regulation of ribogenesis.

61 ults provide the first mechanistic model for BER and MMR functioning within the same pathway to media

62 herein the activity of several enzymes [four BER-initiating DNA glycosylases and the downstream proce

63 advantages in comparison to other functional BER assays with no need of electrophoretic separation, s

64 he oxidatively modified DNA base OG to guide BER activity in a gene promoter and impact cellular phen

65 recent advances in the understanding of how BER mediates this critical component of epigenetic regul

66 However, BER also performs essential functions in processes other

67 In contrast, the human BER glycosylase NEIL1 exhibited robust activity for all

68 lls and blasts of AML patients have impaired BER activity.

69 hypoxia with consequences including impaired BER and down regulation of the ATMIN transcriptional tar

70 w key regulation point for pathway choice in BER.

71 Cells defective in BER or MMR display a cisplatin-resistant phenotype.

72 epair of these lesions, and as deficiency in BER activity results in DNA damage it has been proposed

73 1 mutation frequencies in yeast deficient in BER endonucleases or DNA damage tolerance proteins.

74 olely responsible for the deglycosylation in BER enzymes, however our results suggest an alternative

75 ed these reporters to measure differences in BER capacity across a panel of cell lines collected from

76 This fall in BER activity was associated with small changes in methyl

77 at aberrant BER, resulting from mutations in BER genes, can lead to genomic instability and cancer.

78 S229L participates in BER, but due to its lower catalytic rate, does so more s

79 strand (NTS) of yeast genes, particularly in BER-deficient strains, due to higher damage formation on

80 t Rev1 could serve as a backup polymerase in BER and could potentially contribute to AID-initiated an

81 beta and there is a significant reduction in BER polymerase extension beyond 1 nt, creating a strikin

82 thus has an indirect but significant role in BER in vivo that may also be important for NPM1c+ tumori

83 The first step in BER is catalyzed by DNA N-glycosylases.

84 zymes that catalyze the first three steps in BER can act at many sites in nucleosomes without the aid

85 s no longer provided to the plants to induce BER.

86 s within nucleosomes significantly influence BER efficiency; moreover, this effect is asymmetric rela

87 action is a possible strategy for inhibiting BER selectively in cancer cells.

88 N-methylpurines from DNA and do not initiate BER, display strongly reduced levels of methylation-indu

89 ate the detrimental effects of Aag-initiated BER during I/R and sterile inflammation, and present a n

90 cterization of in vitro uracil-DNA initiated BER in C. elegans.

91 increase repair fidelity of MUTYH-initiated BER.

92 t pre-excision step(s) during OGG1 initiated BER evoked by ROS facilitates NF-kappaB DNA occupancy an

93 ities enabling suppression of OGG1-initiated BER and coordination of TDG-initiated BER at this tandem

94 In contrast, the OGG1-initiated BER pathway is blocked due to the 5'-flanking T:G mispai

95 tiated BER and coordination of TDG-initiated BER at this tandem alteration in the CpG dinucleotide.

96 The overall TDG-initiated BER of the Tp8-oxoG dinucleotide is significantly reduce

97 Furthermore, in TDG-initiated BER, TDG remains bound to its product AP site blocking O

98 emethylation process involving TDG-initiated BER.

99 urine-DNA glycosylase (MPG), which initiates BER of epsilonA.

100 mine DNA glycosylase (hTDG), which initiates BER of mutagenic and cytotoxic G:T and G:U mispairs in D

101 available data on characterized PTMs of key BER proteins, the functional consequences of these modif

102 and newly emerging questions about mammalian BER pathways, mechanisms regulating BER capacity, BER re

103 limited because most methods used to measure BER activity are cumbersome, time consuming and, for the

104 Measuring BER capacity in living cells is valuable for both basic

105 Rev1 and demonstrated the enzyme can mediate BER in vitro The full-length Rev1 protein and its cataly

106 tivity and enhanced CRT expression mitigated BER in sCAX1 expressing lines.

107 Interaction between mitochondrial BER enzymes was significantly affected in the presence o

108 of hEXOG suggest a pathway for mitochondrial BER that provides an optimal substrate for subsequent ga

109 weak against the 5'-AMP-dRP block in a model BER substrate, and this activity was not able to complem

110 These studies also suggest that most BER-generated DSBs will occur in linker DNA and in genom

111 did not affect BER activity of the mothers, BER increased in the offspring at weaning (P=0.052).

112 However, the role of mitochondrial (mt) BER and SSBR proteins in mt genome maintenance is not co

113 NA lesions, suggesting that the relative NER/BER product ratios may depend on competitive BER and NER

114 t a role for the redistribution of nucleolar BER factors in determining cisplatin toxicity.

115 ice between long-patch and single-nucleotide BER, thereby modulating cellular sensitivity to DNA dama

116 mammalian cells induces the accumulation of BER intermediate substrates, chromosomal aberrations, an

117 Here, we performed a proteomic analysis of BER deficient human cells using stable isotope labelling

118 Biochemical characterization of BER in the context of (CTG)20 repeats further revealed t

119 known to be involved in the coordination of BER activity through a mechanism regulated by the sirtui

120 equires temporal and spatial coordination of BER and cell cycle progression to prevent replication of

121 y unrecognized mechanism for coordination of BER by p53, and its dysfunction in p53-inactivated cells

122 Step-by-step coordination of BER is facilitated by multiple interactions between enzy

123 , we demonstrate that MMR acts downstream of BER and is dependent on the polymerase activity of Polbe

124 ve cisplatin ICL processing is downstream of BER processing and dependent on Polbeta misincorporation

125 ver, little is known about the enzymology of BER of altered in-tandem CpG dinucleotides; e.g. Tp8-oxo

126 mall changes in methylation or expression of BER-related genes.

127 This fundamental and essential function of BER not only necessitates tight control of the continuou

128 ntly induce AID expression and inhibition of BER did not reduce the frequency of genome rearrangement

129 ctionally, knockdown of Tet or inhibition of BER in hippocampal neurons elevated excitatory glutamate

130 Model DNA intermediates of BER are shown to induce significant rearrangement of the

131 Levels of BER-initiating DNA glycosylases can vary between individ

132 . mutans, mutator phenotypes, due to loss of BER enzymes, may confer an advantage to virulence of the

133 nd purine base damage is by a sub-pathway of BER that requires both XRCC1 and PARP1.

134 endent and PARP1-independent sub-pathways of BER.

135 nucleosomes on the frequency and pattern of BER-dependent DSB formation, we incubated nucleosomes co

136 methods to effectively quantify the rate of BER as a whole.

137 A prominent example is the central role of BER in mediating active DNA demethylation, a multistep p

138 results provide new insight into the role of BER in modulating genome stability that is associated wi

139 Here we report that the DNA ligation step of BER is compromised after pol beta insertion of oxidized

140 However, population studies of BER capacity have been limited because most methods used

141 peroxynitrite, is an excellent substrate of BER only.

142 e NTHL1 gene predisposes to a new subtype of BER-associated adenomatous polyposis and CRC.

143 nucleosomes contribute to the suppression of BER-generated DSBs.

144 mbrane leakage, one of the first symptoms of BER.

145 posed that the mechanistic link between OGG1-BER and proinflammatory gene expression is OGG1's guanin

146 Mice deficient in OGG1-BER showed significantly decreased immune responses, whe

147 a the DNA base excision repair pathway (OGG1-BER).

148 presents different levels of constraints on BER, dependent on the structural requirements for enzyme

149 at the protein level, and also the impact on BER in vitro and in vivo.

150 owever, the effect of chromatin structure on BER protein recruitment to DNA damage sites in living ce

151 ctins and Ca(2)(+) bound to the cell wall on BER development in tomato fruit.

152 eraction of NEIL1 with replication and other BER proteins is required for efficient repair of the rep

153 e syndrome group B protein, TFIIH, and other BER proteins.

154 stitutes great sensitivity compared to other BER functional assays.

155 ts, we propose a revised model of long-patch BER and a new key regulation point for pathway choice in

156 major sub-pathway of conventional long-patch BER that involves formation of a 9-nucleotide gap 5' to

157 ic switch, shunting repair toward long-patch BER upon correct dCMP incorporation, thus enhancing repa

158 s the fourth and final step in (short-patch) BER.

159 fy a PPI inhibitor, 26 PPIs in DDR pathways (BER, MMR, NER, NHEJ, HR, TLS, and ICL repair) are specif

160 tween this altered dinucleotide and purified BER enzymes, the DNA glycosylases TDG and 8-oxoG DNA gly

161 on (16-QAM OFDM) data with a bit error rate (BER) of 3.1 x 10(-3) over a 60-cm free-space link.

162 rmodal crosstalk, and system bit error rate (BER).

163 Thus, we demonstrate that RAD9 regulates BER by controlling NEIL1 protein levels, albeit by diffe

164 ammalian BER pathways, mechanisms regulating BER capacity, BER responses to DNA damage and their link

165 , a core enzyme in base excision DNA repair (BER) of DNA lesions, specifically interacts with NPM1 wi

166 The base excision DNA repair (BER) pathway known to occur in Caenorhabditis elegans ha

167 lved in base and nucleotide excision repair (BER and NER).

168 and H3 N-tails rescues base excision repair (BER) activity but not MMS sensitivity.

169 eding from weaning, on base excision repair (BER) and DNA methylation and expression of selected BER-

170 kylating agent-induced base excision repair (BER) and formation of DPCs is enhanced by a PARP inhibit

171 Base excision repair (BER) and mismatch repair (MMR) pathways play an importan

172 ase (AID) and requires base excision repair (BER) and mismatch repair (MMR).

173 and the efficiency of base excision repair (BER) and RER enzymes (OGG1, MUTYH, and RNase H2) when pr

174 oxidative DNA damage, base excision repair (BER) and TNR expansion, which is demonstrated by the obs

175 fficient processing by base excision repair (BER) are among the factors suggested to contribute to TN

176 ng strands, initiating base excision repair (BER) by 8-oxoguanine DNA glycosylase (OGG1), yielding an

177 a) plays a key role in base excision repair (BER) by filling in small gaps that are generated after b

178 ylase, which initiates base excision repair (BER) by removing damaged DNA bases.

179 es have shown that DNA base excision repair (BER) can mediate TNR expansion and deletion by removing

180 Base Excision Repair (BER) efficiently corrects the most common types of DNA d

181 is shown that the DNA base excision repair (BER) enzyme, DNA glycosylase NEIL1, efficiently recogniz

182 ing DNA strands by the base excision repair (BER) enzymes can produce double-strand DNA breaks (DSBs)

183 chondrial-specific DNA base excision repair (BER) enzymes, namely EXOG and DNA polymerase gamma (Polg

184 ognition of 5'-AODN by base excision repair (BER) enzymes.

185 nsense mutation in the base-excision repair (BER) gene NTHL1.

186 n to be substrates for base excision repair (BER) glycosylases; however, large Sp-amine adducts would

187 DNA base excision repair (BER) has a critical role in genome maintenance by preven

188 vation led to impaired base-excision repair (BER) in cardiomyocytes in vitro, accompanied by loss of

189 d to be substrates for base excision repair (BER) in the framework of active demethylation.

190 agments in addition to base excision repair (BER) incision products.

191 APTX activity, blocked base excision repair (BER) intermediates containing the 5'-AMP or 5'-adenylate

192 Base excision repair (BER) is a frontline repair system that is responsible fo

193 Base excision repair (BER) is a highly conserved DNA repair pathway throughout

194 Base excision repair (BER) is an essential DNA repair pathway involved in the

195 Base excision repair (BER) is initiated by DNA glycosylases and is crucial in

196 Base excision repair (BER) is one of several DNA repair pathways found in all

197 Base excision repair (BER) is one of the most frequently used cellular DNA rep

198 Furthermore, base excision repair (BER) is responsible for causing CAG repeat contractions

199 Base excision repair (BER) is the main repair pathway to eliminate abundant ox

200 Base excision repair (BER) is the major cellular pathway responsible for repai

201 Base excision repair (BER) is the predominant pathway for coping with most for

202 ortive ligation during base excision repair (BER) leads to blocked repair intermediates containing a

203 ese maps revealed that base excision repair (BER) of alkylation damage is significantly modulated by

204 Base excision repair (BER) of an oxidized base within a trinucleotide repeat (

205 During mammalian base excision repair (BER) of lesion-containing DNA, it is proposed that toxic

206 nitiate prereplicative base excision repair (BER) of oxidized bases in the replicating genome, thus p

207 n that operates in the base excision repair (BER) pathway and is responsible for >/=95% of the total

208 damaged bases via the base excision repair (BER) pathway is a long-standing question.

209 The base excision repair (BER) pathway is mainly responsible for repairing oxidize

210 ally, we find that the base excision repair (BER) pathway is required to maintain expression of AREG

211 The DNA base excision repair (BER) pathway is the frontline mechanism handling the maj

212 r of these lesions via base excision repair (BER) pathway maintains genomic fidelity.

213 ced DNA lesions by the base excision repair (BER) pathway prevents mutation, a form of genomic instab

214 The base excision repair (BER) pathway repairs oxidized lesions in the DNA that re

215 glycosylase (TDG) and base excision repair (BER) pathway, but it is unclear to what extent and at wh

216 key enzyme in the DNA base excision repair (BER) pathway, is pivotal in maintaining the integrity an

217 lesions as part of the base excision repair (BER) pathway.

218 ethylation through the base-excision repair (BER) pathway.

219 the first step of the base excision repair (BER) pathway.

220 cluding members of the base excision repair (BER) pathway.

221 the first step in the base excision repair (BER) pathway.

222 is not repaired by the base excision repair (BER) pathway.

223 functions through the base excision repair (BER) pathway.

224 he initial step in the base excision repair (BER) pathway.

225 osylase1 (OGG1) during base excision repair (BER) pathway.

226 Base excision repair (BER) processes non-helix distorting lesions (e.g., uraci

227 known as a key nuclear base excision repair (BER) protein, in mitochondrial protein extracts derived

228 ce suggests a role for base excision repair (BER) proteins in the response to DNA interstrand crossli

229 Base excision repair (BER) recognizes and repairs minimally helix-distorting D

230 Base excision repair (BER) removes at least 20,000 DNA lesions per human cell

231 unknown if subsequent base excision repair (BER) steps function on replication-associated ssDNA.

232 nase (AID) followed by base excision repair (BER) was found not to be involved.

233 is mainly repaired by base excision repair (BER), a process initiated by DNA glycosylases that recog

234 idized bases in DNA is base excision repair (BER), and in vertebrates DNA polymerase beta (pol beta)

235 onuclease in mammalian base excision repair (BER), apurinic/apyrimidinic endonuclease 1 (APE1).

236 primarily processed by base excision repair (BER), either initiated by uracil-DNA glycosylase (UNG) o

237 is removed mainly via base excision repair (BER), however, whether there is preferential strand repa

238 ibute to DNA repair by base excision repair (BER), nucleotide excision repair (NER), mismatch repair

239 amage and fulfilled by base excision repair (BER), suggesting active roles for oxidative DNA damage a

240 reak repair (SSBR) and base excision repair (BER), the p1p2 and p1p2k80 mutants were shown to be sens

241 cation interferes with base excision repair (BER), the predominant pathway for repairing methylated b

242 polymerase involved in base excision repair (BER), which is a pathway responsible for the repair of t

243 s vitally important in base excision repair (BER).

244 sylase (TDG) initiated base excision repair (BER).

245 ge that is repaired by base excision repair (BER).

246 lesions are subject to base excision repair (BER).

247 luenced by IFN-induced base excision repair (BER).

248 ir intermediate during base excision repair (BER).

249 ld also be involved in base excision repair (BER).

250 endent MUTYH-initiated base excision repair (BER).

251 These results reveal BER enzyme specificities enabling suppression of OGG1-in

252 Blossom-end rot (BER) in tomato fruit (Solanum lycopersicum) is believed

253 Furthermore, blossom-end rot (BER) in tomato may be linked to changes in CAX activity

254 d DNA methylation and expression of selected BER-related genes in the brain of adult offspring.

255 lating the nucleolar localization of several BER enzymes.

256 The presence of the SN BER in C. elegans is supported by these results, despite

257 Whether single nucleotide (SN)-BER of a damaged base requires histone deposition or nuc

258 sion to 1 nt, suggesting a preference for SP BER.

259 main are similar in their ability to support BER in vitro The dRP lyase activity in both of these pro

260 cations of this behaviour for the GO system (BER of 8-oxo-dG lesions).

261 n cell culture (SILAC), and demonstrate that BER deficiency, which induces genetic instability, resul

262 nt locations of a TNR tract, indicating that BER can promote or prevent TNR expansion in a damage loc

263 These results suggest the possibility that BER mediated toxic strand breaks are produced in cells u

264 We have previously shown that BER in a TNR hairpin loop can lead to removal of the hai

265 nal resistance to cisplatin, suggesting that BER and MMR play epistatic roles in mediating cisplatin

266 The BER enzyme methyl-CpG binding domain protein 4 (MBD4) ha

267 The BER pathway is widely used to repair DNA damage in cells

268 mice provide evidence that MSH2-MSH3 and the BER machinery promote trinucleotide repeat (TNR) expansi

269 In R137Q knock-in mouse embryos, the BER efficiency was severely impaired, which subsequently

270 remove the 5'-adenylated-dRP group from the BER intermediate.

271 However, the mechanism(s) governing the BER process are poorly understood.

272 tion of oxidized purine nucleotides into the BER intermediate in vitro.

273 c of many cancers, leads to a failure of the BER coordination mechanism, overexpression of APE1, accu

274 yocytes in vitro, accompanied by loss of the BER enzyme OGG1, while BER activity was rescued by recom

275 hich MSH2-MSH3 is used as a component of the BER machinery to cause expansion.

276 MutY) and endonucleases (Smx and Smn) of the BER pathway and their relative role in adaptation and vi

277 APE1 acetylation is an integral part of the BER pathway for maintaining genomic integrity.

278 Regulation of the BER pathway for mutagenic oxidized bases, initiated by N

279 osylases that catalyze the first step of the BER pathway, i.e. recognition and excision of DNA lesion

280 e of APE1 as a representative protein of the BER pathway, our data suggest a function for BER protein

281 Situated within the middle of the BER pathway, Pol beta must efficiently locate its substr

282 nderstanding the fundamental features of the BER pathway.

283 nderlying coordination and regulation of the BER process.

284 Enzymatic characterization of the BER system showed that it protects the organism against

285 s therefore play key roles in regulating the BER pathway and are consequently crucial for coordinatin

286 Our results suggest that the BER enzyme, APE1, has acquired distinct surface residues

287 protecting against contractions, but through BER rather than nucleotide excision repair.

288 s whether TNR is expanded or deleted through BER.

289 ll, and also reduced fruit susceptibility to BER.

290 d thereby increasing fruit susceptibility to BER.

291 ling BER protein levels, 2) regulating total BER capacity, and 3) modulating the nucleolar localizati

292 op (FCL) motif in the structurally unrelated BER glycosylases MutY and Endonuclease III and therefore

293 cells, suggesting that genetically unstable BER deficient cells may be a source of pre-cancerous cel

294 rate that TNR expansion can be prevented via BER in hairpin loops that is coupled with the removal of

295 e of substrate channeling for steps in vitro BER and was proficient in in vitro repair of substrates

296 ning DNA appears to be a suicidal event when BER is overwhelmed or disrupted.

297 panied by loss of the BER enzyme OGG1, while BER activity was rescued by recombinant OGG1 (control vs

298 el role for NPM1 as a modulator of the whole BER pathway by 1) controlling BER protein levels, 2) reg

299 In contrast, yeast BER-defective cells accumulate endogenous damage prefere

300 We also documented that yeast BER-defective cells have significantly higher levels of