ライフサイエンスコーパス: NER

1 NER and normalization systems are also typically used in

2 NER crossing the midline was the only morphologic featur

3 NER protects against skin cancer.

4 me (XPC-1) and transcription-coupled (CSB-1) NER in ICL sensing were exposed.

5 y, this results in an increased binding of a NER protein, Rad14, to damaged DNA.

6 in the observed biocompatibility by using a NER-deficient human cell line.

7 o replicative stress significantly abrogates NER uniquely during S phase.

8 Accurate NER systems require task-specific, manually-annotated da

9 went above and beyond the assessment of all NER imaging features, as well as clinical and genomic fe

10 Together, these analyses identify an NER-related mutational signature and highlight the relat

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

12 uct ratios may depend on competitive BER and NER protein binding to these lesions.

13 base and nucleotide excision repair (BER and NER).

14 ons are excellent substrates of both BER and NER.

15 sm that delays chromosome decondensation and NER in response to incomplete chromosome separation duri

16 that prevents chromosome decondensation and NER until effective separation of sister chromatids is a

17 t and promoted chromosome decondensation and NER.

18 so important were KPS, age at diagnosis, and NER crossing the midline.

19 d damage recognition domains of MutS/MSH and NER helicase XPB, respectively, as well as with the puta

20 e relationship between protein oxidation and NER inhibition was investigated in cultured human cells

21 y and another tie between the proteasome and NER regulators.

22 Patients with high rCBVNER and NER crossing the midline and those with high rCBVNER and

23 he XPB helicase subunit of transcription and NER factor TFIIH.

24 opose collaborations between Fanconi anemia, NER, and MMR are necessary to initiate checkpoint activa

25 ncreased cell survival is independent of any NER subpathways.

26 ure XPA-photodamage interactions, and assess NER function.

27 erage, the multi-task models produced better NER results than the single-task models trained on a sin

28 e used to estimate the formation of biogenic NER.

29 onsidered as a potential risk while biogenic NER from incorporation of labeled carbon into microbial

30 transcription in human cells that lack both NER and TCR.

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

32 ) expedites the recognition of DNA damage by NER components via transcription-coupled DNA repair (TCR

33 DNA lesions are initially detected by NER factors XPC and XPE or stalled RNA polymerases, but

34 Here, we show that dual incision by NER endonucleases, including XPF and XPG, promotes the S

35 sized to evaluate the relative processing by NER and BER.

36 sincorporated ribonucleotides are removed by NER followed by error-prone resynthesis with DnaE.

37 y analogy, signal such lesions for repair by NER.

38 bulky lesions are preferentially repaired by NER.

39 n Human Exposure to Environmental Chemicals [NER; Centers for Disease Control and Prevention (2012)]

40 and that oxidative damage to RPA compromises NER capability.

41 zeta-dependent filling of lesion-containing, NER-generated gaps.

42 elial cancer, a tumor type in which the core NER gene ERCC2 is significantly mutated.

43 nucleotide polymorphisms (rSNPs) of the core NER genes modulate clinical outcome of patients with adv

44 07) and chemicals (BioCreative 5 CDR corpus, NER f-score: 0.914, normalization f-score 0.895).

45 erformance on diseases (NCBI Disease corpus, NER f-score: 0.829, normalization f-score: 0.807) and ch

46 eficient in GG-NER and transcription-coupled NER, but not in XPC cell lines lacking GG-NER only.

47 Defective NER is associated with photosensitivity and a high skin

48 nerate reactive oxygen species that diminish NER capacity by causing protein damage.

49 allowing UvrB to orchestrate the downstream NER reactions.

50 ate in the damage recognition process during NER, allowing dynamic DNA damage detection at a distance

51 We show that MMSET is required for efficient NER and that it catalyzes the dimethylation of histone H

52 involving XPC, TFIIH, and XPA for efficient NER.

53 s a positive function in promoting efficient NER in yeast.

54 aspect of chromatin that regulates efficient NER, and we provide a model for how Htz1 influences NER

55 vestigated associations of 25 rSNPs in eight NER genes with progression free survival (PFS) and overa

56 Mutations in genes encoding NER factors are associated with xeroderma pigmentosum (X

57 the two overlapping branches that encompass NER, transcription-coupled repair or global genome repai

58 damage, which is essential for cAMP-enhanced NER.

59 e recognition and verification in eukaryotic NER still remained elusive.

60 om The Cancer Genome Atlas dataset exhibited NER alterations, including nonsynonymous or splice site

61 Moreover, we show that RNF111 facilitated NER by regulating the recruitment of XPC to UV-damaged D

62 nd mimicking that functioning on a bona fide NER substrate.

63 classifier, with a rich feature approach for NER and supervised semantic indexing for normalization.

64 nuclear import of XPA from the cytoplasm for NER is regulated in cellular DNA damage responses in S-p

65 ds trainable for many entity types exist for NER, normalization methods are usually specialized to a

66 We show here that RPA is limiting for NER and that oxidative damage to RPA compromises NER cap

67 We present a single-task model for NER, a Multi-output multi-task model and a Dependent mul

68 XPA serves as a scaffold for NER, interacting with several other NER proteins as well

69 [c]Ph-N(6)-dA, which is a poor substrate for NER but also blocks transcription in vitro, was tested.

70 data showing that it is a poor substrate for NER.

71 d breaks are most likely poor substrates for NER.

72 may then trigger the recruitment of further NER proteins.

73 syndrome group B (CSB) and the global genome NER-initiating factor XPC are implicated in the protecti

74 lls and cells defective in the global genome-NER (GG-NER) subpathway, we establish how this alters th

75 e excision repair (TC-NER) or global genomic NER (GG-NER).

76 efficient XPC recruitment and global genomic NER.

77 in Core7 to promote NER, whereas non-genuine NER substrates have no such effect.

78 evels were elevated in cells deficient in GG-NER and transcription-coupled NER, but not in XPC cell l

79 ZRF1 is an essential factor in GG-NER, and its function at damaged chromatin sites is link

80 y step that leads to downstream events in GG-NER.

81 ed NER, but not in XPC cell lines lacking GG-NER only.

82 cells defective in the global genome-NER (GG-NER) subpathway, we establish how this alters the distri

83 of the global genomic subpathway of NER (GG-NER), associates with PARP-1 in the vicinity of UV-damag

84 on repair (TC-NER) or global genomic NER (GG-NER).

85 We also examined the genomic locations of GG-NER factor binding to chromatin before and after UV irra

86 facilitate the lesion recognition step of GG-NER via its interaction with DDB2 at the lesion site.

87 iciency of the lesion recognition step of GG-NER.

88 at the UV-induced DNA lesions to promote GG-NER.

89 subpathway of nucleotide excision repair (GG-NER) for removal of UV-induced direct photolesions from

90 global genome nucleotide excision repair (GG-NER) pathway.

91 global-genome nucleotide excision repair (GG-NER).

92 and after UV irradiation, revealing that GG-NER is organized and initiated from specific genomic loc

93 tyl-transferase Gcn5 is controlled by the GG-NER complex, which regulates histone H3 acetylation and

94 dent on the ubiquitination of Rad4 by the GG-NER E3 ligase, promotes UV survival in yeast cells.

95 Chromatin remodeling during the GG-NER process is therefore organized into these genomic do

96 the adduct but not as effectively as global NER.

97 The interplay between global NER and TCR in repairing the polycyclic aromatic hydroca

98 Hence, both global NER and TCR enhance the recovery of gene expression foll

99 ipt production in cells proficient in global NER but lacking TCR, indicating that TCR is necessary fo

100 at measuring the combined status of MMR, HR, NER, and MGMT provided a more robust prediction of temoz

101 nts and uncertainties in (i) total NER, (ii) NER formed from the parent pool, and (iii) NER formed fr

102 ) NER formed from the parent pool, and (iii) NER formed from the metabolite pool vary considerably am

103 rms of RPA that are associated with impaired NER.

104 ecruitment of XPA to UV-damaged DNA, impairs NER and increases UV-induced mutagenesis.

105 be possible to use them together to improve NER performance.

106 In NER, ERCC1-XPF is recruited to DNA lesions by interactio

107 irs growth in cells genetically deficient in NER, but did not show any sensitivity to the repair gene

108 and energetic origins of this difference in NER-incision efficiencies.

109 omplementary views of the k-mers involved in NER and NDR.

110 s, indicating that TFIIE was not involved in NER.

111 ong suppression of two-strand mutagenesis in NER-deficient backgrounds and demonstrated that neither

112 fect on transcription in cells proficient in NER but lacking TCR, indicating that NER can remove the

113 ntified lysines of Htz1 plays little role in NER or cell survival after UV.

114 r, XPB-R appears to function specifically in NER.

115 To elucidate substrate specificity in NER, we have prepared homogeneous human ten-subunit TFII

116 and the DNA-binding activity of human XPA in NER, we used NMR to investigate the interaction of its D

117 operating upon immobilization of individual NER factors on undamaged chromatin and mimicking that fu

118 d we provide a model for how Htz1 influences NER in Htz1 nucleosomes.

119 In Escherichia coli, UvrA and UvrB initiate NER, although the mechanistic details of how this occurs

120 o helix-distorting DNA lesions and initiates NER.

121 chanism of telomeric photoproduct removal is NER.

122 e the first machine learning model for joint NER and normalization during both training and predictio

123 of our model as a general toolkit for joint NER and normalization.

124 hich promoted ATR's interaction with the key NER factor xeroderma pigmentosum A (XPA) and facilitated

125 ) at Ser435, which actively recruits the key NER protein xeroderma pigmentosum complementation group

126 In primary human cells lacking NER, (+)-trans-anti-B[a]P-N(6)-dA exhibited a deleteriou

127 g to attack the mitochondrial genome lacking NER machinery and in vivo distribution of the delivery v

128 ndria to attack mitochondrial genome lacking NER machinery can lead to a rationally designed therapy

129 sensitive and quantitative assay to measure NER activity in human cells, which we term the Oligonucl

130 UVRAG as a regulator of CRL4(DDB2)-mediated NER and suggest that its expression levels may influence

131 with UV-damaged DNA and optimize melanocytic NER.

132 nhibitor, 26 PPIs in DDR pathways (BER, MMR, NER, NHEJ, HR, TLS, and ICL repair) are specifically dis

133 We conclude that jointly modeling NER and normalization greatly improves performance.

134 Importantly, neither NER alteration affected HR or conferred sensitivity to P

135 However, normal NER activity appeared when the XPC(-/-) cell extracts we

136 recognition in the global-genomic branch of NER.

137 recognition in the global-genomic branch of NER.

138 omes in the main nuclei before completion of NER.

139 metabolism and is an essential component of NER.

140 e site mutations and homozygous deletions of NER genes.

141 stablish how this alters the distribution of NER rates throughout the genome.

142 ificantly alters the genomic distribution of NER rates; this has implications for the effects of chro

143 s are characterized by lower efficiencies of NER and DSB/R mechanisms, resulting in higher accumulati

144 repair proteins for successful execution of NER.

145 onstrate that ORA can quantify the extent of NER in diverse cell types, including immortalized, prima

146 midline was the only morphologic feature of NER associated with poor survival (log-rank test, P = .0

147 cally characterized by genetic impairment of NER, such as skin and testicular cancers.

148 are characterized by profound inhibition of NER exclusively during S phase.

149 Responders' BMPCs showed slower rates of NER and DSB/R (P <0022), similar rates of ICL/R, and mor

150 larly, RPMI8226 cells showed slower rates of NER and DSB/R, comparable rates of ICL/R, more condensed

151 r results strongly suggest that reduction of NER capacity during periods of enhanced replicative stre

152 C is ubiquitinated during the early stage of NER of UV light-induced DNA lesions.

153 protein of the global genomic subpathway of NER (GG-NER), associates with PARP-1 in the vicinity of

154 ural hearing loss is observed in a subset of NER-associated DNA repair disorders including Cockayne s

155 he dG-C8-AAF adduct is a better substrate of NER than dG-C8-AF in all three NarI sequence contexts.

156 Mutation or aberrant transcription of NER genes reduces repair efficiency and results in the a

157 mechanism that integrates ubiquitination of NER DNA repair factors with the regulation of the transc

158 The broad substrate versatility of NER further includes, among others, various bulky DNA ad

159 increasing relative cerebral blood volume of NER (rCBVNER), which was higher with deep white matter i

160 The vulnerability of NER to inhibition by oxidation provides a connection bet

161 Thus, the effect of Htz1 on NER is specifically relevant to its presence in chromati

162 ng that XPBs specialized in transcription or NER exist beyond the Kinetoplastida.

163 fold for NER, interacting with several other NER proteins as well as the DNA substrate.

164 ersatile nucleotide excision repair pathway (NER) that removes a variety of DNA damages including tho

165 or manifestation of this defect, and S phase NER proficiency is correlated with the capacity of indiv

166 ter involvement (t test, P = .0482) and poor NER margin definition (t test, P = .0147).

167 ties of both XPB and XPD in Core7 to promote NER, whereas non-genuine NER substrates have no such eff

168 nes, activating an Mfd-dependent error-prone NER mechanism.

169 enon, we developed a novel assay to quantify NER kinetics as a function of cell cycle in the model or

170 romatids before nuclear envelope reassembly (NER).

171 depend on accurate named entity recognition (NER) and normalization (grounding).

172 Named Entity Recognition (NER) is a key task in biomedical text mining.

173 corpora suggesting named-entity recognition (NER) to be more challenging than anticipated: 28-77% of

174 into account, several conclusions regarding NER formation and its impact on persistence assessment c

175 osome enriched and depleted genomic regions (NER and NDR for short) that is: (i) exhaustive and withi

176 ered an important role of USP7 in regulating NER via deubiquitinating XPC and by preventing its VCP/p

177 The relative NER efficiencies of all four cyclopurines were measured

178 rcalation pocket that parallels the relative NER efficiencies.

179 Sp DNA lesions, suggesting that the relative NER/BER product ratios may depend on competitive BER and

180 interaction energies correlate with relative NER incision efficiencies, and explain these results on

181 In PBT and vPvB assessment, remobilisable NER are considered as a potential risk while biogenic NE

182 Nucleotide excision DNA repair (NER) pathway mutations cause neurodegenerative and proge

183 or efficient nucleotide excision DNA repair (NER).

184 tor in mammalian nucleotide excision repair (NER) and nuclear import of XPA from the cytoplasm for NE

185 Global nucleotide excision repair (NER) and transcription-coupled DNA repair (TCR) are amon

186 red by the human nucleotide excision repair (NER) apparatus.

187 Given the use of nucleotide excision repair (NER) as a backup pathway for RER in RNase HII-deficient

188 on that enhances nucleotide excision repair (NER) by facilitating recruitment of the XPA protein to s

189 Mutations in nucleotide excision repair (NER) components (e.g. XPA-1 and XPF-1) imparted extreme

190 a subpathway of nucleotide excision repair (NER) dedicated to rapid removal of DNA lesions in the tr

191 ttributed to the nucleotide excision repair (NER) defect as well as to impaired transcription.

192 e differences in nucleotide excision repair (NER) efficiencies in DNA duplexes, which depend on the i

193 to 3-fold lower nucleotide excision repair (NER) efficiencies in Escherichia coli.

194 d by a dedicated Nucleotide Excision Repair (NER) enzyme.

195 Nucleotide excision repair (NER) excises bulky DNA lesions induced by mutagens and c

196 nition factor in nucleotide excision repair (NER) extensively regulated by ultraviolet (UV)-induced S

197 motifs found in nucleotide excision repair (NER) factors and transcription factors known to interact

198 gnaling promotes nucleotide excision repair (NER) in a cAMP-dependent protein kinase A (PKA)-dependen

199 Nucleotide excision repair (NER) is a conserved and versatile DNA repair pathway for

200 Nucleotide excision repair (NER) is a highly conserved pathway that removes helix-di

201 Nucleotide excision repair (NER) is a major repair pathway that recognizes and corre

202 Nucleotide excision repair (NER) is an evolutionarily conserved mechanism that proce

203 Nucleotide excision repair (NER) is critical for maintaining genome integrity.

204 Nucleotide excision repair (NER) is critical for the repair of DNA lesions induced b

205 Nucleotide excision repair (NER) is responsible for the removal of a large variety o

206 Nucleotide excision repair (NER) is shown to not play a role in the observed biocomp

207 Nucleotide excision repair (NER) is the key DNA repair system that eliminates the ma

208 Nucleotide excision repair (NER) is the sole mechanism in humans for the repair of c

209 the multiprotein nucleotide excision repair (NER) machinery.

210 erations in the nucleotide- excision repair (NER) pathway has not yet been identified.

211 l protein in the nucleotide excision repair (NER) pathway, in charge of recruiting the ERCC1-XPF endo

212 air pathway, the nucleotide excision repair (NER) pathway, which may exhibit a discordance in sensiti

213 mutations in the nucleotide excision repair (NER) pathway, which repairs DNA damage from UV exposure.

214 to repair by the nucleotide excision repair (NER) pathway.

215 function in the nucleotide excision repair (NER) pathway.

216 A damage via the nucleotide excision repair (NER) pathway.

217 he substrates of nucleotide excision repair (NER) pathway.

218 y defects in the nucleotide excision repair (NER) pathway.

219 repaired in the nucleotide excision repair (NER) pathway.

220 ticipates in the nucleotide excision repair (NER) pathway.

221 Nucleotide excision repair (NER) plays a vital role in platinum-induced DNA damage d

222 Nucleotide excision repair (NER) protects against sunlight-induced skin cancer.

223 Nucleotide excision repair (NER) proteins have been found to play a prominent role i

224 We find that the nucleotide excision repair (NER) proteins UvrA, UvrB, and UvrC, but not RecA, are re

225 distribution of nucleotide excision repair (NER) rates for UV-induced lesions throughout the budding

226 Nucleotide excision repair (NER) removes chemically diverse DNA lesions in all domai

227 Nucleotide excision repair (NER) removes these photoproducts, but whether NER functi

228 nformation about nucleotide excision repair (NER) stimulated by cAMP-dependent signaling downstream o

229 eins involved in nucleotide excision repair (NER) under normal growth conditions.

230 t USP7 regulates nucleotide excision repair (NER) via deubiquitinating xeroderma pigmentosum compleme

231 ch repair (MMR), nucleotide excision repair (NER), and homologous recombination (HR) capacity contrib

232 nd on functional nucleotide excision repair (NER), but the molecular mechanism of this unique type of

233 In nucleotide excision repair (NER), damage recognition by XPC-hHR23b is described as a

234 Nucleotide excision repair (NER), interstrand cross-links repair (ICL/R), double-str

235 on repair (BER), nucleotide excision repair (NER), mismatch repair (MMR), non-homologous end joining

236 the activity of nucleotide excision repair (NER), the most versatile DNA repair process.

237 suggesting that nucleotide excision repair (NER), translesion synthesis (TLS), and recombination eac

238 port here that a nucleotide excision repair (NER)-associated-factor is required for efficient HCMV DN

239 a characteristic nucleotide excision repair (NER)-induced ladder of short dual incision oligonucleoti

240 ranscription and nucleotide excision repair (NER).

241 photolesions by nucleotide excision repair (NER).

242 e to UV light is nucleotide excision repair (NER).

243 e nucleus by the nucleotide excision repair (NER).

244 ognition step in nucleotide excision repair (NER).

245 ranscription and nucleotide excision repair (NER).

246 dily repaired by nucleotide excision repair (NER).

247 are deficient in nucleotide excision repair (NER).

248 or cAMP-enhanced nucleotide excision repair (NER).

249 rily repaired by nucleotide excision repair (NER).

250 cisplatin-induced DNA damage, which require NER.

251 of the formation of nonextractable residues (NER).

252 ide a biophysical explanation for the severe NER deficiencies caused by this mutation.

253 um complementation group F), leads to severe NER pathway deficiencies.

254 n the single-task models trained on a single NER dataset.

255 Among six NER factors found to be regulated by the proteasome, we

256 fa1 recapitulates defective S phase-specific NER in wild type yeast; moreover, ectopic RPA1-3 overexp

257 hich is of central importance for successful NER, has remained enigmatic.

258 he 5'-3' direction with slow recovery and TC-NER at the 3' end of long genes.

259 oupled nucleotide excision repair factor (TC-NER) Cockayne syndrome group B (CSB) and the global geno

260 cted and potentially deleterious role for TC-NER factors in driving R-loop-induced DNA damage and gen

261 oxidative DNA damage, but proficient for TC-NER.

262 ry 1: XP-A, B, D, F, and G) and preserved TC-NER (category 2: XP-C, E, and V).

263 ption coupled nucleotide excision repair (TC-NER) (category 1: XP-A, B, D, F, and G) and preserved TC

264 ption-coupled nucleotide excision repair (TC-NER) factor Cockayne syndrome group B (CSB), but not the

265 ption-coupled nucleotide excision repair (TC-NER) or global genomic NER (GG-NER).

266 ption-coupled nucleotide excision repair (TC-NER), contains a ubiquitin-binding domain (UBD), but the

267 sponse to chromosomal triplex formation than NER-proficient cells.

268 tected from ultraviolet irradiation and that NER preserves telomere integrity.

269 ient in NER but lacking TCR, indicating that NER can remove the lesion in the absence of TCR, which i

270 We show that NER initiation involves a two-step mechanism in which Uv

271 as BRCA1/2-mutated patients, suggesting that NER pathway inactivation in EOC conferred enhanced plati

272 ional impairments that are distinct from the NER disorder XP.

273 population biomarker concentrations from the NER were compared to the available screening values to g

274 We find that cells deficient in the NER damage recognition proteins, XPA and XPC, accumulate

275 Most analytes in the NER show HQ values of < 1; however, some (including acry

276 the measured biomarker concentrations in the NER with BEs and similar risk assessment values to provi

277 levels for approximately 130 analytes in the NER.

278 Moreover, the NER factor XPA activates unwinding of normal DNA by Core

279 age sites facilitates the recruitment of the NER factor XPA.

280 scription-coupled repair (TCR) branch of the NER pathway and exhibits developmental and neurological

281 the global genome repair (GGR) branch of the NER pathway and have a very high incidence of UV-induced

282 ur findings redraw the initial stages of the NER process in those organisms that express an alkyltran

283 Although the general mechanism of the NER process is well studied, the function of the XPA pro

284 ading errors and limiting the ability of the NER system to directly exploit the lexical information p

285 to FICZ/UVA-induced oxidation damage to the NER proteome and DNA excision repair is impaired in extr

286 cer by promoting photochemical damage to the NER proteome and thereby preventing the removal of UVB-i

287 substrates of XPA as it functions within the NER machinery.

288 may act as a complementary repair pathway to NER to remove S-cdA adducts from 3' DNA termini in E. co

289 in removing DNA damage that is refractory to NER.

290 mechanistically links cAMP-PKA signaling to NER and illustrates potential benefits of cAMP pharmacol

291 rans-anti-B[a]P-N(6)-dA, which is subject to NER and blocks transcription in vitro, and (+)-trans-ant

292 that amounts and uncertainties in (i) total NER, (ii) NER formed from the parent pool, and (iii) NER

293 Moreover, two NER mutations (ERCC6-Q524* and ERCC4-A583T), identified

294 3'-next flanking sequence effect as a unique NER factor for bulky arylamine lesions in E. coli.

295 Using NER-proficient and -deficient cells and in vitro PARP-1

296 The ladders were not observed when NER was inhibited either by mouse monoclonal antibody (5

297 ER) removes these photoproducts, but whether NER functions at telomeres is unresolved.

298 of radiolabeled nucleosides associated with NER.

299 ICLs (TFO-ICLs) in vitro, cooperatively with NER damage recognition proteins, promoted removal of UVC

300 Furthermore, patients with tumors with NER alterations had similar OS and PFS as BRCA1/2-mutate

301 Tumors with NER alterations were associated with improved overall su

302 rvival (PFS), compared with patients without NER alterations or BRCA1/2 mutations.