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 o replicative stress significantly abrogates NER uniquely during S phase.

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

7 d on our results, we created the stand-alone NER tool HUNER incorporating fully trained models for fi

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

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

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

11 ons are excellent substrates of both BER and NER.

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

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

14 are positioned to reduce local stability and NER activity, whereas residues mutated in XP-G/CS have i

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

16 anscription efficiency was similar in WT and NER-deficient human cell lines, suggesting that the 5fC-

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

18 e mutations decreased activity in cell-based NER assays, demonstrating the functional importance of X

19 oyed high-performance machine learning-based NER tools for concept recognition and trained our concep

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

21 s to predict microbial turnover and biogenic NER have been developed, having limited use when metabol

22 e used to estimate the formation of biogenic NER.

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

24 tity recognition (NER), including biomedical NER.

25 and suggest how XPG complexes may bind both NER bubble junctions and replication forks.

26 DB is a general sensor of DNA damage in both NER and BER pathways, facilitating damage recognition in

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

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

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

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

31 bulky lesions are preferentially repaired by NER.

32 and that oxidative damage to RPA compromises NER capability.

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

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

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

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

37 nomic NER (GG-NER) and transcription coupled NER (TC-NER) subpathways.

38 Defective NER is associated with photosensitivity and a high skin

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

40 allowing UvrB to orchestrate the downstream NER reactions.

41 dinating damage incision by nucleases during NER, but the underlying mechanisms remain unclear.

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

43 regulate the helicase activity of XPD during NER, p62 is thought to be purely structural.

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

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

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

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

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

49 XPA is an essential protein in eukaryotic NER, although reports about its stoichiometry and role i

50 unwinding and damage incision in eukaryotic NER.

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

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

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

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

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

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

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

58 C-polypeptide lesion is a weak substrate for NER.

59 2, the major sensor initiating global genome NER (GG-NER), and that the interaction was enhanced upon

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

61 sion repair (NER) consists of global genomic NER (GG-NER) and transcription coupled NER (TC-NER) subp

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

63 efficient XPC recruitment and global genomic NER.

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

65 nuate GG-NER, do not substantially affect GG-NER or TC-NER.

66 e genomic locations, which we refer to as GG-NER complex binding sites (GCBSs).

67 t for T73F and T73Y that mildly attenuate GG-NER, do not substantially affect GG-NER or TC-NER.

68 ith histone H2B, significantly attenuates GG-NER and Rad26-independent TC-NER but does not affect TC-

69 chromatin remodeling is initiated during GG-NER.

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

71 air (NER) consists of global genomic NER (GG-NER) and transcription coupled NER (TC-NER) subpathways.

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

73 ajor sensor initiating global genome NER (GG-NER), and that the interaction was enhanced upon UV irra

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

75 The attenuation of GG-NER and Rad26-independent TC-NER by the H4H75E mutation

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

77 We demonstrate that initiation of GG-NER in chromatin is accompanied by the disruption of dyn

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

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

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

81 global genome-nucleotide excision repair (GG-NER) in chromatin is organized into domains in relation

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

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

84 In undamaged cells, we show that the GG-NER complex occupies chromatin, establishing the nucleos

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

86 namic nucleosomes that flank GCBSs by the GG-NER complex.

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

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

89 the adduct but not as effectively as global NER.

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

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

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

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

94 The identified NER-DDXs were categorized into three groups according to

95 rms of RPA that are associated with impaired NER.

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

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

98 nucleosomes shows the opposite asymmetry in NER-proficient skin cancers, but not in NER-deficient ca

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

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

101 ve may be a common way to interrogate DNA in NER.

102 tion, the role of UvrA's 2 ATPase domains in NER remains elusive.

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

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

105 y in NER-proficient skin cancers, but not in NER-deficient cancers, indicating that asymmetric repair

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

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

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

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

110 chanism of telomeric photoproduct removal is NER.

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

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

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

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

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

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

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

118 with UV-damaged DNA and optimize melanocytic NER.

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

120 aled how XPA DBD and RPA70AB orient on model NER DNA substrates.

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

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

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

124 ll known to profoundly inhibit the access of NER proteins.

125 recognition in the global-genomic branch of NER.

126 recognition in the global-genomic branch of NER.

127 metabolism and is an essential component of NER.

128 e site mutations and homozygous deletions of NER genes.

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

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

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

132 Evolution of NER, unlike DSB, is shaped primarily by sunlight exposur

133 of the LRS domain, or lowered expression of NER proteins.

134 n, and thermochemolysis to study the fate of NER-DDX along different environmental aquatic-terrestria

135 d results, a conceptual model of the fate of NER-DDXs on their different environmental aquatic-terres

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

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

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

139 his mechanism, pharmacological inhibition of NER using spironolactone abolished SIRT2-mediated TC-NER

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

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

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

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

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

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

146 s ablated the stimulatory effect of SIRT6 on NER and destabilized the genome due to (i) partial loss

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

148 ly reduce transcription efficiency, are poor NER substrates, and do not cause transcription errors.

149 f UvrA, the initiating enzyme of prokaryotic NER, to an alkyl lesion by ATL.

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

151 Overall, we demonstrate that SIRT6 promotes NER by deacetylating DDB2, thereby preventing the onset

152 2-independent function for EZH2 in promoting NER through DDB2 stabilization, suggesting a rationale f

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

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

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

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

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

158 oncept embeddings, named-entity recognition (NER) tools are first used to identify and normalize conc

159 tate-of-the-art in named entity recognition (NER), including biomedical NER.

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

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

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

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

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

165 or efficient nucleotide excision DNA repair (NER).

166 proteins of the nucleotide excision repair (NER) and base excision repair (BER) pathways work in a c

167 DDB2 to promote nucleotide excision repair (NER) and govern cisplatin resistance in SCLC.

168 thways including nucleotide excision repair (NER) and inter-strand crosslink repair (ICLR).

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

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

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

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

173 Nucleotide excision repair (NER) consists of global genomic NER (GG-NER) and transcr

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

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

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

177 Nucleotide excision repair (NER) in eukaryotes is orchestrated by the core form of t

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

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

180 Nucleotide excision repair (NER) is a major DNA repair pathway for a variety of DNA

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

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

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

184 the multiprotein nucleotide excision repair (NER) machinery.

185 in multi-protein nucleotide excision repair (NER) machinery.

186 leosomes inhibit nucleotide excision repair (NER) of the nontranscribed strand (NTS) of genes in an a

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

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

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

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

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

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

193 in the bacterial nucleotide excision repair (NER) pathway.

194 repaired via the nucleotide excision repair (NER) pathway.

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

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

197 Nucleotide excision repair (NER) protects cells against diverse types of DNA damage,

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

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

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

201 SIRT6 regulates nucleotide excision repair (NER) remains unknown.

202 Nucleotide excision repair (NER) removes a wide range of DNA lesions, including UV-i

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

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

205 Nucleotide excision repair (NER) removes various DNA lesions caused by UV light and

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

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

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

209 in human global nucleotide excision repair (NER), binds avidly to abasic sites and 8-oxo-guanine (8-

210 repair, but not nucleotide excision repair (NER), coevolves with longevity.

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

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

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

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

215 photolesions by nucleotide excision repair (NER).

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

217 endonuclease in nucleotide excision repair (NER).

218 are deficient in nucleotide excision repair (NER).

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

220 rily repaired by nucleotide excision repair (NER).

221 ranscription and nucleotide excision repair (NER).

222 of global-genome nucleotide excision repair (NER).

223 Nonextractable residues (NER) are pollutants incorporated into the matrix of natu

224 of the formation of nonextractable residues (NER).

225 n, and formation of nonextractable residues (NER).

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

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

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

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

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

231 embeddings generally suffer from suboptimal NER tools, small-scale evaluation, and limited availabil

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

233 ns to the nucleotide excision repair system (NER).

234 TC-NER deficiency in humans is associated with the severe n

235 26-independent TC-NER but does not affect TC-NER in the presence of Rad26.

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

237 mplicated in transcriptional stalling and TC-NER in the cell remain unknown.

238 tes error-free transcriptional bypass and TC-NER of UV photoproducts.

239 a key transcription elongation factor and TC-NER repressor, from the chromatin.

240 olog CSB have been proposed to facilitate TC-NER in part by positioning and stabilizing stalling of R

241 ypass of DNA lesions by Rad26 facilitates TC-NER.

242 6 and its ATPase activity is critical for TC-NER downstream of the first (+1) nucleosome in gene codi

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

244 scription stalling might be important for TC-NER.

245 Furthermore, TC-NER interacts with mismatch repair (MMR) under physiolog

246 However, TC-NER on the transcription start site (TSS)-proximal half

247 nstrate that the requirement for Rad26 in TC-NER is modulated by the distribution of TFIIH and Spt4/S

248 ide misincorporation is not implicated in TC-NER, and moderate eviction of Spt5 and promotion of erro

249 ver, the genome-wide role of CSB/Rad26 in TC-NER, particularly in the context of the chromatin organi

250 y attenuates GG-NER and Rad26-independent TC-NER but does not affect TC-NER in the presence of Rad26.

251 tenuation of GG-NER and Rad26-independent TC-NER by the H4H75E mutation is not due to decreased chrom

252 g spironolactone abolished SIRT2-mediated TC-NER activity in differentiated neuronal cells and protec

253 R (GG-NER) and transcription coupled NER (TC-NER) subpathways.

254 Initiation of TC-NER is mediated by specific factors such as the human Co

255 ER, do not substantially affect GG-NER or TC-NER.

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

257 downstream of the +1 nucleosome to remove TC-NER suppression by Spt4/Spt5.

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

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

260 Transcription coupled repair (TC-NER) is a subpathway of nucleotide excision repair trigg

261 ption-coupled nucleotide excision repair (TC-NER) is an important DNA repair mechanism that removes R

262 ption-coupled nucleotide excision repair (TC-NER) of cisplatin-induced DNA cross-links.

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

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

265 ption-coupled nucleotide excision repair (TC-NER).

266 t deletion of SPT4 significantly restores TC-NER across the genome in a rad26Delta mutant, particular

267 on elongation factor Spt4/Spt5 suppresses TC-NER in Rad26-deficient cells.

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

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

270 rom UV-irradiated human cells indicates that NER activity along the NTS is also elevated on the 5' si

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

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

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

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

275 eview focuses on recent data showing how the NER proteins, XPA, XPC, XPG, CSA, CSB and UV-DDB, work t

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

277 r results identified SIRT2's function in the NER pathway as a key underlying mechanism of preventing

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 f the structure and mechanical action of the NER machinery.

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

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

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 troversy about where XPA is bound within the NER bubble, provide structural insights into the molecul

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

289 sions are probably directly repaired through NER.

290 in removing DNA damage that is refractory to NER.

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

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

293 This finding was confirmed by in vitro NER assays in cell-free extracts from human HeLa cells,

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

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

296 of radiolabeled nucleosides associated with NER.

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

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

299 Tumors with NER alterations were associated with improved overall su

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