ライフサイエンスコーパス: glycosylase

1 se) and DNA repair enzymes (e.g., uracil-DNA glycosylase).

2 o inactivation of MUTYH, which encodes a DNA glycosylase.

3 e (MnSOD) and mitochondrial 8-oxoguanine DNA glycosylase.

4 instead depends, in part, on the thymine DNA glycosylase.

5 pair pathway initiated by human alkyladenine glycosylase.

6 lational modification of the human MutYH DNA glycosylase.

7 in a coupled assay in principle with any DNA glycosylase.

8 are repair intermediates of bifunctional DNA glycosylases.

9 l inhibition of other DNA repair enzymes and glycosylases.

10 se interrogation during lesion search by DNA glycosylases.

11 ar DNA translocation by two human DNA repair glycosylases.

12 DNA sliding is human 8-oxoguanine ((o)G) DNA glycosylase 1 (hOGG1), which repairs mutagenic (o)G lesi

13 the DNA glycosylase gene 3-MethylAdenine DNA Glycosylase 1 (MAG1), which is part of the base-excision

14 recently shown to stimulate 8-oxoguanine DNA glycosylase 1 (OGG1), an enzyme that removes oxidized pu

15 mes, the DNA glycosylases TDG and 8-oxoG DNA glycosylase 1 (OGG1), apurinic/apyrimidinic (AP) endonuc

16 8-oxoG is repaired by the 8-oxoguanine glycosylase 1 (OGG1)-initiated DNA base excision repair

17 8-Oxoguanine-DNA glycosylase-1 (OGG1) is the primary enzyme for repairing

18 8-Oxoguanine DNA glycosylase-1 (OGG1)-initiated base excision repair path

19 tion of TIMP1 expression by 8-oxoguanine DNA glycosylase-1 binding to DNA:RNA hybrid.

20 report that the suppression of Nei-like DNA glycosylase 2 (NEIL2), a mammalian DNA glycosylase that

21 selectively killed by inhibiting uracil DNA glycosylase 2 (UNG) and that this synthetic lethal pheno

22 Uracil N-glycosylase 2 (UNG2), the nuclear isoform of UNG, cataly

23 CRL4 to trigger the degradation of uracil-N-glycosylase 2 (UNG2).

24 e 3alpha (TOP3alpha) and NEIL3 (Nei-like DNA glycosylase 3), as well as transcription and RNA regulat

25 The major DNA glycosylase, 8-oxoguanine glycosylase (OGG1), is respons

26 We examined the role of the viral uracil DNA glycosylase, a protein conserved among all herpesviruses

27 PRs in mice lacking the BER-initiating DNA glycosylase AAG did not exhibit alkylation-induced necro

28 n repair (BER) initiated by alkyladenine DNA glycosylase (AAG) is essential for removal of aberrantly

29 Human alkyladenine DNA glycosylase (AAG) is thought to initiate base excision r

30 In human alkyladenine DNA glycosylase (AAG), the enzyme that initiates base excisi

31 n repair (BER) initiated by alkyladenine DNA glycosylase (AAG).

32 ONS-induced DNA damage; the alkyladenine DNA glycosylase (Aag/Mpg) excises several DNA base lesions i

33 monstrate that Pms2/Mlh1 and multiple uracil glycosylases act jointly, each one with a distinct stran

34 , T/I, and A/I base pairs and a xanthine DNA glycosylase acting on all double-stranded and single-str

35 A/U base pairs, but also a hypoxanthine DNA glycosylase acting on G/I, T/I, and A/I base pairs and a

36 n nucleobase and aromatic side chains in the glycosylase active site.

37 categories: those that are necessary for (1) glycosylase activity (C146 and C255), (2) lyase activity

38 establish that the NEIL3 GRF domain inhibits glycosylase activity against monoadducts and ICLs.

39 ycosylases in real time as well as profiling glycosylase activity in cell lysates.

40 The AP lyase activity is more coupled with glycosylase activity in R.CcoLI than in R.PabI.

41 ugh the female lineage due to widespread DNA glycosylase activity in the male germline, and extensive

42 can be cleaved by DNA glycosylases; however, glycosylase activity is blocked if Pot1 binds.

43 C/I, matching the trend of hypoxanthine DNA glycosylase activity observed in vitro.

44 ain of ROS1 is indispensable for the 5mC DNA glycosylase activity of ROS1.

45 08) Nevertheless, G.T substrate affinity and glycosylase activity of TDG(82-308) greatly exceeds that

46 G) from Escherichia coli is known to exhibit glycosylase activity on three mismatched base pairs, T/U

47 glycosylases for oxidized bases carry both a glycosylase activity that removes the faulty base and an

48 al sensing of 8-oxoguanine and uracil repair glycosylase activity within DNA monolayers on gold by mu

49 IL1 are catalytically inactive for their DNA glycosylase activity, these deficiencies may increase su

50 nine adduct cytotoxicity and MUTYH-dependent glycosylase activity.

51 of base-excision repair independently of its glycosylase activity.

52 Using the DNA glycosylase AlkD from Bacillus cereus, we crystallograph

53 uantitative measurements of 8-oxoguanine DNA glycosylase, alkyl-adenine DNA glycosylase, MutY DNA gly

54 we observed that Nrf2, p53 and 8-oxoguanine glycosylase alpha dependent antitumor mechanisms were la

55 of intercalation for human alkyladenine DNA glycosylase, an enzyme that initiates repair of alkylati

56 AID/APOBEC enzymes, here we used uracil-DNA glycosylase and an alkoxyamine to covalently tag and seq

57 II) and demonstrated their DNA cleavage, DNA glycosylase and AP lyase activities in vitro at 37 degre

58 s Zf-GRF repeat) are dispensable for its DNA glycosylase and AP lyase activity; however, the potentia

59 anine-containing DNA and stimulated both the glycosylase and apurinic/apyrimidinic lyase activities o

60 es Schiff base formation, and stimulates its glycosylase and apyrimidinic/apurinic lyase enzymatic ac

61 VACV D4 protein serves both as a uracil-DNA glycosylase and as an essential component required for p

62 additional uracil glycosylases, thymine-DNA glycosylase and SMUG1.

63 interact with the 8-oxoguanine (8-oxoG) DNA glycosylase and stimulate its enzymatic activities.

64 trand cross-link repair pathways via its DNA glycosylase and/or AP lyase activity, which are consider

65 es in opposing DNA strands with selected DNA glycosylases and human apurinic/apyrimidinic endonucleas

66 se excision repair (BER) is initiated by DNA glycosylases and is crucial in repairing RONS-induced DN

67 be operative in related base excision repair glycosylases and provides a critical framework for analy

68 of several enzymes [four BER-initiating DNA glycosylases and the downstream processing apurinic/apyr

69 paralleled by a compromised TDG (thymine DNA glycosylase) and TET1 (ten-eleven translocation protein

70 lycosylase, MutY DNA glycosylase, uracil DNA glycosylase, and APE1 activity.

71 tarate-dependent dioxygenases, base excision glycosylases, and sequence-specific transcription factor

72 nd G241R was observed on a pre-assembled DNA glycosylase.AP-DNA complex as well.

73 Glycosylase/apurinic lyase activity was reduced in Rad9(

74 DNA glycosylases are enzymes that perform the initial steps

75 DNA glycosylases are important editing enzymes that protect

76 Finally, since many glycosylases are inhibited from working on damage in the

77 evious fluorescence methods for assaying DNA glycosylases are often complex and/or limited in scope t

78 HD model R6/2 mice indicates that these DNA glycosylases are present in brain areas affected by neur

79 DEMETER family of 5-methylcytosine (5mC) DNA glycosylases are the first genetically characterized DNA

80 thyltransferase) and APNG (alkylpurine-DNA-N-glycosylase) are key enzymes capable of repairing temozo

81 lly generates lesions that are recognized by glycosylases as being foreign to DNA.

82 part, only allow for the analysis of one DNA glycosylase at a time.

83 ized bases, initiated by NEIL1 and other DNA glycosylases at the chromatin level remains unexplored.

84 of the base excision repair (BER) enzyme DNA glycosylase augments PD-L1 upregulation in response to H

85 These glycosylase base editors (GBEs) consist of a Cas9 nickas

86 l nucleosomes following base excision by DNA glycosylases but prior to handover to APEX1.

87 NEIL3 glycosylase can cleave the crosslink(1); however, if thi

88 Thymine DNA glycosylase can further remove 5fC and 5caC, connecting

89 Also, the NEIL1 and NEIL3 DNA glycosylases can remove hydantoin lesions but none of th

90 Levels of BER-initiating DNA glycosylases can vary between individuals, suggesting th

91 described both vertebrate and microbial DNA glycosylases capable of unhooking highly toxic interstra

92 DNA glycosylases catalyze the first step of the base excisio

93 her nuclease incision of the DNA backbone or glycosylase cleavage of the crosslinked nucleotide.

94 We show that human methylpurine DNA glycosylase cleaves N-glycosidic bonds on RNA and that h

95 In summary, CREB1 and DNA glycosylases compete for damaged CRE in vitro and in viv

96 ns, we investigated whether CREB1 and repair glycosylases compete with each other.

97 DNA glycosylases constitute a biologically and biomedically

98 lts suggest that Fpg, and possibly other DNA glycosylases, convert part of the binding energy into ac

99 Uracil DNA glycosylase could hydrolyze deoxyuracils of the aptamer

100 Alkylpurine glycosylase D (AlkD) exhibits a unique base excision str

101 -associated genes in a Tet3- and thymine DNA glycosylase-dependent fashion in DRG neurons.

102 Why mammalian cells possess multiple DNA glycosylases (DGs) with overlapping substrate ranges for

103 an N-terminal MBD (MBD4MBD) and a C-terminal glycosylase domain (MBD4GD) separated by a long linker.

104 the enzyme harbors a helix-hairpin-helix DNA glycosylase domain followed by a unique C-terminal domai

105 We show that the isolated glycosylase domain is inactive for base excision but ret

106 In addition to its N-terminal catalytic glycosylase domain, NEIL3 contains two tandem C-terminal

107 repair of nearby mCpG/TpG mismatches by the glycosylase domain.

108 study the [Fe4S4] clusters in the DNA repair glycosylases EndoIII and MutY to evaluate the effects of

109 enerally requires five enzymatic activities: glycosylase, endonuclease, lyase, polymerase, and ligase

110 anded biological utility are specialized DNA glycosylases - enzymes that selectively excise damaged,

111 se, an Escherichia coli-derived uracil DNA N-glycosylase (eUNG) and a rat APOBEC1 cytidine deaminase

112 MutY glycosylase excises adenines misincorporated opposite th

113 nds, but one restriction enzyme (restriction glycosylase) excises unmethylated bases from its recogni

114 s by thymine DNA (TDG) or Nei-like 1 (NEIL1) glycosylases followed by base excision repair to restore

115 DNA glycosylases for oxidized bases carry both a glycosylase

116 cation sites was developed that utilizes DNA glycosylases found in the base excision repair pathway t

117 Formamidopyrimidine-DNA glycosylase (Fpg) excises 8-oxoguanine (oxoG) from DNA b

118 y the repair enzyme, formamidopyrimidine-DNA glycosylase (Fpg), likely involves multiple gates.

119 aled introduction of formamidopyrimidine-DNA glycosylase (Fpg)-sensitive oxidative DNA lesions suppre

120 Unlike uracil-DNA glycosylases from diverse sources, where the C termini a

121 tative PCRs (qPCRs) targeting the uracil DNA glycosylase gene (udg) or the 23S rRNA gene are describe

122 ed in DNA repair pathways, including the DNA glycosylase gene 3-MethylAdenine DNA Glycosylase 1 (MAG1

123 y circuit centered on a 5-methylcytosine DNA glycosylase gene is required for long-term epigenetic fi

124 Their processing by the OGG1 and MUTYH DNA glycosylases generates closely spaced incisions on oppos

125 Mammalian MutY glycosylases have a unique architecture that features an

126 Human N-methylpurine DNA glycosylase (hMPG) initiates base excision repair of a n

127 These results reveal how the human oxoG DNA glycosylase hOGG1 locates the lesions inside the DNA hel

128 g the localization of the human 8-oxoguanine glycosylase (hOGG1) to damaged DNA.

129 Human DNA glycosylase, hOGG1, is known to perform DNA repair by cl

130 structures of human 8-oxoguanine (oxoG) DNA glycosylase, hOGG1, that interact with the DNA containin

131 Notably, for both hTDG and a second glycosylase, hOGG1, which recognizes structurally differ

132 The MutY DNA glycosylase homologue (MutYH) recognizes A:8-oxo-G mispa

133 nce, all three analogs can be cleaved by DNA glycosylases; however, glycosylase activity is blocked i

134 to study damage search by human thymine DNA glycosylase (hTDG), which initiates BER of mutagenic and

135 DNA repair enzymes such as human uracil-DNA glycosylase (hUNG) perform the initial step in the base

136 he probability that nuclear human uracil DNA glycosylase (hUNG2) excised two uracil lesions spaced 10

137 ndo III possesses two types of activities: N-glycosylase (hydrolysis of the N-glycosidic bond) and AP

138 ss to read and catalyze removal of OG via OG-glycosylase I (OGG1), yielding an abasic site (AP).

139 ers for base excision repair initiated by OG-glycosylase I (OGG1).

140 ponses, whereas a lack of other Nei-like DNA glycosylases (i.e., NEIL1 and NEIL2) had no significant

141 in (MBD) family, MBD4 serves as a potent DNA glycosylase in DNA mismatch repair specifically targetin

142 latory mechanism for the essential MutYH DNA glycosylase in human cells.

143 acil creation by AID and its removal by UNG2 glycosylase in splenocytes undergoing maturation and in

144 from the DNA backbone by human alkyladenine glycosylase in vitro is similarly affected by nearest-ne

145 analysis of gene expression profiles of DNA glycosylases in gastric specimens linked the reduced Nei

146 of Mag1, as compared with alkylation repair glycosylases in other organisms, could explain the extre

147 of the UBER probe by assaying five different glycosylases in real time as well as profiling glycosyla

148 can remove hydantoin lesions but none of the glycosylases, including OGG1, are able to remove 8-oxoG

149 Knockdown of thymine DNA glycosylase increased 5caC in genome, affected cell prol

150 This strategy utilizes glycosylase-induced excimer formation of pyrenes, and mo

151 r-like effector array proteins, and a uracil glycosylase inhibitor resulted in RNA-free DddA-derived

152 ird-generation base editors that fuse uracil glycosylase inhibitor, and that use a Cas9 nickase targe

153 Coupled with a uracil-DNA glycosylase inhibitor, dCas9-AIDx converted targeted cyt

154 either replication-dependent dilution or DNA glycosylase-initiated base excision repair.

155 Finally, we demonstrate that uracil glycosylase initiates the bypass of DNA damage induced b

156 methyltransferases and 5-methylcytosine DNA glycosylases interact to maintain epigenetic homeostasis

157 uclease VIII-like protein 1 (NEIL1) is a DNA glycosylase involved in initiating the base excision rep

158 CSA, CSB and UV-DDB, work to stimulate known glycosylases involved in the removal of certain forms of

159 The NEIL3 DNA glycosylase is a base excision repair enzyme that excise

160 bacterial MutY (MUTYH in humans) adenine DNA glycosylase is able to initiate the repair of A:oxoG by

161 MUTYH DNA glycosylase is responsible for recognizing and removing

162 Ogg1 (8-oxoguanine DNA glycosylase) is one such silenced base excision repair e

163 nced by either UNG1/2, SMUG1, or thymine-DNA glycosylase knockdown, strongly suggesting that there ar

164 Bacillus cereus AlkD is the only DNA glycosylase known to catalyze base excision without extr

165 HDAC1 stimulates OGG1, a DNA glycosylase known to remove 8-oxoG lesions that are asso

166 Although uracil DNA glycosylases limit APOBEC-induced mutation, it is unknow

167 fications, and thus, the mechanisms by which glycosylases locate DNA damage are of particular interes

168 The 5-methylcytosine DNA glycosylase/lyase REPRESSOR OF SILENCING 1 (ROS1)-mediat

169 NA demethylation by the 5-methylcytosine DNA glycosylase/lyase ROS1.

170 1 (ROS1) is a multi-domain bifunctional DNA glycosylase/lyase, which excises 5-methylcytosine (5mC)

171 eukaryotic and prokaryotic bifunctional DNA glycosylases/lyases (NEIL1, Nei, Fpg, Nth, and NTH1) and

172 Here we investigate the bifunctional DNA glycosylases/lyases NEIL1 and NEIL2, which act in repair

173 ly of genes that encode 5-methylcytosine DNA glycosylases/lyases.

174 ng with the base excision repair pathway DNA glycosylase MAG1 renders the tpa1Deltamag1Delta double m

175 By fusing the yeast 3-methyladenine DNA glycosylase MAG1 to a tetR DNA-binding domain, we are ab

176 the basal and MMS-induced expression of DNA glycosylase Mag1.

177 The NEIL3 DNA glycosylase maintains genome integrity during replicatio

178 Thus, the NEIL DNA glycosylases may be involved in both telomere maintenanc

179 we present the first, to our knowledge, DNA glycosylase mechanism that does not require base flippin

180 e mechanistic details and general utility of glycosylase-mediated ICL repair in other bacteria are un

181 In bacteria, glycosylase-mediated ICL unhooking was described in Stre

182 o inefficient turnover of N-methylpurine-DNA glycosylase (MPG), which initiates BER of epsilonA.

183 Mitochondria-targeted human 8-oxoguanine DNA glycosylase (mt-hOgg1) and aconitase-2 (Aco-2) each redu

184 Family 2 mismatch-specific uracil DNA glycosylase (MUG) from Escherichia coli is known to exhi

185 The DNA glycosylase MutY prevents deleterious mutations resultin

186 xoguanine DNA glycosylase, alkyl-adenine DNA glycosylase, MutY DNA glycosylase, uracil DNA glycosylas

187 emonstrated that the bacterial and human DNA glycosylases Nei and NEIL1 excise unhooked psoralen-deri

188 The human DNA glycosylase NEIL1 was recently demonstrated to initiate

189 e DNA base excision repair (BER) enzyme, DNA glycosylase NEIL1, efficiently recognizes and excises th

190 Compared with the other DNA glycosylases NEIL1 and NEIL2, Xenopus laevis NEIL3 C ter

191 elevated expression of the bifunctional DNA glycosylase, NEIL2, sensitizes breast cancer cells to A3

192 The DNA glycosylase NEIL3 has been implicated in DNA repair path

193 forming the cross-link is cleaved by the DNA glycosylase NEIL3.

194 in naked DNA, products generated by the DNA glycosylase NTHL1 were efficiently processed by the down

195 proximately 18000 regions when the OG repair glycosylase Ogg1 was knocked out.

196 ic sites, which are repaired by 8-oxoguanine glycosylase (OGG1) and apurinic/apyrimidinic endonucleas

197 supplemented with exogenous 8-oxoguanine DNA glycosylase (OGG1) did so.

198 ating the DNA repair enzyme 8-oxoguanine DNA glycosylase (OGG1) in the PyMT transgenic mouse model of

199 8-Oxoguanine glycosylase (OGG1) is a base excision repair enzyme resp

200 and relies on the upstream 8-oxoguanine-DNA glycosylase (OGG1) to recognise and excise 8-oxoG.

201 The major DNA glycosylase, 8-oxoguanine glycosylase (OGG1), is responsible for removing the most

202 se excision repair (BER) by 8-oxoguanine DNA glycosylase (OGG1), yielding an abasic site (AP).

203 en not repaired properly by 8-oxoguanine DNA glycosylase (Ogg1).

204 (8-oxoG) primarily via the 8-Oxoguanine DNA glycosylase (OGG1).

205 Uracil DNA glycosylase plays a key role in DNA maintenance via base

206 Some DNA glycosylases possess AP lyase activities that nick the D

207 DNA glycosylases preserve genome integrity and define the sp

208 MutY adenine glycosylases prevent DNA mutations by excising adenine f

209 In promoter G-quadruplex DNA, the NEIL glycosylases primarily remove Gh from Na(+)-coordinated

210 DNA glycosylases protect genomic integrity by locating and e

211 Thus, NEIL1 and NEIL2 DNA glycosylases protect mitochondrial DNA against oxidative

212 SMUG1 or thymine-DNA glycosylase uracil-DNA glycosylases, proving that it is base excision by UNG1/2

213 ntribute to removal of uracils by uracil DNA glycosylase regardless of the translational or rotationa

214 The relative in vivo contributions of each glycosylase remain elusive.

215 The DNA glycosylase ROS1 was only partially decreased in activit

216 n flowering or DNA repair, including the DNA glycosylase ROS1, which facilitates DNA demethylation.

217 tures have captured for the first time a DNA glycosylase scanning the genome for a damaged base in th

218 e-strand selective monofunctional uracil DNA glycosylase (SMUG1).

219 The uracil DNA glycosylase superfamily consists of several distinct fam

220 NA polymerase B (polB) and methyladenine DNA glycosylase (tag) genes responsible for the repair of po

221 NTH1, a major glycosylase targeting oxidized pyrimidines, prevents mut

222 nucleotide and purified BER enzymes, the DNA glycosylases TDG and 8-oxoG DNA glycosylase 1 (OGG1), ap

223 the base excision repair enzyme thymine DNA glycosylase (TDG) could be such a target for its dual ro

224 lated in the presence of TET and thymine DNA glycosylase (TDG) enzymes.

225 tosine dioxygenase 2 (TET2), and Thymine DNA glycosylase (TDG) genes.

226 C and 5caC subject to removal by thymine DNA glycosylase (TDG) in conjunction with base excision repa

227 ir, and this step is followed by thymine DNA glycosylase (TDG) initiated base excision repair (BER).

228 Thymine DNA glycosylase (TDG) initiates the repair of G.T mismatches

229 Thymine DNA Glycosylase (TDG) is a base excision repair enzyme funct

230 Thymine DNA glycosylase (TDG) is an essential enzyme playing multipl

231 Thymine DNA Glycosylase (TDG) performs essential functions in mainta

232 Thymine-DNA glycosylase (TDG) plays critical roles in DNA base excis

233 DNA demethylases, we found that thymine DNA glycosylase (TDG) up-regulated Wnt signaling.

234 between chromatin structure and thymine DNA glycosylase (TDG) using chemically defined nucleosome ar

235 (caC), excision of fC or caC by thymine DNA glycosylase (TDG), and subsequent base excision repair.

236 tively recognized and excised by thymine DNA glycosylase (TDG), leading to DNA demethylation.

237 recognized by the monofunctional thymine DNA glycosylase (Tdg), which cleaves the glycosidic bond of

238 Many TET2- and thymine-DNA glycosylase (TDG)-dependent 5mC and 5hmC changes directl

239 eplication-dependent dilution or thymine DNA glycosylase (TDG)-dependent base excision repair.

240 fC)/5-carboxylcytosine (5caC) by thymine DNA glycosylase (TDG).

241 nd excision of oxidized bases by thymine DNA glycosylase (TDG).

242 tory proteins, including p53 and thymine DNA glycosylase (TDG).

243 elves contribute to AML, such as thymine DNA glycosylase (TDG).

244 ine from G.T mispairs, including thymine DNA glycosylase (TDG).

245 as a function of (i) the lesion type and DNA glycosylase tested, (ii) local sequence context and the

246 here are RNA abasic sites, and we identify a glycosylase that generates these sites and an AP endonuc

247 Family 4 UDGa is a robust uracil DNA glycosylase that only acts on double-stranded and single

248 cherichia coli protein YcaQ as an ICL repair glycosylase that protects cells against the toxicity of

249 iroi AlkZ (previously Orf1), a bacterial DNA glycosylase that protects its host by excising ICLs deri

250 e DNA glycosylase 2 (NEIL2), a mammalian DNA glycosylase that specifically removes oxidized bases, is

251 NEIL1 is one of the 11 human DNA glycosylases that catalyze the first step of the BER pat

252 ructural and mechanistic features of the DNA glycosylases that enable these functions.

253 Countering this threat are three types of glycosylases that excise thymine from G.T mispairs, incl

254 AP sites are also generated by DNA glycosylases that initiate DNA base excision repair.

255 nophosphate, or that lack MutM and MutY, DNA glycosylases that process base pairs involving 8-oxo-dGT

256 t it is significantly faster than DNA repair glycosylases that recognize and excise some of the same

257 otion of single molecules of three bacterial glycosylases that recognize oxidized bases, Fpg, Nei, an

258 Base excision repair is initiated by DNA glycosylases that recognize specific altered bases.

259 s of this or any type are not excised by DNA glycosylases that use a traditional base-flipping mechan

260 at A-T bases depend on two additional uracil glycosylases, thymine-DNA glycosylase and SMUG1.

261 on on E141 mediates the recruitment of Neil3 glycosylase to the sites of DNA damage for BER.

262 The abilities of the DNA glycosylases to incise the DNA strand adjacent to G*, wh

263 The ability of DNA glycosylases to rapidly and efficiently detect lesions a

264 potentially general concept of sculpting of glycosylases to their targets, allowing them to exploit

265 d 2'-deoxyuridine (dU) residue by uracil DNA glycosylase (UDG) and apurinic/apyrimidinic endonuclease

266 Enzymes like uracil DNA glycosylase (UDG) can achieve ground state destabilizati

267 Enzymes in Uracil DNA glycosylase (UDG) superfamily are essential for the remo

268 UDGb belongs to family 5 of the uracil DNA glycosylase (UDG) superfamily.

269 enzymes, in particular by MutM and MutY DNA glycosylases, ultimately contributes to cell death.

270 iosensor is able to detect both uracil DNA N-glycosylase (UNG) and AP-endonuclease 1 (APE1) within fe

271 tidine deaminase are processed by uracil-DNA glycosylase (UNG) and mismatch repair (MMR) pathways to

272 zygotes (AID+/-), and patients with uracil N-glycosylase (UNG) deficiency, which impairs CSR but not

273 Family 1 uracil N-glycosylase (UNG) from E. coli is an extremely efficient

274 repair (BER), either initiated by uracil-DNA glycosylase (UNG) or by single-strand selective monofunc

275 Ig gene loci can be recognized by uracil DNA glycosylase (UNG) or mutS homologs 2 and 6 (MSH2-MSH6) p

276 We show that depletion of the uracil DNA glycosylase (UNG) sensitizes tumor cells to FdUrd.

277 erential access of mismatch repair or uracil glycosylase (UNG) to AID-initiated U:G mismatches.

278 anine mismatches are processed by uracil DNA glycosylase (UNG)-mediated base-excision repair and MSH2

279 ckase, a cytidine deaminase and a uracil-DNA glycosylase (Ung).

280 n depends on protective repair by uracil-DNA glycosylase (UNG).

281 zymatic activity, D4 is an active uracil-DNA glycosylase (UNG).

282 Uracil DNA glycosylases (UNG) are highly conserved proteins that pr

283 with base excision repair enzyme uracil DNA glycosylase (UNG2) and crossover junction endonuclease M

284 epair pathway by antagonizing the uracil DNA glycosylase (Ung2) enzyme.

285 Uracil DNA Glycosylase (UNG2) is the primary enzyme in humans that

286 he recruitment of another target, uracil DNA glycosylase (UNG2), to the CRL4-DCAF1 E3 by Vpr.

287 In conclusion, the Nei-like DNA glycosylases unhook psoralen-derived ICLs in various DNA

288 but not by knockdown of SMUG1 or thymine-DNA glycosylase uracil-DNA glycosylases, proving that it is

289 ase, alkyl-adenine DNA glycosylase, MutY DNA glycosylase, uracil DNA glycosylase, and APE1 activity.

290 ndings support a general mechanism where DNA glycosylases use highly dynamic multidimensional diffusi

291 tructures of Endo III, we conclude that this glycosylase uses a multistep mechanism of damage recogni

292 We found that DNA glycosylases were efficiently recruited to DNA damage in

293 Therefore, various glycosylases were evaluated for their ability to hydroly

294 Repair of A:oxoG is initiated by adenine DNA glycosylase, which catalyzes hydrolytic cleavage of the

295 at cells defective in the N-methylpurine DNA glycosylase, which fail to remove N-methylpurines from D

296 ent DNA repair pathways, including NEIL1 DNA glycosylase, which initiates base excision repair (BER)

297 arising from DNA damage are mitigated by DNA glycosylases, which initiate the base excision repair pa

298 ecific sites in nucleic acids, including DNA glycosylases, which remove modified nucleobases to initi

299 endonuclease III (Endo III or Nth) is a DNA glycosylase with a broad substrate specificity for oxidi

300 model enzymes, exonuclease I and uracil DNA glycosylase with high sensitivity and selectivity.