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 pair pathway initiated by human alkyladenine glycosylase.

3 lational modification of the human MutYH DNA glycosylase.

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

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

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

7 se interrogation during lesion search by DNA glycosylases.

8 ar DNA translocation by two human DNA repair glycosylases.

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

10 d breaks by lesion-specific endonucleases or glycosylases.

11 promiscuity, such as these two unrelated DNA glycosylases.

12 (G) are substrates for repair by various DNA glycosylases.

13 are repair intermediates of bifunctional DNA glycosylases.

14 l inhibition of other DNA repair enzymes and glycosylases.

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

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

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

18 8-oxoG is repaired by the 8-oxoguanine glycosylase 1 (OGG1)-initiated DNA base excision repair

19 8-Oxoguanine-DNA glycosylase-1 (OGG1) is the primary enzyme for repairing

20 e pronounced in the case of 8-oxoguanine-DNA-glycosylase-1 and nei-endonuclease-VIII-like.

21 DNA damage repair molecules 8-oxoguanine-DNA-glycosylase-1, nei-endonuclease-VIII-like, X-ray-repair-

22 Uracil glycosylase 2 (UNG2) is required for CSR, most likely by

23 Processing of U:G base pairs via U N-glycosylase 2 (UNG2) or MutSalpha generates further poin

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

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

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

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

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

29 leobase shape on damage recognition by these glycosylases, a series of four substituted indole nucleo

30 ibosyl moiety of DNA, human alkyladenine DNA glycosylase (AAG) and Escherichia coli 3-methyladenine D

31 Human alkyladenine DNA glycosylase (AAG) employs nonspecific DNA binding intera

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

33 The mouse alkyl adenine DNA glycosylase (AAG, also known as MPG) recognizes such bas

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

35 NA demethylation mediated by the DEMETER DNA glycosylase accounts for all of the demethylation in the

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

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

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

39 dopts both anti and syn conformations in the glycosylase active site.

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

41 mes compare favorably with their known DNA-N-glycosylase activities: AAG removes both methanol and 1,

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

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

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

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

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

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

48 dition, NEIL1 but not mNeil3 showed enhanced glycosylase activity on Gh in the telomeric sequence con

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

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

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

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

53 g these residues did not markedly affect the glycosylase activity.

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

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

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

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

58 ranslocations in plasmacytomas from uracil N-glycosylase and activation-induced cytidine deaminase-de

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

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

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

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

63 duct of 5hmC could be excised by thymine DNA glycosylase and MBD4 glycosylases regardless of context.

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

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

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

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

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

69 related with active DNA demethylation by DNA glycosylases and repressive targeting by the Polycomb gr

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

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

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

73 HmdU, may be cleaved from DNA by thymine DNA glycosylase, and subsequent action of base-excision repa

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

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

76 Near the dyad, uracil DNA glycosylase/APE1 removes an outwardly oriented uracil ef

77 Glycosylase/apurinic lyase activity was reduced in Rad9(

78 DNA glycosylases are enzymes that perform the initial steps

79 DNA glycosylases are important editing enzymes that protect

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

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

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

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

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

85 The question of how mismatch glycosylases attain specificity for excising thymine fro

86 lly related Escherichia coli mismatch uracil glycosylase can excise 5caC as well.

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

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

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

90 MBD4 glycosylase cannot excise 5-formylcytosine (fC) or 5-car

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

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

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

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

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

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

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

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

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

102 Here, we report a crystal structure of the glycosylase domain of human MBD4 (residues 427-580) boun

103 s that would be expected to provide the MBD4 glycosylase domain with specificity for acting at CpG si

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

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

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

107 ctivity on Tg in quadruplex DNA and that the glycosylase exhibited a strong preference for Tg in the

108 DNA glycosylases for oxidized bases carry both a glycosylase

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

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

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

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

113 ned the consequences of compromising the DNA glycosylases (Fpg and MutY) and endonucleases (Smx and S

114 Two key glycosylases, Fpg and hOGG1, function to remove the muta

115 The family 4 uracil-DNA glycosylase from the hyperthermophilic organism Archaeog

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

117 DEMETER (DME), a DNA glycosylase functioning in the base-excision DNA repair

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

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

120 targeted inactivation of the mouse Smug1 DNA glycosylase gene is sufficient to ablate nearly all hmU-

121 ined with inactivation of the Ung uracil-DNA glycosylase gene leads to a loss of nearly all detectabl

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

123 substrates for mNeil3 and NEIL1, none of the glycosylases had activity on quadruplex DNA containing 8

124 Mammalian MutY glycosylases have a unique architecture that features an

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

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

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

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

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

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

131 be substrates for base excision repair (BER) glycosylases; however, large Sp-amine adducts would be e

132 ase excision activities of human thymine DNA glycosylase (hTDG) toward duplex DNA substrates harborin

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

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

135 Human uracil DNA glycosylase (hUNG) plays a central role in DNA repair an

136 e in sliding and hopping by human uracil DNA glycosylase (hUNG), which is an exemplar that efficientl

137 line that had no detectable human uracil DNA glycosylase (hUNG2) activity, establishing that hUNG2 is

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

139 sic site recognition, the rate of uracil-DNA glycosylase hydrolysis of the N-glycosidic bond, convert

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

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

142 AG) and Escherichia coli 3-methyladenine DNA glycosylase II (AlkA) bind tightly to their abasic DNA p

143 3-Methyladenine DNA glycosylase II (AlkA) is an enzyme that cleaves a wide r

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

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

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

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

148 are removed from DNA by specific uracil-DNA glycosylases in the base excision repair pathway.

149 ks caused by base excision from ssDNA by DNA glycosylases, including Nei-like (NEIL) 1, would generat

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

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

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

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

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

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

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

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

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

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

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

164 1 (ROS1) is a multi-domain bifunctional DNA glycosylase/lyase, which excises 5-methylcytosine (5mC)

165 We demonstrate that the bi-functional glycosylase/lyases Nth and MutM share several overlappin

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

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

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

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

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

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

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

173 The mammalian DNA glycosylase--methyl-CpG binding domain protein 4 (MBD4)-

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

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

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

177 Human DNA repair glycosylases must encounter and inspect each DNA base in

178 FCL) motif in the structurally unrelated BER glycosylases MutY and Endonuclease III and therefore ref

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

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

181 In contrast, the human BER glycosylase NEIL1 exhibited robust activity for all Sp-a

182 The human DNA glycosylase NEIL1 was recently demonstrated to initiate

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

184 se excision activities of five mammalian DNA glycosylases (NEIL1, NEIL2, mNeil3, NTH1, and OGG1) on t

185 observed that the endonuclease VIII-like DNA glycosylase, NEIL1, accumulates at sites of oxidative DN

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

187 nstrate that the bi-functional meningococcal glycosylases Nth and MutM can perform strand incisions a

188 esions in the human genome, initiated by DNA glycosylases, occurs via the base excision repair pathwa

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

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

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

192 Human 8-oxoguanine DNA glycosylase (OGG1) is a key enzyme involved in removing

193 8-Oxoguanine-DNA glycosylase (OGG1) removes premutagenic lesion 8-oxoguan

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

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

196 (8-oxoG) primarily via the 8-Oxoguanine DNA glycosylase (OGG1).

197 by DNA glycosylases such as 8-oxoguanine DNA glycosylase (OGG1).

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

199 gar-phosphate backbone and the action of DNA glycosylases on deaminated, oxidized, and alkylated base

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

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

202 DNA glycosylases preserve genome integrity and define the sp

203 MutY adenine glycosylases prevent DNA mutations by excising adenine f

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

205 DNA glycosylases protect genomic integrity by locating and e

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

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

208 excised by thymine DNA glycosylase and MBD4 glycosylases regardless of context.

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

210 mmunoprecipitate of human NEIL1, a major DNA glycosylase responsible for oxidized base repair.

211 The DNA glycosylase ROS1 was only partially decreased in activit

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

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

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

215 n repair, a pathway that is catalyzed by DNA glycosylases such as 8-oxoguanine DNA glycosylase (OGG1)

216 The uracil DNA glycosylase superfamily consists of several distinct fam

217 5fC and 5caC are excised by mammalian DNA glycosylase TDG, implicating 5mC oxidation in DNA demeth

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

219 generate unmodified cytosines by thymine-DNA glycosylase (TDG) and base excision repair (BER) pathway

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

221 The mammalian thymine DNA glycosylase (TDG) excises the mismatched base, uracil, t

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

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

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

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

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

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

228 The mammalian thymine DNA glycosylase (TDG) is implicated in active DNA demethylat

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

230 ET) enzymes (TET1/TET2/TET3) and thymine DNA glycosylase (TDG) play crucial roles in early embryonic

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

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

233 (caC), excision of fC or caC by thymine DNA glycosylase (TDG), and restoration of cytosine via follo

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

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

236 A key player is thymine DNA glycosylase (TDG), which excises thymine from mutagenic

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

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

239 through iterative oxidation and thymine DNA glycosylase (TDG)-mediated 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 as a function of (i) the lesion type and DNA glycosylase tested, (ii) local sequence context and the

243 clease III (EndoIII), a base excision repair glycosylase that also contains a [4Fe-4S] cluster.

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

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

246 Endonuclease VIII-like 1 (NEIL1) is a DNA glycosylase that recognizes a broad range of oxidative l

247 MutM is a bacterial DNA glycosylase that serves as the first line of defense aga

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

249 ke protein 1], one of the five mammalian DNA glycosylases that excise oxidized DNA base lesions in th

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

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

252 ion repair (BER), a process initiated by DNA glycosylases that recognize and remove damaged DNA bases

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

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

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

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

257 ivo-targeted mutagenesis in yeast, targeting glycosylases to embedded arrays for mutagenesis (TaGTEAM

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

259 CING 1 (ROS1) family of 5-methylcytosine DNA glycosylases to protect these genes from silencing.

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

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

262 e interest surrounds the question of how DNA glycosylases translocate efficiently along DNA while mai

263 ion in plants is mediated by a family of DNA glycosylases typified by Arabidopsis ROS1 (repressor of

264 Uracil-DNA glycosylase (UDG) compromises the replication strategies

265 y of both bacterial and mammalian uracil-DNA glycosylase (UDG) enzymes.

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

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

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

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

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

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

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

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

274 entary pathways, initiated by the uracil-DNA glycosylase (UNG) or the mismatch repair factor MSH2/MSH

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

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

277 Processing of dUs by uracil DNA glycosylase (UNG) yields abasic sites, which are excised

278 We investigated the enzyme uracil-DNA glycosylase (UNG), which detects and cleaves uracil from

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

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

281 n depends on protective repair by 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 The hOGG1 glycosylase was also found to catalyze removal of three

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

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

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

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

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

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

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.