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1 clease) and DNA repair enzymes (e.g., uracil-DNA glycosylase).
2 ranslational modification of the human MutYH DNA glycosylase.
3 effects were observed previously for thymine DNA glycosylase.
4 osphate and from genomic DNA by 8-oxoguanine-DNA glycosylase.
5 and into the active site of the 8-oxoguanine-DNA glycosylase.
6 adducts that can be removed by alkyladenine DNA glycosylase.
7 ue to inactivation of MUTYH, which encodes a DNA glycosylase.
8 utase (MnSOD) and mitochondrial 8-oxoguanine DNA glycosylase.
9 but instead depends, in part, on the thymine DNA glycosylase.
10 tic promiscuity, such as these two unrelated DNA glycosylases.
11 ine (G) are substrates for repair by various DNA glycosylases.
12 rent catalytic mechanism from those of other DNA glycosylases.
13 y a unique catalytic center in this class of DNA glycosylases.
14 nteractions in modulating the specificity of DNA glycosylases.
15 ich are repair intermediates of bifunctional DNA glycosylases.
16 ) base interrogation during lesion search by DNA glycosylases.
18 of DNA sliding is human 8-oxoguanine ((o)G) DNA glycosylase 1 (hOGG1), which repairs mutagenic (o)G
19 ere recently shown to stimulate 8-oxoguanine DNA glycosylase 1 (OGG1), an enzyme that removes oxidize
20 enzymes, the DNA glycosylases TDG and 8-oxoG DNA glycosylase 1 (OGG1), apurinic/apyrimidinic (AP) end
23 of DNA damage repair molecules 8-oxoguanine-DNA-glycosylase-1, nei-endonuclease-VIII-like, X-ray-rep
24 eral host cellular proteins including uracil DNA glycosylase-2 (UNG2) and a cullin-RING E3 ubiquitin
25 erase 3alpha (TOP3alpha) and NEIL3 (Nei-like DNA glycosylase 3), as well as transcription and RNA reg
27 We examined the role of the viral uracil DNA glycosylase, a protein conserved among all herpesvir
30 oxyribosyl moiety of DNA, human alkyladenine DNA glycosylase (AAG) and Escherichia coli 3-methyladeni
35 ng RONS-induced DNA damage; the alkyladenine DNA glycosylase (Aag/Mpg) excises several DNA base lesio
36 ve DNA demethylation mediated by the DEMETER DNA glycosylase accounts for all of the demethylation in
37 G/I, T/I, and A/I base pairs and a xanthine DNA glycosylase acting on all double-stranded and single
38 and A/U base pairs, but also a hypoxanthine DNA glycosylase acting on G/I, T/I, and A/I base pairs a
39 aired by the HCV core protein due to reduced DNA glycosylase activity for the excision of 8-oxo-2'-de
41 through the female lineage due to widespread DNA glycosylase activity in the male germline, and exten
44 f NEIL1 are catalytically inactive for their DNA glycosylase activity, these deficiencies may increas
48 or quantitative measurements of 8-oxoguanine DNA glycosylase, alkyl-adenine DNA glycosylase, MutY DNA
49 tion of intercalation for human alkyladenine DNA glycosylase, an enzyme that initiates repair of alky
50 Uracils in DNA can be recognized by uracil DNA glycosylase and abasic endonuclease to produce singl
51 pyAXII) and demonstrated their DNA cleavage, DNA glycosylase and AP lyase activities in vitro at 37 d
52 the VACV D4 protein serves both as a uracil-DNA glycosylase and as an essential component required f
53 poson-based library construction with uracil DNA glycosylase and endonuclease VIII to specifically de
55 product of 5hmC could be excised by thymine DNA glycosylase and MBD4 glycosylases regardless of cont
57 n to interact with the 8-oxoguanine (8-oxoG) DNA glycosylase and stimulate its enzymatic activities.
58 amages in opposing DNA strands with selected DNA glycosylases and human apurinic/apyrimidinic endonuc
59 Base excision repair (BER) is initiated by DNA glycosylases and is crucial in repairing RONS-induce
60 correlated with active DNA demethylation by DNA glycosylases and repressive targeting by the Polycom
61 vity of several enzymes [four BER-initiating DNA glycosylases and the downstream processing apurinic/
62 was paralleled by a compromised TDG (thymine DNA glycosylase) and TET1 (ten-eleven translocation prot
64 d 5-HmdU, may be cleaved from DNA by thymine DNA glycosylase, and subsequent action of base-excision
70 e in HD model R6/2 mice indicates that these DNA glycosylases are present in brain areas affected by
71 OS1/DEMETER family of 5-methylcytosine (5mC) DNA glycosylases are the first genetically characterized
72 rences between E. coli MUG and human thymine DNA glycosylase as well as that between the wild type MU
75 oxidized bases, initiated by NEIL1 and other DNA glycosylases at the chromatin level remains unexplor
80 have described both vertebrate and microbial DNA glycosylases capable of unhooking highly toxic inter
83 results suggest that Fpg, and possibly other DNA glycosylases, convert part of the binding energy int
85 In this issue, Johnson et al. show that a DNA glycosylase derived from Chlorella virus and enginee
87 lf, the enzyme harbors a helix-hairpin-helix DNA glycosylase domain followed by a unique C-terminal d
90 d process in all forms of life is the use of DNA glycosylase enzymes to excise rare damaged bases fro
93 dification sites was developed that utilizes DNA glycosylases found in the base excision repair pathw
94 Endonuclease III (Nth), formamidopyrimidine DNA glycosylase (Fpg) and endonuclease VIII (Nei) are me
96 A glycosylase (UDG) and formamido-pyrimidine-DNA glycosylase (FPG), 3'-5' exonucleases, and enzymes w
97 e, by the repair enzyme, formamidopyrimidine-DNA glycosylase (Fpg), likely involves multiple gates.
98 revealed introduction of formamidopyrimidine-DNA glycosylase (Fpg)-sensitive oxidative DNA lesions su
99 xamined the consequences of compromising the DNA glycosylases (Fpg and MutY) and endonucleases (Smx a
103 antitative PCRs (qPCRs) targeting the uracil DNA glycosylase gene (udg) or the 23S rRNA gene are desc
104 atory circuit centered on a 5-methylcytosine DNA glycosylase gene is required for long-term epigeneti
105 hat targeted inactivation of the mouse Smug1 DNA glycosylase gene is sufficient to ablate nearly all
106 combined with inactivation of the Ung uracil-DNA glycosylase gene leads to a loss of nearly all detec
112 the structure of a human 8-oxoguanine (oxoG) DNA glycosylase, hOGG1, in which a normal guanine from D
115 equence, all three analogs can be cleaved by DNA glycosylases; however, glycosylase activity is block
116 leobase excision activities of human thymine DNA glycosylase (hTDG) toward duplex DNA substrates harb
117 ssay to study damage search by human thymine DNA glycosylase (hTDG), which initiates BER of mutagenic
118 DNA repair enzymes such as human uracil-DNA glycosylase (hUNG) perform the initial step in the b
120 kbone in sliding and hopping by human uracil DNA glycosylase (hUNG), which is an exemplar that effici
121 ell line that had no detectable human uracil DNA glycosylase (hUNG2) activity, establishing that hUNG
122 ed the probability that nuclear human uracil DNA glycosylase (hUNG2) excised two uracil lesions space
123 abasic site recognition, the rate of uracil-DNA glycosylase hydrolysis of the N-glycosidic bond, con
124 responses, whereas a lack of other Nei-like DNA glycosylases (i.e., NEIL1 and NEIL2) had no signific
125 e (AAG) and Escherichia coli 3-methyladenine DNA glycosylase II (AlkA) bind tightly to their abasic D
128 This study provides the first structure of a DNA glycosylase in complex with an inhibitory base lesio
129 domain (MBD) family, MBD4 serves as a potent DNA glycosylase in DNA mismatch repair specifically targ
131 glycosylase (Fpg) are two of the predominant DNA glycosylases in Escherichia coli that remove oxidati
132 dues are removed from DNA by specific uracil-DNA glycosylases in the base excision repair pathway.
135 breaks caused by base excision from ssDNA by DNA glycosylases, including Nei-like (NEIL) 1, would gen
137 Though expression of the 12 known human DNA glycosylases individually did not enhance removal of
141 DNA methyltransferases and 5-methylcytosine DNA glycosylases interact to maintain epigenetic homeost
142 ndonuclease VIII-like protein 1 (NEIL1) is a DNA glycosylase involved in initiating the base excision
143 The bacterial MutY (MUTYH in humans) adenine DNA glycosylase is able to initiate the repair of A:oxoG
145 fluenced by either UNG1/2, SMUG1, or thymine-DNA glycosylase knockdown, strongly suggesting that ther
147 anscripts containing dUTP degraded by Uracil DNA glycosylase, leaving only those transcripts produced
150 ults demonstrate that rice DNG701 is a 5-meC DNA glycosylase/lyase responsible for the demethylation
152 cing 1 (ROS1) is a multi-domain bifunctional DNA glycosylase/lyase, which excises 5-methylcytosine (5
154 l of eukaryotic and prokaryotic bifunctional DNA glycosylases/lyases (NEIL1, Nei, Fpg, Nth, and NTH1)
156 along with the base excision repair pathway DNA glycosylase MAG1 renders the tpa1Deltamag1Delta doub
160 Here we present the first, to our knowledge, DNA glycosylase mechanism that does not require base fli
162 ue to inefficient turnover of N-methylpurine-DNA glycosylase (MPG), which initiates BER of epsilonA.
163 Mitochondria-targeted human 8-oxoguanine DNA glycosylase (mt-hOgg1) and aconitase-2 (Aco-2) each
167 8-oxoguanine DNA glycosylase, alkyl-adenine DNA glycosylase, MutY DNA glycosylase, uracil DNA glycos
168 ditional (fifth) viral gene, encoding uracil-DNA glycosylase (MVADelta5-HIV); or (iii) represent the
169 w the presence of the oxidized base-specific DNA glycosylase Nei-like 2 (NEIL2) and the DNA end-proce
170 we demonstrated that the bacterial and human DNA glycosylases Nei and NEIL1 excise unhooked psoralen-
173 t the DNA base excision repair (BER) enzyme, DNA glycosylase NEIL1, efficiently recognizes and excise
174 e base excision activities of five mammalian DNA glycosylases (NEIL1, NEIL2, mNeil3, NTH1, and OGG1)
175 we observed that the endonuclease VIII-like DNA glycosylase, NEIL1, accumulates at sites of oxidativ
176 e show that the oxidized base-specific human DNA glycosylase NEIL2 associates with RNA polymerase II
178 ing 8-oxoguanine DNA glycosylase (OGG1), the DNA glycosylase NTH1, and the apurinic endonuclease redo
179 ir pathway, initiated with one of four major DNA glycosylases: NTH1 or OGG1 (of the Nth family) or NE
180 se lesions in the human genome, initiated by DNA glycosylases, occurs via the base excision repair pa
181 nes, which are recognized and cleaved by two DNA glycosylases of the base excision repair pathway, en
185 odulating the DNA repair enzyme 8-oxoguanine DNA glycosylase (OGG1) in the PyMT transgenic mouse mode
189 repair (BER) enzymes, including 8-oxoguanine DNA glycosylase (OGG1), the DNA glycosylase NTH1, and th
190 g base excision repair (BER) by 8-oxoguanine DNA glycosylase (OGG1), yielding an abasic site (AP).
194 e sugar-phosphate backbone and the action of DNA glycosylases on deaminated, oxidized, and alkylated
201 n of SMUG1 or thymine-DNA glycosylase uracil-DNA glycosylases, proving that it is base excision by UN
202 oxylcytosine followed by excision by thymine-DNA glycosylase, raises the possibility that active deme
203 y contribute to removal of uracils by uracil DNA glycosylase regardless of the translational or rotat
204 eotide excision repair because humans lack a DNA glycosylase required to initiate base excision repai
205 he immunoprecipitate of human NEIL1, a major DNA glycosylase responsible for oxidized base repair.
208 ed in flowering or DNA repair, including the DNA glycosylase ROS1, which facilitates DNA demethylatio
209 tructures have captured for the first time a DNA glycosylase scanning the genome for a damaged base i
211 ision repair, a pathway that is catalyzed by DNA glycosylases such as 8-oxoguanine DNA glycosylase (O
214 d dinucleotide and purified BER enzymes, the DNA glycosylases TDG and 8-oxoG DNA glycosylase 1 (OGG1)
215 o regenerate unmodified cytosines by thymine-DNA glycosylase (TDG) and base excision repair (BER) pat
220 h 5fC and 5caC subject to removal by thymine DNA glycosylase (TDG) in conjunction with base excision
221 ispair, and this step is followed by thymine DNA glycosylase (TDG) initiated base excision repair (BE
226 nactivation of the DNA repair enzyme thymine DNA glycosylase (TDG) leads to embryonic lethality in mi
228 n (TET) enzymes (TET1/TET2/TET3) and thymine DNA glycosylase (TDG) play crucial roles in early embryo
231 sine (caC), excision of fC or caC by thymine DNA glycosylase (TDG), and restoration of cytosine via f
232 electively recognized and excised by thymine DNA glycosylase (TDG), leading to DNA demethylation.
233 are recognized by the monofunctional thymine DNA glycosylase (Tdg), which cleaves the glycosidic bond
236 by replication-dependent dilution or thymine DNA glycosylase (TDG)-dependent base excision repair.
237 sine through iterative oxidation and thymine DNA glycosylase (TDG)-mediated base excision repair.
240 ied as a function of (i) the lesion type and DNA glycosylase tested, (ii) local sequence context and
241 way, base excision repair (BER), they lack a DNA glycosylase that can initiate BER of dipyrimidine ph
243 hachiroi AlkZ (previously Orf1), a bacterial DNA glycosylase that protects its host by excising ICLs
247 )-like protein 1], one of the five mammalian DNA glycosylases that excise oxidized DNA base lesions i
248 uble-stranded (ds)DNA scanning enzymes, e.g. DNA glycosylases that excise rare aberrant bases, there
250 e monophosphate, or that lack MutM and MutY, DNA glycosylases that process base pairs involving 8-oxo
251 xcision repair (BER), a process initiated by DNA glycosylases that recognize and remove damaged DNA b
253 ducts of this or any type are not excised by DNA glycosylases that use a traditional base-flipping me
256 is critically dependent upon the ability of DNA glycosylases to locate rare sites of damage embedded
257 ILENCING 1 (ROS1) family of 5-methylcytosine DNA glycosylases to protect these genes from silencing.
259 rable interest surrounds the question of how DNA glycosylases translocate efficiently along DNA while
260 ylation in plants is mediated by a family of DNA glycosylases typified by Arabidopsis ROS1 (repressor
261 eotide kinase, the DNA repair enzymes uracil-DNA glycosylase (UDG) and formamido-pyrimidine-DNA glyco
264 undant mutagenic lesion recognized by uracil DNA glycosylase (UDG) in the first step of base excision
269 pair enzymes, in particular by MutM and MutY DNA glycosylases, ultimately contributes to cell death.
270 d cytidine deaminase are processed by uracil-DNA glycosylase (UNG) and mismatch repair (MMR) pathways
272 ion repair (BER), either initiated by uracil-DNA glycosylase (UNG) or by single-strand selective mono
273 plementary pathways, initiated by the uracil-DNA glycosylase (UNG) or the mismatch repair factor MSH2
275 and retroviruses encode a dUTPase or uracil-DNA glycosylase (UNG) to counteract uracil incorporation
279 l-guanine mismatches are processed by uracil DNA glycosylase (UNG)-mediated base-excision repair and
284 ions with base excision repair enzyme uracil DNA glycosylase (UNG2) and crossover junction endonuclea
287 to the recruitment of another target, uracil DNA glycosylase (UNG2), to the CRL4-DCAF1 E3 by Vpr.
289 1/2 but not by knockdown of SMUG1 or thymine-DNA glycosylase uracil-DNA glycosylases, proving that it
290 osylase, alkyl-adenine DNA glycosylase, MutY DNA glycosylase, uracil DNA glycosylase, and APE1 activi
291 e findings support a general mechanism where DNA glycosylases use highly dynamic multidimensional dif
292 hat are commonly employed for studying other DNA glycosylases, we observe an unusual biphasic protein
294 Repair of A:oxoG is initiated by adenine DNA glycosylase, which catalyzes hydrolytic cleavage of
295 w that cells defective in the N-methylpurine DNA glycosylase, which fail to remove N-methylpurines fr
296 fferent DNA repair pathways, including NEIL1 DNA glycosylase, which initiates base excision repair (B
297 ity arising from DNA damage are mitigated by DNA glycosylases, which initiate the base excision repai
298 coli endonuclease III (Endo III or Nth) is a DNA glycosylase with a broad substrate specificity for o
299 two model enzymes, exonuclease I and uracil DNA glycosylase with high sensitivity and selectivity.
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