ライフサイエンスコーパス: translesion synthesis

1 base-substitution fidelity, and abasic-site translesion synthesis.

2 oleta to positively regulate its activity in translesion synthesis.

3 witch between replication, proofreading, and translesion synthesis.

4 loping novel cancer therapeutics to suppress translesion synthesis.

5 in a potentially mutagenic process known as translesion synthesis.

6 eloping novel cancer therapeutics to inhibit translesion synthesis.

7 Rev1 is an essential scaffolding protein in translesion synthesis.

8 al repair enzyme recognition, processing and translesion synthesis.

9 tandard DNA structures in a process known as translesion synthesis.

10 cation of the DNA surrounding the lesion and translesion synthesis.

11 s that both prevent and facilitate mutagenic translesion synthesis.

12 lesion and the incoming nucleotide to assist translesion synthesis.

13 roperties of DNA Pol II that facilitate this translesion synthesis.

14 d thus generate active mutasomal complex for translesion synthesis.

15 PCNA plays an essential role in facilitating translesion synthesis.

16 ectly replicate past a lesion by error-prone translesion synthesis.

17 slipped mutagenic intermediate (SMI) during translesion synthesis.

18 Rad6-Rad18 complex as the initiating step of translesion synthesis.

19 Y family of DNA polymerases that function in translesion synthesis.

20 kappa functions during the extension step of translesion synthesis.

21 recombination, nonhomologous endjoining and translesion synthesis.

22 ll-characterized Y-family DNA polymerase for translesion synthesis.

23 would encounter during the extension step of translesion synthesis.

24 through an as yet poorly understood role in translesion synthesis.

25 dependent roles in the control of vertebrate translesion synthesis.

26 various roles of pol zeta that extend beyond translesion synthesis.

27 show how it catalyzes the extension step of translesion synthesis.

28 s into dsDNA templates by sequential PCR and translesion synthesis.

29 A polymerases that can bypass the lesion via translesion synthesis.

30 pa, catalyze the bypass of DNA damage during translesion synthesis.

31 a set of damage-tolerant DNA polymerases for translesion synthesis.

32 of double-strand breaks (DSBs) and performs translesion synthesis.

33 is a PCNA-interacting protein implicated in translesion synthesis, a DNA damage tolerance process th

34 Y-family of DNA polymerases and mediates DNA translesion synthesis, a major mechanism for DNA damage

35 tion (E664K) within this region that enables translesion synthesis across a template abasic site or a

36 NA synthesis during base-excision repair and translesion synthesis across a wide range of chemically

37 ases, the poxviral holoenzyme cannot perform translesion synthesis across an abasic site.

38 DNA polymerase Polkappa plays a key role in translesion synthesis, an error-prone replication mechan

39 is required in a lesion-specific manner for translesion synthesis and base damage-induced mutagenesi

40 ons for the accuracy of DNA synthesis during translesion synthesis and for the process of Pol exchang

41 anaemia pathway, which promote ICL incision, translesion synthesis and homologous recombination (revi

42 CHN cells to dacomitinib by the loss of both translesion synthesis and homologous recombination pathw

43 ID is essential for ICL repair by excision, translesion synthesis and homologous recombination; howe

44 B-family DNA polymerase that specializes in translesion synthesis and is essential for normal embryo

45 PDE-induced mutagenesis, we examined in vivo translesion synthesis and mutagenesis in yeast cells of

46 Therefore, translesion synthesis and mutagenesis of 1,N(6)-ethenoad

47 he Polzeta pathway is generally required for translesion synthesis and mutagenesis of the (+)- and (-

48 In this mutant strain, whereas translesion synthesis and mutagenesis of UV radiation we

49 pe as the single rev3 mutant with respect to translesion synthesis and mutagenesis.

50 PrimPol employs both translesion synthesis and repriming mechanisms to facili

51 The DDT pathways, which involve translesion synthesis and template switching (TS), are a

52 teins required for homologous recombination, translesion synthesis, and at least two endonucleases, M

53 d DNA oxidation, reduced REV1 expression and translesion synthesis, and elevated resistance to oxidat

54 tial activity of nucleotide excision repair, translesion synthesis, and homologous recombination mech

55 duced by a crosslink plays a crucial role in translesion synthesis, and length of the duplex surround

56 ncluding mono-ubiquitylation, which promotes translesion synthesis, and sumoylation, which inhibits r

57 omotes photoproduct excision, suppression of translesion synthesis, and the localization and activati

58 Our analysis highlights the importance of translesion synthesis as a primary function of the SOS r

59 acilitate replicative bypass of damaged DNA (translesion synthesis) as TRIP interactors.

60 This in vitro translesion synthesis assay will help in understanding t

61 The best-examined situation is translesion synthesis at sites of covalent DNA lesions s

62 line DT40 that REV1, a key regulator of DNA translesion synthesis at the replication fork, is requir

63 tolerated using either a recombination- or a translesion synthesis-based bypass mechanism.

64 The in vitro data suggest that translesion synthesis by another Y-family DNA polymerase

65 monoubiquitylation of PCNA allows mutagenic translesion synthesis by damage-tolerant DNA polymerases

66 Rad6-Rad18-dependent processes that include translesion synthesis by DNA polymerases eta and zeta an

67 These results and biochemical studies of translesion synthesis by mouse Pol eta indicate that Pol

68 ver, this checkpoint clamp did not stimulate translesion synthesis by Pol zeta or by DNA polymerase d

69 pair capacity of the cell has been exceeded, translesion synthesis by polymerase V (Pol V) allows DNA

70 covery and cell survival become dependent on translesion synthesis by polymerase V.

71 To better understand the mechanism of translesion synthesis by the yeast DNA polymerase eta (y

72 erases adhere to this bypass mechanism, then translesion synthesis by these error-prone enzymes is li

73 ted cells accorded with the well-established translesion synthesis bypass caused by 8-oxodG, and the

74 Translesion synthesis came at the expense of lesion-skip

75 lized to the mitochondria with repriming and translesion synthesis capabilities and, therefore, a pot

76 Error-prone translesion synthesis causes the majority of genotoxin-i

77 o better understand the mechanistic basis of translesion synthesis contributing to cisplatin resistan

78 Translesion synthesis depends on the trigger loop and br

79 replication, and the polymerase eta (Poleta) translesion synthesis DNA polymerase additionally promot

80 entional role for PrimPol as a mitochondrial translesion synthesis DNA polymerase for oxidative DNA d

81 tly discovered DNA-dependent DNA primase and translesion synthesis DNA polymerase found in the nucleu

82 of functional DNA polymerase (Pol) eta, the translesion synthesis DNA polymerase that readily insert

83 Polymerase eta (Poleta) is a low fidelity translesion synthesis DNA polymerase that rescues damage

84 was no involvement, however, for the Pol eta translesion synthesis DNA polymerase, the Mms2-Ubc13 pos

85 of the lesion, and bypass of the damage by a translesion synthesis DNA polymerase.

86 d its miscoding potential with four Y-family translesion synthesis DNA polymerases (pols): human pol

87 Translesion synthesis DNA polymerases contribute to DNA

88 belonging to the DinB class of the Y-family translesion synthesis DNA polymerases have a preference

89 uman cells, revealed the roles of individual translesion synthesis DNA polymerases in bypassing these

90 Rev1 is unique among translesion synthesis DNA polymerases in employing a pro

91 The relative roles of the yeast translesion synthesis DNA polymerases Pol zeta and Pol e

92 n vitro replication in the presence of human translesion synthesis DNA polymerases.

93 NA specifically activates two key enzymes in translesion synthesis: DNA polymerase eta, the yeast Xer

94 1) yeast, which depended highly on the known translesion synthesis enzymes Rev1 and DNA polymerase ze

95 dbrain development: neural migration and DNA translesion synthesis, essential for the replication of

96 During translesion synthesis, eukaryotic DNA polymerase zeta (z

97 To examine the role of translesion synthesis in ICL repair, we generated a defi

98 Current models suggest that translesion synthesis in mammalian cells is achieved in

99 DNA damage-induced checkpoint activation and translesion synthesis in mammalian cells.

100 clobutane pyrimidine dimer or abasic site by translesion synthesis in the absence of specialized tran

101 of human Y-family DNA polymerases to perform translesion synthesis in the presence of DNA-distorting

102 The involvement of translesion synthesis in this pathway has been postulate

103 Effective translesion synthesis in vertebrates requires the scaffo

104 merase V was responsible for the error-prone translesion synthesis in vivo.

105 n, nucleotide excision repair, and mutagenic translesion synthesis, in response to genotoxic insults.

106 Here we show, however, that pol-V-catalysed translesion synthesis, in the presence or absence of the

107 Translesion synthesis is a DNA damage tolerance mechanis

108 Translesion synthesis is a fundamental biological proces

109 Translesion synthesis is an essential cell survival stra

110 y incising on both sides of the ICL and then translesion synthesis is conducted across the "half-exci

111 Moreover, translesion synthesis is enhanced by altered partitionin

112 spectrum resulting from deamination without translesion synthesis is similar to a mutational signatu

113 crosslink sites and for interaction with the translesion synthesis machinery.

114 -family polymerases that facilitate accurate translesion synthesis may promote accurate microsatellit

115 e tolerance, employed in both re-priming and translesion synthesis mechanisms to bypass nuclear and m

116 When translesion synthesis occurred, epsilonA-->T mutations i

117 essory factors (PCNA and RPA) indicates that translesion synthesis occurs under replicative condition

118 PCNA also stimulated translesion synthesis of a model abasic site by Pol zeta

119 key cellular proteins involved in repair and translesion synthesis of O (6)-alkyl-dG lesions and prov

120 ic results, we present mechanistic models of translesion synthesis of these two DNA adducts, involvin

121 In particular, translesion synthesis of UV damage-containing DNA is dra

122 her critical DNA processing events including translesion synthesis, Okazaki fragment maturation and D

123 pairing; pol iota may play a limited role in translesion synthesis on bulky N2-G adducts in cells.

124 matic properties: it is less able to perform translesion synthesis on templates containing base lesio

125 n addition, PolDom can perform non-mutagenic translesion synthesis on termini containing modified bas

126 Klenow fragment (DNA polymerase I) performs translesion synthesis on this model substrate.

127 tion when either incorporating 8-oxo-dGTP or translesion synthesis opposite 8-oxo-dG.

128 Y-family hpol eta is known for translesion synthesis opposite the UV-induced DNA lesion

129 silon, to post-replicative processes such as translesion synthesis or post-replicative repair.

130 corporation of T for template G and accurate translesion synthesis past a 5S-thymine glycol (5S-Tg).

131 particularly adept at efficient and accurate translesion synthesis past a 5S-thymine glycol.

132 reproductive organs and are associated with translesion synthesis past bulky DNA adducts.

133 ymerases plays crucial roles in carrying out translesion synthesis past damaged bases in DNA.

134 mily DNA polymerase paralogs that facilitate translesion synthesis past damaged DNA.

135 ppressor genes and are thought to arise from translesion synthesis past deaminated cyclobutane pyrimi

136 ol) iota has been proposed to be involved in translesion synthesis past minor groove DNA adducts via

137 rest, suggesting that pol eta is involved in translesion synthesis past these replication-blocking ad

138 ta support a model in which pol eta-mediated translesion synthesis past this adduct is error-free in

139 Furthermore, POLN can perform translesion synthesis past thymine glycol, a common endo

140 Y-family of DNA polymerases and facilitates translesion synthesis past UV damage.

141 eins are essential components of a mutagenic translesion synthesis pathway in Escherichia coli design

142 y, replicative pol delta and the error-prone translesion synthesis pol zeta were able to accurately b

143 Translesion synthesis polymerase eta (eta) also extends

144 PrimPol, the translesion synthesis polymerase identified inside mamma

145 icase Twinkle and the proposed mitochondrial translesion synthesis polymerase PrimPol to study lesion

146 DNA damage bypass by the translesion synthesis polymerase Rev1 is enhanced by the

147 e absence of polymerase kappa or iota, other translesion synthesis polymerase(s) could incorporate nu

148 naturally in eukaryotic Pol zeta (a family-B translesion synthesis polymerase).

149 Yeast polymerase eta, a prototypical translesion synthesis polymerase, binds both PCNA and Re

150 of Ubc13 in controlling the activity of the translesion synthesis polymerase, Rev1.

151 me-replicating category or is an error-prone translesion synthesis polymerase.

152 olvement of distinct DNA repair pathways and translesion synthesis polymerases (Pols) in ameliorating

153 Translesion synthesis polymerases (TLS Pols) are require

154 uggesting the mutual involvement of multiple translesion synthesis polymerases in bypassing the lesio

155 plicative polymerases but can be bypassed by translesion synthesis polymerases in the nucleus.

156 gated to the C5 position of thymine by human translesion synthesis polymerases leads to large numbers

157 bditis elegans and supports a model in which translesion synthesis polymerases perform a slippage and

158 recombination-associated DNA synthesis, with translesion synthesis polymerases providing a supportive

159 We report here that of two translesion synthesis polymerases tested, only DNA polym

160 sion synthesis in the absence of specialized translesion synthesis polymerases.

161 s, or how the latter process is modulated by translesion synthesis polymerases.

162 While monoubiquitination activates mutagenic translesion synthesis, polyubiquitination activates an e

163 anding the basic mechanism of a postincision translesion synthesis process in ICL repair.

164 erase but has little, if any, bearing on the translesion synthesis properties of the enzyme.

165 is dramatically stimulated by PCNA such that translesion synthesis rates are comparable with replicat

166 anconi anemia, nonhomologous end joining, or translesion synthesis repair pathways did not sensitize

167 ol becomes more promutagenic, has an altered translesion synthesis spectrum and is capable of faithfu

168 f the multi-protein complex that carries out translesion synthesis, the error-prone replication of da

169 that Rev1 plays a non-catalytic function in translesion synthesis, the role of its dCMP transferase

170 ved that although the mutant RNAPs stimulate translesion synthesis, their expression is toxic in vivo

171 NHEJ) (yku70), mismatch repair (MMR) (pms1), translesion synthesis (TLS) (rev3), and checkpoints (mec

172 olymerase (Pol) eta in the insertion step of translesion synthesis (TLS) across the (5'S) diastereome

173 , a translesion polymerase, demonstrate that translesion synthesis (TLS) across these N(2)-dG adducts

174 ty to copy damaged DNA in a process known as translesion synthesis (TLS) and by their low fidelity on

175 rase zeta (Pol zeta) plays a key role in DNA translesion synthesis (TLS) and mutagenesis in eukaryote

176 te unrepaired lesions: potentially mutagenic translesion synthesis (TLS) and nonmutagenic damage avoi

177 ding-deficient family A enzyme implicated in translesion synthesis (TLS) and perhaps in somatic hyper

178 om both nucleotide excision repair (NER) and translesion synthesis (TLS) and predominates during the

179 18 governs at least two distinct mechanisms: translesion synthesis (TLS) and template switching (TS)-

180 r as to which of the lesion bypass processes-translesion synthesis (TLS) and/or template switching-de

181 mediated damage avoidance and Rad18-mediated translesion synthesis (TLS) are two forms of PRR.

182 d mutagenesis through its additional role in translesion synthesis (TLS) as a subunit of DNA polymera

183 Among several hypotheses to explain how translesion synthesis (TLS) by DNA polymerase eta (pol e

184 One process is translesion synthesis (TLS) by DNA polymerases (Pol) del

185 Rad6-Rad18-dependent lesion bypass involves translesion synthesis (TLS) by DNA polymerases eta or ze

186 ponent of Pol delta, it is also required for translesion synthesis (TLS) by Pol zeta.

187 e Rad6-Rad18-dependent pathways that include translesion synthesis (TLS) by Pol(eta) or -zeta and an

188 , p31(comet) can counteract REV7 function in translesion synthesis (TLS) by releasing it from REV3 in

189 Translesion synthesis (TLS) by Y-family DNA polymerases

190 Translesion synthesis (TLS) by Y-family DNA polymerases

191 TRIP13 similarly disassembles the REV7-REV3 translesion synthesis (TLS) complex, a component of the

192 Because mutagenic translesion synthesis (TLS) contributes to chemoresistan

193 ugh AraC that becomes incorporated into DNA, translesion synthesis (TLS) DNA Pols could reduce the ef

194 Both the POLH-1 (pol eta) translesion synthesis (TLS) DNA polymerase and the GEI-1

195 Rev1 is a Y-family translesion synthesis (TLS) DNA polymerase involved in b

196 The Polzeta translesion synthesis (TLS) DNA polymerase is responsibl

197 ave investigated mechanisms that recruit the translesion synthesis (TLS) DNA polymerase Polkappa to s

198 l and structural analyses of replicative and translesion synthesis (TLS) DNA polymerases (Pols) are r

199 Here we examine in human cells the roles of translesion synthesis (TLS) DNA polymerases (Pols) in pr

200 Here, we examine in human cells the roles of translesion synthesis (TLS) DNA polymerases (Pols) in th

201 Translesion synthesis (TLS) DNA polymerases (Pols) promo

202 Here we identify the translesion synthesis (TLS) DNA polymerases (Pols) requi

203 ys a crucial role in promoting the access of translesion synthesis (TLS) DNA polymerases (Pols) to PC

204 sions occurs by the sequential action of two translesion synthesis (TLS) DNA polymerases (Pols), in w

205 nding domains (UBDs) have been identified in translesion synthesis (TLS) DNA polymerases and it has b

206 Instead, translesion synthesis (TLS) DNA polymerases are employed

207 The roles of translesion synthesis (TLS) DNA polymerases in bypassing

208 Error-prone mechanisms rely on specialized translesion synthesis (TLS) DNA polymerases that directl

209 o its previously proposed role in recruiting translesion synthesis (TLS) DNA polymerases to gaps enco

210 ments in the isogenic cells where individual translesion synthesis (TLS) DNA polymerases were deplete

211 This review focuses on eukaryotic translesion synthesis (TLS) DNA polymerases, and the emp

212 Unique among translesion synthesis (TLS) DNA polymerases, pol zeta is

213 However, translesion synthesis (TLS) DNA polymerases, such as Rev

214 milar phenomenon was not observed when other translesion synthesis (TLS) DNA polymerases-hpol iota, k

215 polymerases known to bypass DNA lesions: the translesion synthesis (TLS) DNA polymerases.

216 nous carcinogens using a set of low-fidelity translesion synthesis (TLS) DNA polymerases.

217 In contrast, translesion synthesis (TLS) DNAPs are suitable for repli

218 lved in DpC bypass, we comparatively studied translesion synthesis (TLS) efficiency and mutagenesis o

219 Translesion synthesis (TLS) employs low fidelity polymer

220 Translesion synthesis (TLS) employs specialized DNA poly

221 oles of polymerase (Pol) nu and Pol theta in translesion synthesis (TLS) in cells.

222 Here we identify a role of poltheta in translesion synthesis (TLS) in human cells.

223 DNA translesion synthesis (TLS) is a crucial damage toleranc

224 Translesion synthesis (TLS) is a pathway in which specia

225 Translesion synthesis (TLS) is a potentially mutagenic m

226 ad2B, Mad2L2, and FANCV), a component of the translesion synthesis (TLS) machinery, could potentiate

227 from an origin of replication, we show that translesion synthesis (TLS) makes a prominent contributi

228 ub1 normally functions to promote error-free translesion synthesis (TLS) mediated by DNA polymerase e

229 or, PCNA, as a safeguard against error-prone translesion synthesis (TLS) of DNA.

230 t lysine 164 during polymerase eta-dependent translesion synthesis (TLS) of site-specific cis-syn cyc

231 possibly mediated by its ability to catalyze translesion synthesis (TLS) of these lesions.

232 A polymerase zeta is absolutely required for translesion synthesis (TLS) of this lesion, while loss o

233 Here we show that translesion synthesis (TLS) opposite 1,N(6)-ethenodeoxya

234 ional specificity and the genetic control of translesion synthesis (TLS) opposite an AP site in yeast

235 Because errors incorporated during translesion synthesis (TLS) opposite UV lesions would ge

236 Post-replication repair involves either translesion synthesis (TLS) or damage avoidance via temp

237 DNA polymerases eta, zeta and Rev1 to study translesion synthesis (TLS) past a nitrogen mustard-base

238 pathways of ICLs exist in humans that share translesion synthesis (TLS) past a partially processed I

239 polymerases that are thought to function in translesion synthesis (TLS) past different types of DNA

240 itment of damage-tolerant polymerases in the translesion synthesis (TLS) pathway of DNA damage avoida

241 ts with and regulates several members of the translesion synthesis (TLS) pathway, a DNA damage tolera

242 DNA polymerase (Pol) and a more specialized translesion synthesis (TLS) Pol to overcome the obstacle

243 However, E. coli contains translesion synthesis (TLS) Pols II, IV, and V that also

244 Here we analyzed the roles of translesion synthesis (TLS) Pols in the replication of 3

245 nents of the replication fork, including the translesion synthesis (TLS) polymerase poleta.

246 is indispensable for promoting the access of translesion synthesis (TLS) polymerases (Pols) to PCNA.

247 switches, indicative of MMBIR, are driven by translesion synthesis (TLS) polymerases Polzeta and Rev1

248 ic consequences associated with fork demise, translesion synthesis (TLS) polymerases such as poleta p

249 ng is through the recruitment of specialized translesion synthesis (TLS) polymerases that have evolve

250 sets a kinetic barrier to restrict access of translesion synthesis (TLS) polymerases to the primer/te

251 In addition to translesion synthesis (TLS) polymerases, most eukaryotic

252 ty, replicative polymerases and low fidelity translesion synthesis (TLS) polymerases.

253 s, followed by bypass of the unhooked ICL by translesion synthesis (TLS) polymerases.

254 REV1/POLzeta-dependent mutagenic translesion synthesis (TLS) promotes cell survival after

255 n the bypass of DNA damage, a process called translesion synthesis (TLS) that alleviates replication

256 ce that Pol II has an intrinsic capacity for translesion synthesis (TLS) that enables bypass of the C

257 ein of Saccharomyces cerevisiae functions in translesion synthesis (TLS) together with DNA polymerase

258 Consistent with activation of translesion synthesis (TLS) under these conditions, SAHA

259 ll's reliance on the potentially error-prone translesion synthesis (TLS), and an error-free, template

260 sting that nucleotide excision repair (NER), translesion synthesis (TLS), and recombination each play

261 of interstrand cross-links (ICLs) involving translesion synthesis (TLS), biochemical support for thi

262 esizing past DNA lesions in a process called translesion synthesis (TLS), but how TLS polymerases gai

263 repair requires the concerted activities of translesion synthesis (TLS), Fanconi anemia (FA), and ho

264 onse to 8-oxoG lesions involves 'on-the-fly' translesion synthesis (TLS), in which a specialized TLS

265 The DNA synthesis across DNA lesions, termed translesion synthesis (TLS), is a complex process influe

266 The cellular DNA repair pathway, translesion synthesis (TLS), is disrupted by BPLF1, whic

267 log 1,N (6)-ethenoadenosine (1,N (6)-erA) on translesion synthesis (TLS), mediated by human DNA polym

268 A-damage processing defects are reported for translesion synthesis (TLS), non-homologous end joining

269 Three modes of DDT have been documented: translesion synthesis (TLS), template switching (TS), an

270 ice deficient for Rev1, a core factor in DNA translesion synthesis (TLS), the postreplicative bypass

271 replication of damaged genomes by promoting translesion synthesis (TLS), this comes at a cost of pot

272 by the ubiquitin ligase (E3) yRad18 promotes translesion synthesis (TLS), whereas the lysine-63-linke

273 This constitutes one of the initial steps in translesion synthesis (TLS)--a critical pathway for cell

274 charomyces cerevisiae, we have reconstituted translesion synthesis (TLS)-mediated restart of a eukary

275 ivation of pol V for DNA synthesis including translesion synthesis (TLS).

276 ble to assist pol delta in 8-oxo-G bypass by translesion synthesis (TLS).

277 with stalled replication forks and promoting translesion synthesis (TLS).

278 romoting replication although DNA lesions by translesion synthesis (TLS).

279 merases in the DNA damage tolerance pathway, translesion synthesis (TLS).

280 e involved in the tolerance of DNA damage by translesion synthesis (TLS).

281 ination (HR), nonhomologous end joining, and translesion synthesis (TLS).

282 atalyzes proficient bypass of damaged DNA in translesion synthesis (TLS).

283 therwise stall replication--a process termed translesion synthesis (TLS).

284 tive bypass of DNA lesions, a process called translesion synthesis (TLS).

285 is the large increase in mutations caused by translesion synthesis (TLS).

286 A polymerase (pol) eta, which is involved in translesion synthesis (TLS).

287 ring replication, but is believed to inhibit translesion synthesis (TLS).

288 atic relationship between the FA pathway and translesion synthesis (TLS, a post-replication DNA repai

289 The contribution of translesion synthesis to survival was minor compared to

290 Biochemical assays of translesion synthesis using m6G lesion-containing templa

291 Translesion synthesis was reduced by approximately 26-37

292 Overall, 8-oxodG translesion synthesis was seen to be potentially mutagen

293 on, but only Pol eta, an enzyme efficient in translesion synthesis, was able to fully bypass the addu

294 ing of how this substitution interferes with translesion synthesis, we have determined the X-ray crys

295 e the relevance of its catalytic function in translesion synthesis, we separated the Rev1 dCMP transf

296 normal DNA with high efficiency yet conduct translesion synthesis when needed.

297 duced lesions are bypassed predominantly via translesion synthesis, whereas the error-free pathway fu

298 o the G2 phase, cells utilize REV3-dependent translesion synthesis, which requires a MEC1-dependent d

299 n that can facilitate both high fidelity and translesion synthesis within the replisome during DNA re

300 help cells tolerate DNA damage by performing translesion synthesis, yet they also can be highly error