ライフサイエンスコーパス: translesion

1 s, blocking lesion entry to the active site, translesion A rule synthesis, and translocation block ar

2 sion of inverted repeats, while genes in the translesion branch have no detectable role.

3 old factor for other Y-family polymerases in translesion bypass events.

4 named the 1-BD duplex) models the product of translesion bypass of 1,N(2)-epsilondG by Sulfolobus sol

5 en in asf1 mutants, which was independent of translesion bypass polymerases but showed an increased d

6 termining the molecular origins of mutagenic translesion bypass.

7 We related our findings to that of a model translesion DNA pol, Sulfolobus solfataricus Dpo4.

8 either ATM and Rad3-related (ATR) kinase or translesion DNA polymerase eta (i.e. key proteins that p

9 t with some in vitro activities of mammalian translesion DNA polymerase eta: tandem base substitution

10 ding pocket and thus prevents binding of the translesion DNA polymerase IV to the clamp, providing a

11 l, and discuss the potential consequences of translesion DNA polymerase loss.

12 single-strand annealing factors HR Rad52 and translesion DNA polymerase theta to CSR.

13 es an increased involvement of the mutagenic translesion DNA polymerase zeta during DNA replication.

14 g the efficiency and the fidelity of a human translesion DNA polymerase.

15 eriments show that different combinations of translesion DNA polymerases act to bypass lesions in mam

16 epair via recruitment of specific nucleases, translesion DNA polymerases and the homologous recombina

17 of single-stranded DNA regions, error-prone translesion DNA polymerases appear to produce most error

18 ng humans, that suggest both replicative and translesion DNA polymerases are involved in HR-associate

19 to determine the effects of deficiencies in translesion DNA polymerases on the checkpoint response o

20 found that disruption of the genes encoding translesion DNA polymerases Polkappa and Poleta signific

21 eplication blocks, cells utilize specialized translesion DNA polymerases that are intrinsically error

22 hereas Ub-PCNA can signal for recruitment of translesion DNA polymerases, SUMO-PCNA signals for recru

23 on DNA polymerases and poor lesion bypass by translesion DNA polymerases.

24 This rescue strictly depended on translesion DNA polymerases.

25 essential during embryogenesis, unlike other translesion DNA polymerases.

26 astrand cross-links is performed by multiple translesion DNA polymerases.

27 repair/tolerance mechanism over error-prone translesion DNA polymerases.

28 by a complex, multistep mechanism involving translesion DNA polymerases.

29 ing capabilities act as chain terminators of translesion DNA replication while analogs with hydrogen

30 DNA processing (error-free) to low-fidelity translesion DNA synthesis (error-prone) at DNA damage si

31 irradiation, DNA polymerases specialized in translesion DNA synthesis (TLS) aid DNA replication.

32 Translesion DNA synthesis (TLS) allows bypass of DNA les

33 Translesion DNA synthesis (TLS) can use specialized DNA

34 Translesion DNA synthesis (TLS) during S-phase uses spec

35 ored biallelic inactivating mutations of the translesion DNA synthesis (TLS) gene REV7 (also known as

36 zeta (REV3 and REV7) play important roles in translesion DNA synthesis (TLS) in which DNA replication

37 Translesion DNA synthesis (TLS) is the ability of DNA po

38 ions encountered on the template strand, and translesion DNA synthesis (TLS) is used to rescue progre

39 -family DNA polymerase capable of catalyzing translesion DNA synthesis (TLS) on certain DNA lesions,

40 s are converted to dsDNA with an appropriate translesion DNA synthesis (TLS) polymerase, followed by

41 es the cooperative actions of at least three translesion DNA synthesis (TLS) polymerases: Poleta, REV

42 In translesion DNA synthesis (TLS), a specialized TLS pol i

43 pathways such as nucleotide-excision repair, translesion DNA synthesis (TLS), and homologous recombin

44 r processes, including nucleolytic incision, translesion DNA synthesis (TLS), and homologous recombin

45 The two main tolerance strategies are translesion DNA synthesis (TLS), in which low-fidelity D

46 In translesion DNA synthesis (TLS), specialized DNA polymer

47 Given the critical role of pol eta during translesion DNA synthesis (TLS), these findings unveil a

48 s cope with replication-blocking lesions via translesion DNA synthesis (TLS).

49 cialized low fidelity polymerases to perform translesion DNA synthesis (TLS).

50 haracterized for their ability to facilitate translesion DNA synthesis (TLS).

51 nal modification essential for DNA repair by translesion DNA synthesis (TLS).

52 ng that CSCs may have intrinsically enhanced translesion DNA synthesis (TLS).

53 ryonic viability and development through the translesion DNA synthesis activity of Polzeta preserving

54 In addition to translesion DNA synthesis activity, MacDinB-1 synthesize

55 way is believed to be the major mechanism of translesion DNA synthesis and base damage-induced mutage

56 evant platinum-based drugs by promoting both translesion DNA synthesis and DNA repair.

57 the Y-family of DNA polymerases involved in translesion DNA synthesis and genome mutagenesis.

58 of concept for the coordinate inhibition of translesion DNA synthesis as a strategy to improve chemo

59 hat BRCA1 plays a critical role in promoting translesion DNA synthesis as well as DNA template switch

60 the assessment of the mutagenic profiles of translesion DNA synthesis catalyzed by any error-prone D

61 sults suggest that PolN might play a role in translesion DNA synthesis during ICL repair in human cel

62 ein interactions specific for Rev1's role in translesion DNA synthesis in human cells, and I2 acts as

63 It involves either translesion DNA synthesis initiated by proliferating cel

64 Translesion DNA synthesis is an essential process that h

65 Translesion DNA synthesis is an important branch of the

66 have been used to study polymerase-mediated translesion DNA synthesis of abasic sites and TT dimers,

67 PolH to translocate to replication foci for translesion DNA synthesis of UV-induced DNA lesions.

68 T2AA significantly inhibited translesion DNA synthesis on a cisplatin-cross-linked te

69 approach, we examined the effect of impaired translesion DNA synthesis on cisplatin response in aggre

70 gesting their catalytically limited roles in translesion DNA synthesis past deaminated, oxidized base

71 hosphates on DNA polymerases when performing translesion DNA synthesis past the pro-mutagenic DNA add

72 llow us to conveniently screen regulators of translesion DNA synthesis pathway and monitor environmen

73 g., REV1, REV3L) involved in the error-prone translesion DNA synthesis pathway can sensitize intrinsi

74 e, the authors present the structures of the translesion DNA synthesis polymerase Rev1 in complex wit

75 is would preserve the substrate for the REV1 translesion DNA synthesis polymerase to incorporate cyto

76 it of DNA polymerase zeta (Polzeta), 1 of 10 translesion DNA synthesis polymerases known in mammals.

77 A, animal cell mitochondria lack specialized translesion DNA synthesis polymerases to tolerate these

78 seamlessly coordinate both high fidelity and translesion DNA synthesis requires a means to regulate r

79 inks (ICLs) are repaired by mechanisms using translesion DNA synthesis that is regulated by monoubiqu

80 V serve dual roles by facilitating efficient translesion DNA synthesis while simultaneously introduci

81 epair of ICLs requires sequential incisions, translesion DNA synthesis, and homologous recombination,

82 Polymerase eta (PolH) is necessary for translesion DNA synthesis, and PolH deficiency predispos

83 e identify a function of PAF, a component of translesion DNA synthesis, in modulating Wnt signaling.

84 on have direct implications for low-fidelity translesion DNA synthesis, most of which is found to be

85 how that NDP kinase mutants are dependent on translesion DNA synthesis, often a mutagenic form of DNA

86 Due to the critical role of PolH in translesion DNA synthesis, the activity of PolH is tight

87 NA damage are the consequence of error-prone translesion DNA synthesis, which could be responsible fo

88 that PARP10 binding to PCNA is required for translesion DNA synthesis.

89 ro-8-oxo-2'-deoxyguanosine (8-oxo-dG) during translesion DNA synthesis.

90 zeta (Pol zeta) and Rev1 are key players in translesion DNA synthesis.

91 , including T2 amino alcohol (T2AA), inhibit translesion DNA synthesis.

92 amily DNA polymerases play a crucial role in translesion DNA synthesis.

93 atch repair, nucleotide excision repair, and translesion DNA synthesis.

94 ward loop to enhance PCNA ubiquitylation and translesion DNA synthesis.

95 of accessory proteins retained on DNA during translesion DNA synthesis.

96 oid and induced expression of genes encoding translesion DNA synthesis.

97 A provides a novel biochemical tool to study translesion DNA synthesis.

98 ons coordinates homologous recombination and translesion DNA synthesis.

99 s and elucidate the interplay between HR and translesion DNA synthesis.

100 vily on hydrogen-bonding interactions during translesion DNA synthesis.

101 ination in response to UV-induced damage for translesion DNA synthesis.

102 equires specialized polymerases that perform translesion DNA synthesis.

103 We have termed this method translesion excision repair-sequencing (tXR-seq).

104 ns was the same as the surface implicated in translesion polymerase binding.

105 to interact with the beta clamp and act as a translesion polymerase but did not require its "little f

106 and structure determination of a quaternary translesion polymerase complex consisting of the Rev1 CT

107 structural elucidation of such a quaternary translesion polymerase complex encompassing both inserti

108 identify important interface residues of the translesion polymerase complex.

109 iate the assembly of extension and insertion translesion polymerase complexes and provide a molecular

110 NA crosslinking agents, which identified the translesion polymerase eta (PolH) as a p53-regulated tar

111 hway requiring the tumor suppressor p53, the translesion polymerase iota (POLiota), the ubiquitin lig

112 pass by Poldelta itself independently of the translesion polymerase Polzeta of which POLD3 is also a

113 reaches them and also enable the appropriate translesion polymerase to sample each lesion as it is en

114 -terminal domain (CTD), which interacts with translesion polymerase zeta through the Rev7 subunit and

115 ns are strong replication blocks and DinB, a translesion polymerase, facilitates the mutagenic bypass

116 Recent evidence suggests that loss of the translesion polymerase, Polzeta, can sensitize tumor cel

117 e template strand act both as substrates for translesion polymerases and as signals for checkpoint ac

118 To probe the mechanism by which translesion polymerases bypass M1dG, kinetic and structu

119 for repair, suggesting replicative or other translesion polymerases can bypass the C-C remnant.

120 t to the toolbelt model, the replicative and translesion polymerases do not form a stable complex on

121 In contrast, functionally related Y-family translesion polymerases exhibit a severely reduced abili

122 by nucleotide excision repair or bypassed by translesion polymerases in the nucleus.

123 e is highly organized, the exchange with the translesion polymerases is stochastic and is not determi

124 licative DNA polymerase Pol IIIcore with the translesion polymerases Pol II and Pol IV.

125 e flow cytometry revealed that cells lacking translesion polymerases replicate UV-damaged DNA at the

126 Surprisingly, we found no evidence that the translesion polymerases Rev1 and Polzeta repair structur

127 How untimely access of translesion polymerases to DNA is prevented is poorly un

128 mage leads to the recruitment of specialized translesion polymerases to the damage locus.

129 duced replication, errors are independent of translesion polymerases, and many mutations have the sig

130 ctor to chromatin but also directly recruits translesion polymerases, such as Polymerase eta and Rev1

131 m DNA "repair" enzymes including error-prone translesion polymerases.

132 nosis severity, systolic blood pressure, and translesion pressure gradient (peak systolic and mean) a

133 e polymerases display distinct mutagenic and translesion specificities.

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

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

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

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

138 18 governs at least two distinct mechanisms: translesion synthesis (TLS) and template switching (TS)-

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

159 Translesion synthesis (TLS) employs low fidelity polymer

160 Translesion synthesis (TLS) employs specialized DNA poly

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

208 PrimPol employs both translesion synthesis and repriming mechanisms to facili

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

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

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

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

213 Translesion synthesis came at the expense of lesion-skip

214 Translesion synthesis depends on the trigger loop and br

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

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

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

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

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

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

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

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

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

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

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

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

227 Effective translesion synthesis in vertebrates requires the scaffo

228 Translesion synthesis is a fundamental biological proces

229 Translesion synthesis is an essential cell survival stra

230 Moreover, translesion synthesis is enhanced by altered partitionin

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

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

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

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

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

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

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

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

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

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

241 Translesion synthesis polymerase eta (eta) also extends

242 PrimPol, the translesion synthesis polymerase identified inside mamma

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

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

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

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

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

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

249 Translesion synthesis polymerases (TLS Pols) are require

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

282 oleta to positively regulate its activity in translesion synthesis.

283 witch between replication, proofreading, and translesion synthesis.

284 loping novel cancer therapeutics to suppress translesion synthesis.

285 in a potentially mutagenic process known as translesion synthesis.

286 eloping novel cancer therapeutics to inhibit translesion synthesis.

287 Rev1 is an essential scaffolding protein in translesion synthesis.

288 al repair enzyme recognition, processing and translesion synthesis.

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

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

291 s that both prevent and facilitate mutagenic translesion synthesis.

292 lesion and the incoming nucleotide to assist translesion synthesis.

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

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

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

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

297 DNA replication, unless they are bypassed by translesion (TLS) DNA polymerases.

298 We further show that translesion (TLS) polymerase PolH chromatin localization

299 Thus, translesion transcription becomes essential for cell sur

300 Of the "translesion" Y-family human DNA polymerases (hpols), hpo