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

3 Amongst replicative DNA Pols, translesion DNA Pols play a particular role: replication

4 Remarkably, however, DinB is the only known translesion DNA polymerase active in RecA-mediated stran

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

6 he evolutionarily conserved Escherichia coli translesion DNA polymerase IV (DinB) is one of three enz

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

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

9 prine et al report that up-regulation of the translesion DNA polymerase Polkappa mediates resistance

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

11 genes, linking the function of this putative translesion DNA polymerase to host immune evasion by ant

12 While c-TDR requires reverse transcriptase, translesion DNA polymerase zeta (Pol zeta) plays a major

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

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

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

18 Translesion DNA polymerases may also contribute.

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

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

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

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

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

24 This rescue strictly depended on translesion DNA polymerases.

25 e highly conserved in DinB, but not in other translesion DNA polymerases.

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

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

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

29 Translesion DNA synthesis (TLS) and homologous recombina

30 Translesion DNA synthesis (TLS) can use specialized DNA

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

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

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

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

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

36 Translesion DNA synthesis (TLS) mediated by low-fidelity

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

38 the replication of AraC, the lower-fidelity translesion DNA synthesis (TLS) polymerase Poleta is pro

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

40 randed DNA (dsDNA) form by using appropriate translesion DNA synthesis (TLS) polymerases and then can

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 ession, promoting replication fork reversal, translesion DNA synthesis (TLS), and repriming.

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

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

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

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

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

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

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

53 red during S-phase and may be carried out by translesion DNA synthesis (TLS).

54 is specialized for the extension reaction in translesion DNA synthesis (TLS).

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

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 Acting as a suicide enzyme, HMCES prevents translesion DNA synthesis and the action of endonuclease

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

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

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

62 in melanoma development besides its bonafide translesion DNA synthesis function, and suggest that tar

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

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

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

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

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

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

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

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

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

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

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

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

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

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

80 a ubiquitin-conjugating enzyme critical for translesion DNA synthesis, potentiates beta-catenin stab

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

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

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

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

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

86 equires specialized polymerases that perform translesion DNA synthesis.

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

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

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

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

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

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

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

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

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

96 n DNA damage tolerance through their role in translesion DNA synthesis.

97 e associated with homopolymer instability or translesion DNA synthesis.

98 h DPCs causes their proteolysis, followed by translesion DNA synthesis.

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

100 However, Pso2 lacks translesion nuclease activity in vitro, and mechanistic

101 Importantly, Hrq1 also stimulated Pso2 translesion nuclease activity through a site-specific IC

102 we describe a dual function of one putative translesion Pol in African trypanosomes, which we now na

103 All cells express a range of translesion Pols, but little work has examined their fun

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

114 , Pol32, and the catalytic domain of Rev1, a translesion polymerase, act together in the same pathway

115 ted with DNA polymerase zeta, an error-prone translesion polymerase, and the APOBEC family of DNA dea

116 er extension studies using E. coli Pol IV, a translesion polymerase, demonstrate that translesion syn

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

118 utant, specifically dependent on the Polzeta translesion polymerase, yields COSMIC signature 3 observ

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

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

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

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

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

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

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

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

127 est through the lesion to provide access for translesion polymerases.

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

129 a2 instead of being processed by error-prone translesion polymerases.

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

131 volved in nucleotide addition, can stimulate translesion RNA synthesis by Escherichia coli RNAP witho

132 e polymerases display distinct mutagenic and translesion specificities.

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

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

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

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

137 18 governs at least two distinct mechanisms: translesion synthesis (TLS) and template switching (TS)-

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

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

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

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

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

143 Because mutagenic translesion synthesis (TLS) contributes to chemoresistan

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

159 Translesion synthesis (TLS) employs low fidelity polymer

160 Translesion synthesis (TLS) employs specialized DNA poly

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

210 PrimPol employs both translesion synthesis and repriming mechanisms to facili

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

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

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

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

215 Translesion synthesis came at the expense of lesion-skip

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

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

218 Translesion synthesis depends on the trigger loop and br

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

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

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

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

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

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

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

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

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

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

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

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

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

232 Effective translesion synthesis in vertebrates requires the scaffo

233 Translesion synthesis is a fundamental biological proces

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

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

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

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

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

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

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

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

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

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

244 Translesion synthesis polymerase eta (eta) also extends

245 PrimPol, the translesion synthesis polymerase identified inside mamma

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

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

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

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

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

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

252 Translesion synthesis polymerases (TLS Pols) are require

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

271 During translesion synthesis, eukaryotic DNA polymerase zeta (z

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

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

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

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

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

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

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

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

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

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

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

286 oleta to positively regulate its activity in translesion synthesis.

287 witch between replication, proofreading, and translesion synthesis.

288 loping novel cancer therapeutics to suppress translesion synthesis.

289 in a potentially mutagenic process known as translesion synthesis.

290 eloping novel cancer therapeutics to inhibit translesion synthesis.

291 Rev1 is an essential scaffolding protein in translesion synthesis.

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

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

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

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

296 Thus, translesion transcription becomes essential for cell sur

297 dary channel factors DksA and GreA modulated translesion transcription by RNAP, depending on changes

298 We conclude that the efficiency of translesion transcription can be significantly modulated

299 e of key elements of the RNAP active site in translesion transcription.

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