ライフサイエンスコーパス: TLS

1 TLS activity is an important risk factor for the initiat

2 TLS and TS depend on site-specific PCNA K164 monoubiquit

3 TLS density and GC formation were each reduced in chemot

4 TLS is carried out by low-fidelity DNA polymerases that

5 TLS is initiated when the Rad6/Rad18 complex monoubiquit

6 TLS polymerases are capable of bypassing a distorted tem

7 TLS RNA can provide a glimpse into the structural basis

8 TLS(+) tissues exhibited a significantly increased expre

9 TLSs in this model were spatially associated with >90% o

10 PrimPol was recently identified as a TLS primase and polymerase involved in DNA damage tolera

11 (poleta), and that NPM1 deficiency causes a TLS defect due to proteasomal degradation of poleta.

12 The E3 ubiquitin ligase RAD18 activates TLS by promoting recruitment of Y-family DNA polymerases

13 hat the E3 ubiquitin ligase, which activates TLS repair by monoubiquitination of PCNA, is also affect

14 In addition, TLS has been implicated as a major cellular mechanism pr

15 ly involved in priming replication, are also TLS proficient and therefore may play important roles in

16 gy, and gene expression profiling to analyze TLS formation in human lung squamous cell carcinoma (LSC

17 the opposite effects of RecA on Pol III and TLS replisomes, we propose that RecA acts as a switch to

18 mportant role in PCNA monoubiquitination and TLS in a FANCD2 monoubiquitination and HR-independent ma

19 uclear antigen (PCNA) monoubiquitination and TLS polymerase recruitment; however, the regulatory step

20 nalyzed the effects of PolDIP2 on normal and TLS by five different human specialized Pols from three

21 As with another TLS polymerase, Pol IV, increasing concentrations of Pol

22 ritic cells (DC) present in tumor-associated TLS can provide a specific marker of these structures.

23 patient survival, and makes the link between TLS and a protective B cell-mediated immunity.

24 of these three lesions is tolerated by both TLS and HDR.

25 nce the efficiency and fidelity of bypass by TLS polymerases.

26 east triggers a switch to MMBIR catalyzed by TLS polymerases.

27 capable of directly bypassing DNA damage by TLS, as well as repriming replication downstream of impe

28 , our results show how tumors infiltrated by TLS-associated mature DC generate a specific immune cont

29 structural insights into PCNA recognition by TLS DNA polymerases that help better understand TLS regu

30 Resonant absorption by TLSs in the dielectric poses a serious limitation to the

31 basic site bypass independently of canonical TLS polymerases.

32 prokaryotes and eukaryotes possess canonical TLS polymerases (Y-family Pols) capable of traversing bl

33 ients treated with neoadjuvant chemotherapy, TLS density was similar, but GC formation was impaired a

34 ecifically activates replisomes that contain TLS Pols.

35 In contrast, TLS(+) tissues contained significantly more NIK(+) ECs a

36 evated mutagenesis during pol iota-dependent TLS.

37 In contrast, loss of Rad18-dependent TLS potentiates the collapse of stalled forks and leads

38 cleotide lesions by ggNER and Rev1-dependent TLS, respectively.

39 Whereas different TLS groupings yielded similar Bragg intensities, they yi

40 indicated that mRNAs harboring a distinctive TLS can move from transgenic roots into wild-type leaves

41 r low fidelity of synthesis opposite 3-dMeA, TLS opposite this lesion replicates DNA in a highly erro

42 cells can, at different times, modulate DNA TLS for improved cell survival.

43 tide insertion opposite these lesions during TLS in human genomes.

44 ing to the lymphatic vascular network during TLS development have not been studied.

45 t and passive exchange of polymerases during TLS on the lagging strand.

46 Y-family and replicative polymerases during TLS.

47 yeast, POLD3 is required for fully effective TLS, its loss resulting in hypersensitivity to a variety

48 nd demonstrate that ubiquitination of either TLS polymerase is a prerequisite for their physical and

49 e binding of pol eta to PCNA and the ensuing TLS are both independent of PCNA ubiquitination.

50 reover, we observed that MSH2 can facilitate TLS across cyclobutane pyrimidine dimers photoproducts i

51 lled replication forks where they facilitate TLS.

52 Rev1 stands alone from other Y-family TLS enzymes since it lacks the consensus PCNA-interactin

53 , a function unique to Poleta among Y-family TLS polymerases and dissociable from its catalytic activ

54 an important role in recruitment of Y-family TLS polymerases to stalled replication forks after DNA d

55 polymerase exchange that gains low-fidelity TLS polymerases access to DNA is mediated by their inter

56 they display remarkably low efficiencies for TLS compared to normal DNA synthesis.

57 tin-conjugating enzyme RAD6 is essential for TLS.

58 ts and showed that Rev1 is indispensable for TLS mediated by Poleta, Poliota, and Polkappa but is not

59 ng that PolDIP2 is an important mediator for TLS.

60 sed on these results, we propose a model for TLS across S-cdA and S-cdG in human cells, where Pol eta

61 ise, or consecutive, thermodynamic model for TLS folding is developed, which is in good agreement wit

62 s the implications of these observations for TLS mechanisms in human cells.

63 oliota, and Polkappa but is not required for TLS by Polzeta.

64 C-terminal polymerase domain is required for TLS opposite TG in human cells.

65 Here, we investigated roles for TLS polymerase eta, (poleta) in preserving telomeres fol

66 east, Rev1 promotes predominantly error-free TLS opposite UV lesions in humans.

67 eta function together and mediate error-free TLS, whereas in the other, poltheta functions in an erro

68 Whereas TS is mainly error-free, TLS can work in an error-prone manner and, as such, the

69 creasing amounts of the PIP-box peptide from TLS DNA polymerase poleta, suggesting that Rev1-BRCT and

70 etal-ion dependent formation of a functional TLS domain from unfolded RNAs via two consecutive steps:

71 Furthermore, TLS affords human cancer cells the ability to counteract

72 Furthermore, TLS density correlated with GC formation and expression

73 mmon molecular players including TDP-43, FUS/TLS, ubiquilin-2, VCP, and expanded hexanucleotide repea

74 s indicate that HuR regulates TDP-43 and FUS/TLS expression and that loss of HuR-mediated RNA process

75 f HuR in regulating two RBPs, TDP-43 and FUS/TLS, that have been linked genetically to amyotrophic la

76 of specific ASO-binding proteins such as FUS/TLS (FUS) and PSF/SFPQ (PSF).

77 Dominant mutations in FUS/TLS cause a familial form of amyotrophic lateral scleros

78 Mutations in the RNA-binding protein FUS/TLS (FUS) have been linked to the neurodegenerative dise

79 s associate with the RNA-binding protein Fus/TLS (fused in sarcoma/translocated in liposarcoma).

80 used-in-sarcoma/translocated-in-sarcoma (FUS/TLS).

81 from Pol delta to Pol lambda during 8-oxo-G TLS.

82 However, little is known about how TLS develop in cancer, how their function affects surviv

83 called translesion synthesis (TLS), but how TLS polymerases gain access to the DNA template remains

84 elegans and zebrafish embryos, and show how TLS-SPIM can facilitate cell biology research in multice

85 Is in DDR pathways (BER, MMR, NER, NHEJ, HR, TLS, and ICL repair) are specifically discussed for inhi

86 Human TLS involves the conjugation of ubiquitin to PCNA clamps

87 ients, so we evaluated whether they impaired TLS development independently of chemotherapy.

88 e POLD3 subunit of Poldelta are deficient in TLS.

89 very low numbers, but not differentially in TLS(+) tissues.

90 highlight the importance of GC formation in TLS during tumor development and treatment.Significance:

91 ta, Poliota, and Polkappa, which function in TLS in highly specialized ways opposite a diverse array

92 cialized DNA repair polymerase, functions in TLS and allows for DNA replication complexes to bypass l

93 However, how Rev1 functions in TLS and mutagenesis in human cells has remained unclear.

94 ota (pol iota), which has been implicated in TLS of oxidative and UV-induced lesions.

95 A) are expressed early and genes involved in TLS (i.e., Pol V) are expressed late during the bacteria

96 rgeting the LTalpha1beta2/LTbetaR pathway in TLS-associated pathologies might impair a natural prores

97 e establish that UV-induced recombination in TLS mutants is not attributable to DSBs.

98 Surprisingly, repair in TLS-deficient G2 cells required HR repair genes RAD51 an

99 Here we determined the role of Rev1 in TLS opposite UV lesions in human and mouse fibroblasts a

100 ied as a common transposon insertion site in TLS-ERG-induced disease, strongly validating the coopera

101 ong the common transposon insertion sites in TLS-ERG-driven leukemia, suggesting that a key mechanism

102 andard tunnelling model (STM) of independent TLS.

103 ons, as well as recent studies of individual TLS lifetimes in superconducting qubits.

104 results establish the role of NPM1 as a key TLS regulator, and suggest a mechanism for the better pr

105 ells expressing translocated in liposarcoma (TLS)-ERG, an activated form of ERG found in human leukem

106 confirmed in the experimental model of lung TLS induction.

107 (LSCC) and in an experimental model of lung TLS induction.

108 siRNA-based functional screen for mammalian TLS genes and identify 17 validated TLS genes.

109 one at inserting nucleotides opposite 1-MeA, TLS opposite this lesion in human cells occurs in a high

110 ion of DNA polymerase complexes that mediate TLS and describe how this knowledge is beginning to tran

111 is in CSCs, indicating that Pol eta-mediated TLS contributes to the survival of CSCs upon cisplatin t

112 have intrinsically enhanced Pol eta-mediated TLS, allowing CSCs to survive cisplatin treatment, leadi

113 as monoubiquitination by Rad6/Rad18 mediates TLS, extension of this ubiquitin to a polyubiquitin chai

114 eet selective plane illumination microscopy (TLS-SPIM) with real-time light-sheet optimization was de

115 fusing RNA constructs resembling the minimal TLS element of brome mosaic virus RNA3.

116 slate into the development of small molecule TLS inhibitors.

117 des significant interaction between multiple TLSs, which fully describes these observations, as well

118 In contrast to its role in mutagenic TLS in yeast, Rev1 promotes predominantly error-free TLS

119 the laser return intensity of green (532-nm) TLS correlates with changes in the de-epoxidation state

120 than the wild type enzyme, with over 90% of TLS events resulting in dA incorporation.

121 quenching (NPQ), and compare the ability of TLS to quantify these parameters with the passively meas

122 e demonstrate the 3D live imaging ability of TLS-SPIM by imaging cellular and subcellular behaviours

123 ic RAD18-binding partner and an activator of TLS.

124 s, the material recovers a typical amount of TLS.

125 tion method for the simultaneous analysis of TLS and HDR across defined DNA lesions in mammalian geno

126 The cellular composition of TLS was investigated by immunohistochemistry.

127 Lastly, a high density of TLS-associated DC correlated with long-term survival, wh

128 This suggests that the in vivo fidelity of TLS Pols is regulated by factors such as post-translatio

129 r findings highlight the pivotal function of TLS in shaping the immune character of the tumor microen

130 X, thereby recapitulating major hallmarks of TLS deficiency.

131 In this study, we evaluated the influence of TLS on the characteristics of the immune infiltrate in c

132 D2 monoubiquitinations (surrogate markers of TLS and FA pathway activation, respectively) and with at

133 ith Rev1 mediates a highly mutagenic mode of TLS.

134 Using a viral-induced, resolving model of TLS formation in the salivary glands of adult mice we de

135 The error-prone nature of TLS may provide mechanistic understanding of the accumul

136 Reconstituting the entire process of TLS in vitro using E. coli replication machinery and Pol

137 In the process of TLS, high-fidelity replicative DNA polymerases stalled b

138 nd RAD52, directly revealing a redundancy of TLS and HR functions in repair of ssDNAs.

139 or ZBTB1 is a critical upstream regulator of TLS.

140 ertion and extension steps, respectively, of TLS across S-cdA and S-cdG; human Pol kappa and Pol eta

141 However, the role of TLS in tumors has yet to be investigated carefully.

142 (4)-alkyldT lesions and defined the roles of TLS polymerases in bypassing these lesions in human cell

143 n impurities in Al2O3 are the main source of TLS resonant absorption.

144 We also characterized sequential stages of TLS maturation in LSCC culminating in the formation of g

145 ut both the insertion and extension steps of TLS opposite 3-dMeA, and in the Polzeta pathway, Polzeta

146 nucleotide insertion and extension steps of TLS, and in the third pathway, Polzeta would extend from

147 rocess, provide our current understanding of TLS on leading and lagging strand templates, and propose

148 However, the utility of TLS data for the quantification of plant physiological p

149 ion was impaired and the prognostic value of TLS density was lost.

150 cing BAFF in vivo prevented the formation of TLSs and lupus nephritis; however, it did not reduce imm

151 ment but also contribute to the formation of TLSs in chronic inflammation.

152 n NIK(+) ECs, (pre)FDCs, and the presence of TLSs, indicating that NIK(+) ECs may not only be importa

153 UV irradiation does not exclusively rely on TLS events.

154 ry of DDT in the late 1960s, most studies on TLS in eukaryotes have focused on DNA lesions resulting

155 mation of foci containing Polkappa and other TLS polymerases after UV irradiation of cells.

156 We show that, unlike other TLS polymerases, PrimPol is not stimulated by PCNA and d

157 with the T residue, Poliota would carry out TLS opposite 1-MeA, the ability of Poleta to replicate t

158 In untreated patients, TLS density was the strongest independent prognostic mar

159 i S, primase small subunit) can also perform TLS.

160 of a high-fidelity DNA polymerase to perform TLS with 8-oxo-guanine (8-oxo-G), a highly pro-mutagenic

161 deficient human Poldelta holoenzyme performs TLS of abasic sites in vitro much more efficiently than

162 Regulatory mechanisms that prevent TLS-associated mutagenesis are unknown; however, our rec

163 accumulate in late S and G2 when productive TLS is critical for cell survival.

164 ed by DNA damage are replaced by error-prone TLS enzymes responsible for the majority of mutagenesis

165 ly carry out the majority of the error-prone TLS of dG-C8-IQ, whereas pol eta is involved primarily i

166 tosum variant (XPV) results from error-prone TLS of UV-damaged DNA.

167 ation of POLD3 with Rev1 and the error-prone TLS polymerase Pol zeta, and elevates mutagenesis that r

168 t increased recruitment of other error-prone TLS polymerases (Polkappa and Poliota) after UV irradiat

169 lows bypass of DNA lesions using error-prone TLS polymerases.

170 hat Spartan negatively regulates error-prone TLS that is dependent on POLD3, the accessory subunit of

171 Results from a quantitative TLS assay showed that, in human cells, S-cdA and S-cdG i

172 We also calculate the expected qubit-TLS coupling and find it to lie between 16 and 20 MHz, c

173 Consistent with the role of RAD6/TLS in late-S phase, SMI#9-induced DNA replication inhib

174 deepen insights into the vital role of RAD6/TLS in platinum drug tolerance and reveal clinical benef

175 By reconstituting TLS at the single-molecule level, we show that the Esche

176 el purports that ubiquitinated PCNA recruits TLS polymerases such as pol eta to sites of DNA damage w

177 We show that NPM1 (nucleophosmin) regulates TLS via interaction with the catalytic core of DNA polym

178 ed role in lupus nephritis by inducing renal TLSs and regulating the position of T cells within the g

179 n ICL, its bypass may not absolutely require TLS polymerases.

180 nome replication in vivo and, when required, TLS of abasic sites.

181 This significantly restored TLS in pold3 mutants, enhancing dA incorporation opposit

182 Thus, in addition to revealing TLS and HR functional redundancy, we establish that UV-i

183 slocated in liposarcoma or fused in sarcoma (TLS/FUS or FUS).

184 Terrestrial laser scanning (TLS) data allow spatially explicit (x, y, z) laser retur

185 ment, we tested translation-libration-screw (TLS), liquid-like motions (LLM), and coarse-grained norm

186 was able to successfully perform abasic site TLS without template realignment and inserting preferabl

187 anslesion DNA synthesis (TLS), a specialized TLS pol is recruited to catalyze stable, yet often erron

188 thesis (TLS) during S-phase uses specialized TLS DNA polymerases to replicate a DNA lesion, allowing

189 ts made with the Tunable Laser Spectrometer (TLS) on Curiosity using a distinctive spectral pattern s

190 at Mars (SAM)'s tunable laser spectrometer (TLS).

191 bath of fluctuating two-level defect states (TLSs) embedded in the material.

192 -studied systems is the tRNA-like structure (TLS) domain, which has been found to occur in many plant

193 , a prototype being the tRNA-like structure (TLS) found at the 3' end of the turnip yellow mosaic vir

194 associated with tertiary lymphoid structure (TLS) has been reported in numerous studies.

195 he presence of tertiary lymphoid structures (TLS) in patients with non-small cell lung cancer (NSCLC)

196 uctures called tertiary lymphoid structures (TLS) is associated with improved patient survival.

197 tures known as tertiary lymphoid structures (TLS).

198 transcripts harboring tRNA-like structures (TLSs) that were found to be enriched in the phloem strea

199 Tertiary lymphoid structures (TLSs) in chronic inflammation, including rheumatoid arth

200 ation of renal tertiary lymphoid structures (TLSs).

201 (+) and PD-L1(+) epithelial cells supporting TLS formation.

202 es specialized in translesion DNA synthesis (TLS) aid DNA replication.

203 Translesion DNA synthesis (TLS) allows bypass of DNA lesions using error-prone TLS

204 Translesion DNA synthesis (TLS) can use specialized DNA polymerases to insert and/o

205 Translesion DNA synthesis (TLS) during S-phase uses specialized TLS DNA polymerases

206 mutations of the translesion DNA synthesis (TLS) gene REV7 (also known as MAD2L2), which encodes the

207 Trans-lesion DNA synthesis (TLS) is a DNA damage-tolerance mechanism that uses low-f

208 Translesion DNA synthesis (TLS) is the ability of DNA polymerases to incorporate nu

209 plate strand, and translesion DNA synthesis (TLS) is used to rescue progression of stalled replisomes

210 ble of catalyzing translesion DNA synthesis (TLS) on certain DNA lesions, and accumulating data sugge

211 th an appropriate translesion DNA synthesis (TLS) polymerase, followed by PCR amplification and next-

212 In translesion DNA synthesis (TLS), a specialized TLS pol is recruited to catalyze sta

213 -excision repair, translesion DNA synthesis (TLS), and homologous recombination (HR).

214 ce strategies are translesion DNA synthesis (TLS), in which low-fidelity DNA polymerases bypass the b

215 In translesion DNA synthesis (TLS), specialized DNA polymerases replicate the damaged

216 nsically enhanced translesion DNA synthesis (TLS).

217 cking lesions via translesion DNA synthesis (TLS).

218 erases to perform translesion DNA synthesis (TLS).

219 ity to facilitate translesion DNA synthesis (TLS).

220 gase Rad18 activates Trans-Lesion Synthesis (TLS) and the Fanconi Anemia (FA) pathway.

221 Trans-lesion synthesis (TLS) is an important DNA-damage tolerance mechanism that

222 the insertion step of translesion synthesis (TLS) across the (5'S) diastereomers of cdA and cdG.

223 potentially mutagenic translesion synthesis (TLS) and nonmutagenic damage avoidance (DA).

224 distinct mechanisms: translesion synthesis (TLS) and template switching (TS)-dependent pathways.

225 ts additional role in translesion synthesis (TLS) as a subunit of DNA polymerase zeta.

226 Translesion synthesis (TLS) by Y-family DNA polymerases alleviates replication

227 Rev1 is a Y-family translesion synthesis (TLS) DNA polymerase involved in bypass replication acros

228 Translesion synthesis (TLS) DNA polymerases (Pols) promote replication through

229 Here we identify the translesion synthesis (TLS) DNA polymerases (Pols) required for replicating thr

230 The roles of translesion synthesis (TLS) DNA polymerases in bypassing the C8-2'-deoxyguanosi

231 ells where individual translesion synthesis (TLS) DNA polymerases were depleted by the CRISPR/Cas9 ge

232 However, translesion synthesis (TLS) DNA polymerases, such as Rev1, have the ability to

233 a set of low-fidelity translesion synthesis (TLS) DNA polymerases.

234 In contrast, translesion synthesis (TLS) DNAPs are suitable for replicating modified templat

235 Translesion synthesis (TLS) employs low fidelity polymerases to replicate past

236 Translesion synthesis (TLS) employs specialized DNA polymerases to bypass repli

237 a role of poltheta in translesion synthesis (TLS) in human cells.

238 DNA translesion synthesis (TLS) is a crucial damage tolerance pathway that oversees

239 to promote error-free translesion synthesis (TLS) mediated by DNA polymerase eta (Poleta).

240 s ability to catalyze translesion synthesis (TLS) of these lesions.

241 everal members of the translesion synthesis (TLS) pathway, a DNA damage tolerance pathway, and that t

242 nd a more specialized translesion synthesis (TLS) Pol to overcome the obstacle.

243 ver, E. coli contains translesion synthesis (TLS) Pols II, IV, and V that also function with the heli

244 analyzed the roles of translesion synthesis (TLS) Pols in the replication of 3-MeA-damaged DNA in hum

245 MMBIR, are driven by translesion synthesis (TLS) polymerases Polzeta and Rev1.

246 In addition to translesion synthesis (TLS) polymerases, most eukaryotic cells contain a multif

247 f the unhooked ICL by translesion synthesis (TLS) polymerases.

248 age, a process called translesion synthesis (TLS) that alleviates replication stalling.

249 nt with activation of translesion synthesis (TLS) under these conditions, SAHA and cisplatin cotreatm

250 xcision repair (NER), translesion synthesis (TLS), and recombination each play a role in drug toleran

251 s in a process called translesion synthesis (TLS), but how TLS polymerases gain access to the DNA tem

252 ncerted activities of translesion synthesis (TLS), Fanconi anemia (FA), and homologous recombination

253 r DNA repair pathway, translesion synthesis (TLS), is disrupted by BPLF1, which deubiquitinates the D

254 have been documented: translesion synthesis (TLS), template switching (TS), and repriming.

255 a core factor in DNA translesion synthesis (TLS), the postreplicative bypass of damaged nucleotides.

256 genomes by promoting translesion synthesis (TLS), this comes at a cost of potentially error-prone le

257 A synthesis including translesion synthesis (TLS).

258 s believed to inhibit translesion synthesis (TLS).

259 Dissipative two-level systems (TLS) have been a long-standing problem in glassy solids

260 he existence of tunneling two-level systems (TLS).

261 TA-TLSs have been described in human lung cancers, but thei

262 Thus, we propose that Treg cells in TA-TLSs can inhibit endogenous immune responses against tum

263 d T cell proliferation rates increased in TA-TLSs upon Treg cell depletion, leading to tumor destruct

264 -associated tertiary lymphoid structures (TA-TLSs).

265 nature of DNA replication, it is likely that TLS on the leading and lagging strand templates is uniqu

266 We show that TLS through the thymine glycol (TG) lesion, the most com

267 g through 1-MeA in human cells and show that TLS through this lesion is mediated via three different

268 xacerbate a local immune response, such that TLS formation in tumors may help promote an efficacious

269 Our results suggest that TLS by Pol IV smoothes the way for the replication fork

270 SOS response, it has long been thought that TLS was the last recourse to bypass DNA lesions when rep

271 The TLS is thus structured to perform several functions and

272 In addition, the TLS structure is 'two faced': one face closely mimics tR

273 These interactions also allow the TLS to readily switch conformations.

274 Interestingly, Rad51 and the TLS polymerase poleta modulate the elongation of nascent

275 In this work, folding dynamics for the TLS domain of Brome Mosaic Virus have been investigated

276 e three-fold increase in recombinants in the TLS mutants over that in WT cells.

277 ase in ssDNA gaps for cells deficient in the TLS polymerases eta (Rad30) and zeta (Rev3).

278 suggesting a possible role of PolDIP2 in the TLS reaction.

279 This remarkable suppression of the TLS found in ultrastable glasses of indomethacin is argu

280 survival after DNA damage, inhibition of the TLS pathway has emerged as a potential target for the de

281 r, PCNA, and inhibits the recruitment of the TLS polymerase, polymerase eta (Pol eta), after damage t

282 ings establish that PolDIP2 can regulate the TLS polymerase and primer extension activities of PrimPo

283 efined against the diffuse data, whereas the TLS and NM models provide more detailed and distinct des

284 This TLS not only acts like a tRNA to drive aminoacylation of

285 In contrast to TLS mediated by polkappa and polzeta, in which polzeta w

286 These data support Poldelta contributing to TLS in vivo and suggest that the mutagenesis resulting f

287 at POLD3 makes a significant contribution to TLS independently of Polzeta in DT40 cells.

288 Via application of SB mutagenesis to TLS-ERG-induced erythroid transformation, we identified

289 xic stress, bacterial cells give priority to TLS, a minor pathway able to generate genetic diversity

290 +) ECs, (pre)FDCs, and ILC3s with respect to TLSs in RA ST.

291 on, unless they are bypassed by translesion (TLS) DNA polymerases.

292 We further show that translesion (TLS) polymerase PolH chromatin localization is decreased

293 rough a physical interaction between the two TLS pols.

294 t the crystal structure of the complete TYMV TLS to 2.0 A resolution.

295 DNA polymerases that help better understand TLS regulation in eukaryotes.

296 ammalian TLS genes and identify 17 validated TLS genes.

297 In vitro TLS using yeast pol zeta showed that it can extend G3*:A

298 thway unfolds, in particular, where and when TLS occurs on each template strand.

299 Consistent with TLS organization, all stages of B-cell differentiation w

300 i) are executed in chronological order, with TLS coming first, followed by DA.