ライフサイエンスコーパス: Pol eta

1 error-prone polymerase, DNA polymerase eta (pol eta).

2 unted for by the activity of polymerase eta (POL eta).

3 leotide incorporation by DNA polymerase eta (pol eta).

4 undamaged bases by yeast DNA polymerase eta (pol eta).

5 , by 2-3 fold, compared to Pol zeta alone or Pol eta.

6 rosatellites was: Pol kappa >/= Pol delta4 > Pol eta.

7 nt results are obtained with human and mouse Pol eta.

8 oint and with much lower fidelity than yeast Pol eta.

9 subfamily of the Y-family polymerases, as is pol eta.

10 already robust TT dimer bypass efficiency of pol eta.

11 mplate bulges are extended so efficiently by pol eta.

12 sory proteins enhance the fidelity of TLS by pol eta.

13 ucts at both sites, being most favorable for pol eta.

14 the same cells complemented with functional pol eta.

15 stacking in the selection of nucleotides by pol eta.

16 ite G and 8-oxoG by Saccharomyces cerevisiae Pol eta.

17 k on blocking and misincorporation in TLS by pol eta.

18 ly tractable system, we created mice lacking pol eta.

19 ts resembles that observed with the Y family pol eta.

20 g dCMP opposite the dG-N(2)-3MeE lesion than pol eta.

21 two other Y-family polymerases, Pol iota and Pol eta.

22 s an effective inhibitor of DNA synthesis by pol eta.

23 epsilon but not with Pol delta, RB69 gp43 or Pol eta.

24 and the extension of the DL by Pol delta and Pol eta.

25 h the literature: Pol delta4 >> Pol kappa or Pol eta.

26 isincorporation frequency (0.71) followed by pol eta (0.63).

27 Polymerase eta (Pol eta), a specialized DNA repair polymerase, functions

28 We demonstrated that Pol eta accumulated at CFSs upon partial replication str

29 ate how the state of an unhooked ICL affects pol eta activity.

30 tment of the TLS polymerase, polymerase eta (Pol eta), after damage to DNA by UV irradiation.

31 With pol eta, all diastereoisomers of dG-N2-TAM promoted smal

32 Under nucleotide deprivation, Pol eta allows cells to accumulate at the G1/S boundary

33 T-T) dimers and other bulky DNA lesions, but pol eta also has other cellular roles.

34 To determine whether Pol eta also makes such functionally important contacts

35 Furthermore, Pol zeta, but not Pol eta, also contributes to 4-NQO resistance.

36 lls strongly suggest that, in the absence of Pol eta, an abnormally error-prone polymerase substitute

37 opposite a phenanthriplatin lesion, but only Pol eta, an enzyme efficient in translesion synthesis, w

38 omyces cerevisiae Pol delta, Pol epsilon and Pol eta and a series of matched and mismatched primer te

39 ogen-derived DNA adducts were explored using pol eta and a truncated form of human pol kappa (pol kap

40 o the physiological role of DNA synthesis by pol eta and have implications for our understanding of h

41 nd therefore we generated mice deficient for pol eta and heterozygous for pol zeta.

42 r increased by loss of the bypass polymerase Pol eta and inhibition of ataxia-telangiectasia and Rad3

43 slightly increase the processivity of yeast pol eta and its ability to recycle to new template prime

44 When taken together, the properties of pol eta and kappa are consistent with the mutagenic even

45 r dNTPs were retarded at the dX lesion while pol eta and kappa readily bypassed the lesion.

46 e O(6)-alkylG adducts for dCTP and dTTP with pol eta and kappa; pol iota showed a strong preference f

47 Pol eta and kappaDeltaC showed more broad miscoding spec

48 The miscoding frequencies induced by pol eta and kappaDeltaC were at least 8 times higher tha

49 involving localized translesion synthesis by Pol eta and mismatch excision and polymerization by a ma

50 With pol eta and O(6)-BzG, products were also obtained with -

51 duplexes and the Y-family polymerases human Pol eta and P2 Pol IV (Dpo4) from Sulfolobus solfataricu

52 T2AA decreased PCNA/pol eta and PCNA/REV1 chromatin colocalization but did n

53 s from three families: Pol delta (family B), Pol eta and Pol iota (family Y), and Pol lambda and Pol

54 We find that, whereas Pol eta and Pol iota provide alternate pathways for muta

55 The properties of pol eta and pol kappa are consistent with the mutagenic

56 In addition, pol eta and pol kappa bypassed the lesion by incorporati

57 Both pol eta and pol kappa incorporated dCMP, the correct bas

58 Steady-state kinetic studies with pol eta and pol kappa indicated that dTMP, the correct b

59 in centers of viral DNA replication and that Pol eta and Pol kappa play an important role in HBoV1 DN

60 In primer extension assays, pol eta and pol kappa replicated through N(2),3-epsilonG

61 Both Pol eta and Pol zeta extended the DL more efficiently th

62 ion and exclusively directed G->A mutations; Pol eta and Pol zeta participated in error-prone bypass

63 ersion spectra indicates a hierarchy between Pol eta and Pol zeta with respect to the bypass of UV-in

64 suggesting that T2AA hinders interactions of pol eta and REV1 with monoubiquitinated PCNA.

65 Here we report that BPLF1 interacts with Pol eta and that Pol eta protein levels are increased in

66 We show a role for pol eta and the complexity of different chemical adducts

67 l structures of Saccharomyces cerevisiae apo-pol eta and the Dpo4-CPD complex suggests unique feature

68 etry in the selection of nucleotides by both pol eta and the Klenow fragment, and the lesser role of

69 vity, suggest a role for AICDA in regulating POL eta and uracil DNA-glycosylase activity.

70 across S-cdA and S-cdG in human cells, where Pol eta and/or Pol iota carries out nucleotide insertion

71 Although DNA polymerase eta (Pol eta) and other Y family polymerases differ in sequen

72 Recruitment of DNA polymerase eta (Pol eta) and other Y-family TLS polymerases to damaged D

73 including RAD5, REV3/REV7 (Pol zeta), RAD30 (Pol eta), and POL30 (PCNA).

74 on, phenanthriplatin is highly toxic to both Pol eta+ and Pol eta- cells.

75 ons catalyzed by DNA polymerase (pol) alpha, pol eta, and pol kappa.

76 recombinase and DNA polymerase (Pol) delta, Pol eta, and Pol zeta.

77 olumn fraction II (CFII) included pol delta, pol eta, and RFC.

78 ed in wild-type cells that was diminished in pol eta- and pol iota-deficient mouse cells and abolishe

79 DNA repair DNA polymerases (polymerase eta [Pol eta] and polymerase kappa [Pol kappa]) are recruited

80 bypass polymerases, of which polymerase eta (pol eta) appears to be specifically adapted to synthesiz

81 iciencies in the order of pol kappa > REV1 > pol eta approximately pol iota, and dTTP misincorporatio

82 Mice homozygous for a null mutation in pol eta are viable, fertile, and do not show any obvious

83 namely polymerase (pol) theta, pol zeta and pol eta, are induced in B cells by the stimuli that are

84 in conjunction with pol kappa, but not with pol eta, at a replication fork stalled by the adduct, re

85 We found that Pol eta binds the incoming correct dCTP opposite both G

86 Down-regulation of Pol eta blocked cisplatin-induced CSC enrichment both in

87 Yeast Pol delta and yeast Pol eta both bypass 8-oxoG and misincorporate adenine du

88 in-terminating inhibitor of DNA synthesis by pol eta but not by Klenow fragment or T7 DNA polymerase.

89 opposite N2,N2-diMeG compared with N2-EtG by pol eta but not by pol iota is consistent with Hoogsteen

90 observed in AAF-induced mutagenesis and that pol eta, but not pol kappa, may play a role in this proc

91 ore efficiently past the adduct than that of pol eta by incorporating dCMP, a correct base, opposite

92 to help suppress UV mutagenesis by improving pol eta bypass fidelity per se.

93 cycle of processive DNA synthesis, Dpo4 and Pol eta bypass synthetic AP sites with 13-30 and 10-13%,

94 Pol eta bypasses a dimer with low fidelity and with high

95 Pol eta can also bypass other DNA damage adducts in vitr

96 In contrast, pol eta cannot insert pyrene nucleotide opposite the 5'-

97 minor groove, here we examine the effects on Pol eta-catalyzed nucleotide incorporation when 3-deazag

98 demonstrate that pol eta deficiency in mice (pol eta(-/-)) causes obesity with visceral fat accumulat

99 f the POLH gene encoding DNA polymerase eta (pol eta) causes the UV-sensitivity syndrome xeroderma pi

100 iplatin is highly toxic to both Pol eta+ and Pol eta- cells.

101 Here, we present evidence that pol eta competes with DNA polymerases alpha and delta fo

102 we show that although in yeast a stable Rev1-Pol eta complex can be formed, this complex formation in

103 X-ray structural characterization of Pol eta complexed with site-specifically platinated DNA

104 se nucleotide triphosphate, dATP or dGTP, to Pol eta complexed with undamaged or damaged DNA.

105 Human pol eta copied past all three adducts.

106 ed mutagenesis in vivo despite the fact that pol eta copies DNA with low fidelity, here we test wheth

107 We show that Pol eta copies thymine dimers and the flanking bases wit

108 Although pol eta could accommodate large bulges and continue synt

109 across S-cdA and S-cdG; human Pol kappa and Pol eta could also extend past these lesions, albeit muc

110 Yeast pol eta could bypass all three modified nucleosides; alt

111 This finding suggested that pol eta could play a role in translesion synthesis past

112 We found that pol eta could stabilize a frayed primer terminus, which

113 A model of the pol eta-CPD complex built from the crystal structures of

114 Herein, we demonstrate that pol eta deficiency in mice (pol eta(-/-)) causes obesity

115 Pol eta deficiency led to persistence of checkpoint-blin

116 nduced mutagenesis was investigated in human pol eta-deficient (XP-V) cells through whole-exome seque

117 dent with hydroxyurea-induced S-phase delay, Pol eta-deficient cells undergo more replication fork br

118 uently enter apoptosis at a faster rate than Pol eta-deficient cells.

119 to killing by exposure to UV light, and all Pol eta-deficient mice develop skin tumors after UV irra

120 one had no effect, UV-induced skin tumors in pol eta-deficient mice developed 4 weeks earlier in mice

121 se and other Pol eta functions, we generated Pol eta-deficient mice.

122 Finally, we provide evidence that a pol eta dependent signature is also found to be lagging

123 ion synthesis by mouse Pol eta indicate that Pol eta-dependent bypass of cyclobutane pyrimidine dimer

124 data are consistent with the requirement of Pol eta-dependent DNA synthesis during S phase at replic

125 ion bypass pathway is not epistatic with the Pol eta-dependent pathway and, as a consequence, protect

126 of the incoming nucleotide; in this regard, Pol eta differs from high-fidelity DNA polymerases that

127 The stalling of Pol eta directly past the ICL is attributed to its autoi

128 duced normal amounts of IgG, indicating that pol eta does not affect class switch recombination.

129 sser role of shape selection in insertion by pol eta due to its more open and less constrained active

130 ntosum who accumulate dimers, errors made by Pol eta during dimer bypass could contribute to mutagene

131 Given the critical role of pol eta during translesion DNA synthesis (TLS), these fi

132 Mouse Pol kappa, Rev7, Pol iota and Pol eta each bind to the same approximately 100 amino ac

133 Pol eta effectively bypassed N2-methyl(Me)G, N2-ethyl(Et

134 DNA polymerase eta (pol eta), encoded by the xeroderma pigmentosum (XP-V) ge

135 When human DNA polymerase eta (pol eta) encounters N6-deoxyadenosine adducts formed by

136 A deficiency in mouse DNA polymerase eta (pol eta) enhanced UV-induced Hprt mutant frequencies.

137 expression of miR-93 in ovarian CSCs reduced Pol eta expression and increased their sensitivity to ci

138 in, thus revealing a general requirement for pol eta expression in providing tolerance to these plati

139 owever, unlike in XP-A cells, the absence of pol eta expression resulted in a reduced ability to over

140 n, the efficacies of which are influenced by Pol eta expression, phenanthriplatin is highly toxic to

141 Mass spectrometry of pol eta extension products revealed a single major produ

142 human polymerases kappa (Pol kappa) and eta (Pol eta) fidelities to that of replicative human polymer

143 en perform a comprehensive analysis of yeast pol eta fidelity.

144 with attenuated FANCD2, RAD6, gammaH2AX, and POL eta foci formation and cisplatin-adduct removal.

145 o highlighted an accumulation of nuclei with pol eta foci that correlated with the formation of monou

146 sults help explain the proficient ability of Pol eta for bypassing distorting DNA lesions.

147 ing of monoubiquitinated PCNA and a purified pol eta fragment containing the UBZ and PIP-box was inhi

148 or PIAS1- and STUbL-mediated displacement of Pol eta from DNA damage sites.

149 position of the TTD in the previous step of Pol eta function.

150 gh accessory proteins clearly participate in pol eta functions in vivo, they do not appear to help su

151 To better understand these and other Pol eta functions, we generated Pol eta-deficient mice.

152 ts with mutations in the DNA polymerase eta (pol eta) gene are hypersensitive to sunlight and have gr

153 Although the presence of Pol eta generally suppresses UV-induced mutagenesis, our

154 that C is preferentially mutated in vivo and pol eta generates hypermutation in the mu and gamma swit

155 Relative to the replicative polymerases, Pol eta has a greater tolerance for distorted DNA geomet

156 obutane pyrimidine dimers, XPV cells lacking Pol eta have diminished capacity to replicate UV-damaged

157 The fact that yeast and mammalian Pol eta have intrinsically different catalytic propertie

158 Primer extension studies with purified pol eta have shown that this polymerase is highly error-

159 Moreover, 37.5% of pol eta heterozygous mice also developed skin cancer dur

160 two crystal structures of Dpo4, an archaeal pol eta homologue, complexed with CPD-containing DNA, wh

161 reported previously that purified human DNA pol eta (hpol eta) can incorporate both deoxyribonucleos

162 To study the role of pol eta in a genetically tractable system, we created mi

163 hriplatin on DNA interacts with and inhibits Pol eta in a manner distinct from that of cisplatin-DNA

164 rradiation and further indicating a role for pol eta in dealing with cisplatin-induced damage.

165 which firmly establishes a central role for pol eta in hypermutation.

166 Second, MSH2 binds to pol eta in solution, and endogenous MSH2 associates with

167 are consistent with the established role of Pol eta in suppressing ogg1-dependent mutagenesis in yea

168 s significantly different from that by yeast pol eta in that the latter was more error-prone opposite

169 The results suggest the involvement of pol eta in the cellular error-prone translesion synthesi

170 esion synthesis DNA polymerases Pol zeta and Pol eta in UV survival and mutagenesis were examined usi

171 H2-MSH6 stimulates the catalytic activity of pol eta in vitro.

172 n elevated expression of DNA polymerase eta (Pol eta) in ovarian CSCs isolated from both ovarian canc

173 rbed cells and its complementary roles, with Pol Eta, in damage tolerance in human cells.

174 While Pol eta incorporates an incorrect A opposite 8-oxoG with

175 ession of a catalytically inactive mutant of Pol eta increased replication fork stalling and activate

176 al studies of translesion synthesis by mouse Pol eta indicate that Pol eta-dependent bypass of cyclob

177 Moreover, both KF- and yeast pol eta induced a considerable amount of -2 frameshift p

178 In 1-base incorporation studies, pol eta inserted C and A, pol iota inserted T, and pol k

179 Pol eta inserted dAMP opposite 4-OHEN-dC, accompanied by

180 netic studies showed that both pol kappa and pol eta inserted dCMP and dAMP opposite the 4-OHEN-dC an

181 The Y family DNA polymerase yeast pol eta inserts pyrene deoxyribose monophosphate (dPMP)

182 Pol eta inserts pyrene nucleotide with greater efficienc

183 of the SUMO modification pathway in limiting Pol eta interactions with DNA damage sites in human cell

184 Based on methylphosphonate-DNA mapping, pol eta interacts with the single strand template but no

185 pol eta, iota, and kappa showed pre-steady-state kinetic

186 However, yeast Pol eta is 10-fold more efficient than Pol delta, and fo

187 Given that increased expression of Pol eta is a known mechanism by which cells resist cispl

188 We have recently observed that Pol eta is also required for the stability of common fra

189 Moreover, yeast Pol eta is at least 10-fold more accurate than yeast Pol

190 atin-induced S phase arrest, suggesting that pol eta is involved in translesion synthesis past these

191 of the error-prone TLS of dG-C8-IQ, whereas pol eta is involved primarily in its error-free bypass.

192 Translesion synthesis by pol eta is likely to be predominantly error-free, since

193 ons involving T induced by UVA indicate that pol eta is not responsible for correctly replicating T-c

194 how that the low fidelity class Y polymerase Pol eta is recruited to proliferating cell nuclear antig

195 nsistent with the localization observed when Pol eta is recruited to sites of DNA damage.

196 However, as Pol eta is reported to require higher nucleotide concent

197 under conditions of nucleotide deprivation, Pol eta is required for S-phase progression but is proap

198 ing proteomic profiling, we demonstrate that Pol eta is targeted for multisite SUMOylation, and that

199 To examine if pol eta is the primary mutagenic translesion polymerase

200 DNA polymerase eta (Pol eta) is a member of a new class of DNA polymerases t

201 DNA polymerase eta (pol eta) is best known for its ability to bypass UV-indu

202 Human DNA polymerase eta (Pol eta) is best known for its role in responding to UV

203 s in primer extension reactions catalyzed by pol eta, kappa and iota.

204 kappa, whereas it was increased by 10-24% in pol eta knockdown cells.

205 From these studies, we conclude that Pol eta makes only a single functional contact with the

206 humans who are heterozygous for mutations in pol eta may also have an increased risk of skin cancer.

207 The results with pol eta may be relevant to some mutations previously rep

208 We reasoned that the presence of pol eta may mask the contribution of pol zeta, and there

209 acterize the relationship between AICDA- and POL eta-mediated mutations, 1470 H chain and 1313 kappa-

210 n-induced apoptosis in CSCs, indicating that Pol eta-mediated TLS contributes to the survival of CSCs

211 hat ovarian CSCs have intrinsically enhanced Pol eta-mediated TLS, allowing CSCs to survive cisplatin

212 These data support a model in which pol eta-mediated translesion synthesis past this adduct

213 n comparison to WT mice, adipose tissue from pol eta(-/-) mice exhibits increased DNA damage and a gr

214 llular senescence in the adipose tissue from pol eta(-/-) mice was observed and measured by up-regula

215 Treatment of pol eta(-/-) mice with a p53 inhibitor, pifithrin-alpha,

216 te senescence and metabolic abnormalities in pol eta(-/-) mice.

217 Human DNA polymerase eta (Pol eta) modulates susceptibility to skin cancer by prom

218 BPLF1 promotes a nuclear relocalization of Pol eta molecules which are focus-like in appearance, co

219 Analysis of the pol eta O(6)-PobG products indicated that the insertion

220 ished that synthesis past T or U in a CPD by pol eta occurs in a highly error-free manner, the only i

221 examine the role in Saccharomyces cerevisiae Pol eta of three conserved residues, tyrosine 64, argini

222 e wild-type PCNA stimulates incorporation by pol eta opposite an abasic site, the mutant PCNA protein

223 ast, primer extension reactions catalyzed by pol eta or a truncated form of pol kappa (pol kappaDelta

224 t, during translesion synthesis catalyzed by pol eta or pol kappa nucleotides were incorporated oppos

225 Primer extension catalyzed by pol eta or pol kappa occurred rapidly on the unmodified

226 as observed with pol alpha, while with human pol eta or pol kappa, a fraction of the primers was exte

227 Our results showed that deficiency in Pol eta or Pol zeta, but not Pol kappa or Pol iota, led

228 The efficiency of translesion synthesis by pol eta past Pt-GG adducts was very similar to that obse

229 Human DNA polymerase eta (Pol eta) plays an essential protective role against skin

230 support the hypothesis that in cells lacking Pol eta, Pol iota is responsible for the high frequency

231 cally interact with the Y-family polymerases Pol eta, Pol iota, and Pol kappa, and the Rev1 C terminu

232 Additionally, Pol eta, Pol iota, and Pol zeta, but not Pol kappa, had

233 of wild-type mice to mice lacking functional pol eta, pol iota, or both.

234 om wild-type mice to mice lacking functional pol eta, pol iota, or both.

235 The translesion polymerases Pol eta, Pol zeta, and Rev1 are part of a suite of facto

236 ) has been found to physically interact with Pol eta, Pol zeta, and Rev1, suggesting a possible role

237 was faithfully inserted across the ICL-G by Pol eta, Pol zeta, and Rev1-Pol zeta.

238 The data suggest that pol eta preferentially synthesizes a repair patch on the

239 Mass spectrometry analysis of all of the pol eta primer extension products indicated multiple com

240 Targeting Pol eta, probably through enhancement of miR-93 expressi

241 Thus, the pol eta products yielded frame-shifts with the N 2 but n

242 Pol eta promoted incorporation of dAMP and dCMP at the d

243 lecular basis of XP-V worldwide, we measured pol eta protein in skin fibroblasts from putative XP-V p

244 t that BPLF1 interacts with Pol eta and that Pol eta protein levels are increased in the presence of

245 ree cell strains with undetectable levels of pol eta protein, indicating that nonsense-mediated messa

246 oligonucleotide (a six-mer in our study) by Pol eta providing a barrier to further elongation of the

247 merases (Pols): Rev1, Pol zeta (Rev3/7), and Pol eta (Rad30), all with human homologs.

248 ises UV-induced PCNA mono-ubiquitylation and Pol eta recruitment to stalled replication forks.

249 using modified nucleotide analogs show that pol eta relies heavily on hydrogen-bonding interactions

250 Overall, these results show that Pol eta replicates through 8-oxoG without any barriers i

251 Together, these data show that pol eta represents an important determinant of cellular

252 X-ray crystal structures revealed that two pol eta residues, Phe-18 and Tyr-92, behave as steric ga

253 Knockdown of Pol eta resulted in decreased production of infectious v

254 ealed that CRISPR-Cas9-mediated depletion of Pol eta resulted in significant drops in bypass efficien

255 elta and pol epsilon with the TLS pol theta, pol eta, Rev1, pol zeta and, perhaps, pol iota, which ar

256 tic analyses for nucleotide incorporation by pol eta showed that the 3'-cytosine moiety of the cross-

257 alyses for nucleotide incorporation by yeast pol eta showed that the 5'-guanine portion of the lesion

258 In contrast, pol eta shows a combination of high efficiency and low f

259 In reactions catalyzed by pol eta, small amounts of dAMP misincorporation and one-

260 a tendency to stall before the ICL, whereas Pol eta stalled just after insertion across the ICL.

261 at the interaction between MSH2-MSH6 and DNA pol eta stimulates synthesis of mutations at bases locat

262 s with an increased rate of incorporation by pol eta, suggesting a systematic relationship between th

263 esion synthesis (TLS) by DNA polymerase eta (pol eta) suppresses ultraviolet light-induced mutagenesi

264 ficient than Pol delta, and following bypass Pol eta switches to less processive synthesis, similar t

265 e also demonstrate that both yeast and human pol eta synthesize past the 3'-(m)C CPD in a >99% error-

266 anced pro-mutagenic replication catalyzed by pol eta that couples efficient incorporation of damaged

267 ate the existence of a hydrophobic pocket in pol eta that participates in the increased utilization o

268 With pol eta, the bypass frequency past the dA x dG-N2-TAM pa

269 nd sequence specificity of dPMP insertion by pol eta, the kinetics of dPMP insertion opposite various

270 structural element for Pol zeta and not for Pol eta, these observations have raised the possibility

271 base inhibit incorporation and extension by pol eta to a lesser extent than their R counterparts.

272 ant (XP-V) which is linked to the ability of pol eta to accurately bypass UV-induced cyclobutane pyri

273 complex suggests unique features that allow pol eta to efficiently bypass CPDs.

274 Consistent with the ability of Pol eta to efficiently bypass UV light-induced cyclobuta

275 NA-Interacting Protein motif is required for pol eta to function in lagging strand synthesis.

276 at K164 of PCNA is not required in vitro for pol eta to gain access to replication complexes at forks

277 omplete bypass of cisplatin lesions requires Pol eta to insert dCTP opposite the 3' guanine and Pol z

278 ve quantitative evidence that the binding of pol eta to PCNA and the ensuing TLS are both independent

279 This ability of Pol eta to sense the dimer location as synthesis proceed

280 inated PCNA recruits TLS polymerases such as pol eta to sites of DNA damage where they may also displ

281 oubiquitylation of PCNA, and localization of Pol eta to UV damage.

282 tment of the specialized DNA polymerase eta (pol eta) to replication-associated foci after UV.

283 BV recruits cellular repair factors, such as Pol eta, to sites of viral DNA damage via BPLF1, thereby

284 There was no involvement, however, for the Pol eta translesion synthesis DNA polymerase, the Mms2-U

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

286 We found that Pol eta undergoes DNA damage- and protein inhibitor of a

287 bility of correct insertion and extension by pol eta was 1000-2000-fold greater than the probability

288 ass frequency past the 4-OHEN-dA lesion with pol eta was at least 2 orders of magnitude higher than t

289 ass frequency past the 4-OHEN-dC lesion with pol eta was at least 3 orders of magnitude higher than t

290 production of infectious virus, and further, Pol eta was found to bind to EBV DNA, suggesting that it

291 it competition assays, the catalytic core of pol eta was found to insert dGMP opposite the mC of the

292 Pol eta was undetectable in cells from patients in eight

293 Saccharomyces cerevisiae DNA polymerase eta (pol eta) was able to replicate past the cross-link lesio

294 Saccharomyces cerevisiae DNA polymerase eta (pol eta) was able to replicate past the cross-link lesio

295 geometry in the selection of nucleotides by pol eta, we determined the insertion efficiencies of the

296 increase error-prone synthesis catalyzed by pol eta when replicating 8-oxo-G.

297 are consistent with a pro-mutagenic role for pol eta when replicating this DNA lesion.

298 Moreover, we found that the C-terminus of pol eta, which contains a PCNA-Interacting Protein motif

299 ss functioning to curtail the interaction of Pol eta with PCNA at damaged DNA to prevent harmful muta

300 ibe the interaction of the catalytic core of pol eta with primer-templates containing bulge structure