ライフサイエンスコーパス: Pol

1 Pol alpha is enriched at extending Okazaki fragments of

2 Pol beta also was able to perform intersegmental transfe

3 Pol delta, like bacterial replicases, undergoes collisio

4 Pol epsilon contains two flexibly tethered lobes.

5 Pol epsilon has greater contact with the nascent single-

6 Pol II elongation rates of 2.4-3.0 kb/min were observed,

7 Pol III inhibition affects gene reactivation status alon

8 Pol III regulation is thus sensitive to environmental cu

9 Pol IV transcription is considerably more error-prone th

10 The active VSG gene is in a Pol I-transcribed telomeric expression site (ES).

11 This demonstrates the essentiality of a Pol I-transcribed ES, as well as conserved VSG 3'UTR 16-

12 ith the synthesis of one RNA molecule across Pol II genes, suggesting multiple rounds of pre-initiati

13 Binding of initiation factor Rrn3 activates Pol I, fostering recruitment to ribosomal DNA promoters.

14 erases alpha, delta, and epsilon (Pol alpha, Pol delta, and Pol epsilon), are responsible for eukaryo

15 three replicative DNA polymerases Pol alpha, Pol delta, and Pol epsilon; and canonical maturation of

16 Finally, we tested a model that altered Pol II activity sensitizes cells to nucleotide depletion

17 In contrast, although Pol delta contacts the nascent lagging strands of active

18 Furthermore, while the loading of clamp and Pol IIIcore is highly organized, the exchange with the t

19 places the leading Pol epsilon below CMG and Pol alpha-primase at the top of CMG at the replication f

20 elta, and epsilon (Pol alpha, Pol delta, and Pol epsilon), are responsible for eukaryotic genome dupl

21 ve DNA polymerases Pol alpha, Pol delta, and Pol epsilon; and canonical maturation of Okazaki fragmen

22 mRNA counts, Pol II density and Pol II firing rates of the Ccnb1 promoter transgene rese

23 ated by two DNA polymerases, Pol epsilon and Pol delta, that function on the leading and lagging stra

24 f viral DNA replication and that Pol eta and Pol kappa play an important role in HBoV1 DNA replicatio

25 regulate stage-specific gene expression and Pol II pausing will contribute to our continuous search

26 with the translesion polymerases Pol II and Pol IV.

27 suggesting that transcription initiation and Pol II release are the key determinants of gene control

28 nal multisubunit RNA polymerases, Pol IV and Pol V, which synthesize noncoding RNAs that coordinate R

29 n the non-coding RNAs produced by Pol IV and Pol V.

30 onents consisting of polymerases (Pol mu and Pol lambda), a nuclease (the Artemis.DNA-PKcs complex),

31 sh2-Msh3), Exo1, RPA, RFC-Delta1N, PCNA, and Pol epsilon was found to catalyze an MMR reaction that r

32 sh2-Msh3), Exo1, RPA, RFC-Delta1N, PCNA, and Pol epsilon was found to catalyze both short-patch and l

33 de occurs by reduced binding of RARalpha and Pol-II at the Fgf21 promoter.

34 oximal pausing, while Pol II recruitment and Pol II pausing are not correlated among non-NL genes.

35 ciency in mitochondrial extracts from APTX-/-Pol beta-/- cells.

36 teins to be recruited to the lesion-arrested Pol II during the initiation of eukaryotic TCR.

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

38 transcript release from chromatin-associated Pol II.

39 DNA polymerase beta (Pol beta), a member of the DNA polymerase X family that

40 found that Mediator, in addition to binding Pol II promoters, occupies chromosomal interacting domai

41 ereby Cdc45-Mcm2-7-GINS (CMG) helicase binds Pol epsilon and tethers it to the leading strand, and PC

42 Thus, CBP directly stimulates both Pol II recruitment and the ability to traverse the first

43 h reduced catalytic efficiency and that both Pols exhibit a high propensity for inserting a wrong nt

44 of the DNA synthesis domain in the CMG-bound Pol epsilon.

45 ilon binds CMG with a Kd value of 12 nM, but Pol delta binding CMG is undetectable.

46 span; in flies, longevity can be achieved by Pol III inhibition specifically in intestinal stem cells

47 we show that removal of the 5'-dRP block by Pol beta is unaffected by NCP constraints at all sites t

48 t these regions can be scanned for damage by Pol beta.

49 mechanisms of damage search and location by Pol beta are largely unknown, but are critical for under

50 h changes in the non-coding RNAs produced by Pol IV and Pol V.

51 we report the structure of the S. cerevisiae Pol II-Rad26 complex solved by cryo-electron microscopy.

52 ltiple permutations of the reconstituted CMG-Pol epsilon assembly.

53 Based on their subunit compositions, Pols IV and V clearly evolved as specialized forms of Po

54 By contrast, Pol V exhibits high fidelity transcription, similar to P

55 mRNA counts, Pol II density and Pol II firing rates of the Ccnb1 prom

56 e the consequences of increased or decreased Pol II catalysis on gene expression in Saccharomyces cer

57 DNA polymerase delta (Pol delta) is thought to catalyze DNA synthesis to fill

58 hich causes defects in DNA polymerase delta (Pol delta) proofreading (pol3-01) and nucleotide selecti

59 nts of polymerase binding to CMG demonstrate Pol epsilon binds CMG with a Kd value of 12 nM, but Pol

60 t in this case, Runt prevents PESE-dependent Pol II recruitment and preinitiation complex (PIC) assem

61 ly, mNET-seq patterns specific for different Pol II CTD phosphorylation states reveal weak co-transcr

62 (Pol II) recruitment levels tend to display Pol II promoter-proximal pausing, while Pol II recruitme

63 new model for how TCS mutations may disrupt Pol I and III complex integrity.

64 compared the ability of three homologous DNA Pol X family members to perform a processive search for

65 f the vertebrate replisome that includes DNA Pol epsilon is retained on DNA.

66 enzymatic activities of the replicative DNA Pol III are well understood, its dynamics within the rep

67 ive searching ability observed among the DNA Pol X family members correlated with their proposed biol

68 ision release process is triggered, ejecting Pol delta on the leading strand.

69 s economy of design enables Rtt103 to engage Pol II at distinct sets of genes with differentially enr

70 oteins leads to strong depletion of enhancer Pol II occupancy and eRNA synthesis, concomitant with do

71 ases, polymerases alpha, delta, and epsilon (Pol alpha, Pol delta, and Pol epsilon), are responsible

72 rts a model in which DNA polymerase epsilon (Pol epsilon) carries out the bulk of leading strand DNA

73 n has suggested that DNA polymerase epsilon (Pol epsilon) may also play a role in MMR.

74 The replicative DNA polymerase epsilon (Pol epsilon) was shown to activate the S-phase checkpoin

75 nes, POLR1C and POLR1D, encode for essential Pol I/III subunits that form a heterodimer necessary for

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

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

78 tly of mRNA-capping activity in facilitating Pol II's engagement in transcriptional elongation, thus

79 Some promoters have a strong disposition for Pol II pausing and often mediate faster, more synchronou

80 phila melanogaster CTD that is essential for Pol II function in vivo and capitalize on natural sequen

81 restingly, CBP activity is rate limiting for Pol II recruitment to these highly paused promoters thro

82 bunits that form a heterodimer necessary for Pol I/III assembly, and many TCS mutations lie along the

83 on, similar to Pol II, suggesting a need for Pol V transcripts to faithfully reflect the DNA sequence

84 x on transcribed genes when RNA emerges from Pol II, and that loss of EF-RNA interactions upon RNA cl

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

86 processing of HIV-1 polyproteins Gag and Gag-Pol, resulting in immature virions.

87 ssing clade C(CN54) HIV-1 Env(gp120) and Gag-Pol-Nef antigens (NYVAC-C) showed limited immunogenicity

88 h Ad35/Ad26 vectors expressing SIVmac239 Gag/Pol/Env with or without an AS01B-adjuvanted SIVmac32H gp

89 Here we report global Pol III expression/methylation profiles and molecular me

90 Hence, Pol III is a pivotal mediator of this key nutrient-signa

91 Whereas higher Pol III occupancy during the night reflects a MAF1-depen

92 e present the crystal structure of the human Pol B-subunit (p59) in complex with CTD of the catalytic

93 1C and POLR1D) involved in RNA polymerase I (Pol I) transcription account for more than 90% of diseas

94 the selective inhibitor of RNA polymerase I (Pol I) transcription, CX-5461, effectively treats aggres

95 ed a processive search assay to determine if Pol beta has evolved a mechanism for efficient DNA damag

96 Here we employ a set of RNA Polymerase II (Pol II) activity mutants to determine the consequences o

97 Phosphorylation of the RNA polymerase II (Pol II) C-terminal domain (CTD) regulates transcription

98 of Rpb1, a subunit of the RNA polymerase II (Pol II) complex, and therefore hampers global cellular t

99 al inhibitor studies that RNA polymerase II (Pol II) elongation is important for establishing memory

100 Transcription by RNA polymerase II (Pol II) is dictated in part by core promoter elements, w

101 Elongation of RNA polymerase II (Pol II) is thought to be an important mechanism for regu

102 minal domain (CTD) of the RNA polymerase II (Pol II) large subunit cycles through phosphorylation sta

103 of the largest subunit of RNA polymerase II (Pol II) orchestrates dynamic recruitment of specific cel

104 RNA polymerase II (Pol II) pauses downstream of the transcription initiatio

105 ent and the regulation of RNA polymerase II (Pol II) pausing.

106 metazoans is regulated by RNA polymerase II (Pol II) promoter-proximal pausing and its release.

107 tive NL genes with higher RNA polymerase II (Pol II) recruitment levels tend to display Pol II promot

108 at many steps, including RNA polymerase II (Pol II) recruitment, transcription initiation, promoter-

109 The RNA polymerase II (Pol II) transcription elongation factor, Elongin A (EloA

110 Termination of RNA polymerase II (Pol II) transcription is an important step in the transc

111 mechanistic by-product of RNA polymerase II (Pol II) transcription or biologically meaningful.

112 m the mammalian genome by RNA polymerase II (Pol II) transcription.

113 clusively associated with RNA polymerase II (Pol II)-transcribed genes, but is not an unambiguous mar

114 at block translocation of RNA polymerase II (Pol II).

115 promoter-proximal paused RNA polymerase II (Pol II).

116 BocaSR is transcribed by RNA polymerase III (Pol III) from an intragenic promoter at levels similar t

117 RNA polymerase III (Pol III) transcribes medium-sized non-coding RNAs (colle

118 ransposon transcribed by RNA polymerase III (Pol III).

119 and P587L substitutions functionally impair Pol gamma, with greater pathogenicity predicted for the

120 ults demonstrate that the [4Fe4S] cluster in Pol delta can act as a redox switch for activity, and we

121 to 1-10%) in the isogenic cells deficient in Pol kappa, Pol iota or Pol zeta, suggesting the mutual i

122 hown to enter the nucleus and participate in Pol II transcription.

123 We find that a reduction in Pol III extends chronological lifespan in yeast and orga

124 s of many of the amino acid substitutions in Pol delta resemble those of previously identified antimu

125 plexes, followed by the assembly of inactive Pol I homodimers.

126 onal splicing and poly(A) signal-independent Pol II termination of lincRNAs as compared to pre-mRNAs.

127 Hyper-methylation of Pol III genes inhibits Pol III binding to DNA via inducing repressed chromatin

128 nds on the plant-specific RNA polymerase IV (Pol IV), and ARGONAUTE4 (AGO4) is a major het-siRNA effe

129 , and found a coactivator role of MTA1/c-Jun/Pol II coactivator complex upon the IGFBP3 transcription

130 DNA polymerase kappa (Pol kappa), which has been implicated in both nucleotide

131 lymerase eta [Pol eta] and polymerase kappa [Pol kappa]) are recruited to the viral DNA replication c

132 n the isogenic cells deficient in Pol kappa, Pol iota or Pol zeta, suggesting the mutual involvement

133 -tier ahead of the C-tier places the leading Pol epsilon below CMG and Pol alpha-primase at the top o

134 Moreover, Pol I dimers also form after inhibition of either riboso

135 In contrast to model predictions, mutated Pol II retains normal sensitivity to altered nucleotide

136 zation of either Rrn7 N-terminal domain near Pol I wall or the tandem winged helix domain of A49 at a

137 with the intersegmental searching ability of Pol beta being at least 6- and approximately 2-fold high

138 ths, the intramolecular searching ability of Pol beta is at least 4-fold higher than that of Pol mu a

139 ghly resistant to dilution in the absence of Pol III* in solution.

140 te, hydrogen peroxide causes accumulation of Pol II near promoters and enhancers that can best be exp

141 leading to promoter-proximal accumulation of Pol II.

142 ion, PKL is required for the accumulation of Pol V-dependent transcripts and for the positioning of P

143 levels of dNTPs in vivo, and the activity of Pol epsilon is compromised more than lagging-strand poly

144 Inhibiting the activity of Pol III in the gut of adult worms or flies is sufficient

145 y; the growth-promoting anabolic activity of Pol III mediates the acceleration of ageing by TORC1.

146 ch, which was associated with alterations of Pol II-CTD phosphorylation at the target loci.

147 deprivation, cells induce rapid clearance of Pol I-Rrn3 complexes, followed by the assembly of inacti

148 ures of pre- and post-catalytic complexes of Pol mu with a ribonucleotide bound at the active site.

149 The size and complexity of Pol II, TFIID, and TFIIH have precluded their reconstitu

150 The evolutionary conservation of Pol III affirms its potential as a therapeutic target.

151 functional fusion of the endogenous copy of Pol IV to the photoactivatable fluorescent protein PAmCh

152 ing a novel function for the lyase domain of Pol beta.

153 mutations affecting the polymerase domain of Pol epsilon trigger ATR-dependent signaling leading to S

154 ila CBP inhibition results in "dribbling" of Pol II from the pause site to positions further downstre

155 disassembly before productive elongation of Pol II is achieved at most genes in the yeast genome.

156 1 and consequently reduces the engagement of Pol II in transcriptional elongation, leading to promote

157 ranscription that enhances the engagement of Pol II into transcriptional elongation) to the coding se

158 se data suggest that the repair footprint of Pol beta mainly resides within accessible regions of the

159 nd V clearly evolved as specialized forms of Pol II, but their catalytic properties remain undefined.

160 Intriguingly, a significant fraction of Pol III transcription from non-coding regions is not sub

161 ent apoptotic cell death), the inhibition of Pol I transcription also demonstrates potent efficacy in

162 Most strikingly, the acute inhibition of Pol I transcription reduces both the leukemic granulocyt

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

164 Surprisingly, we find that the mechanism of Pol IV recruitment is dependent on the type of DNA lesio

165 ylation profiles and molecular mechanisms of Pol III regulation that have not been as extensively stu

166 Hyper-methylation of Pol III genes inhibits Pol III binding to DNA via induci

167 Pase domain promotes the forward movement of Pol II, and elucidate key roles for Rad26 in both TCR an

168 P-seq allowed transcriptional orientation of Pol II to be determined, which may be useful near promot

169 ssays following electrochemical oxidation of Pol delta reveal a significant slowing of DNA synthesis

170 Similar to Polalpha, p261C of Pol contains a three-helix bundle in the middle and zinc

171 ndent transcripts and for the positioning of Pol V-stabilized nucleosomes at several tested loci, ind

172 environmental cues, yet a diurnal profile of Pol III transcription activity is so far lacking.

173 Here we describe the reconstitution of Pol epsilon-dependent MMR using S. cerevisiae proteins.

174 TFIIIB is required for recruitment of Pol III and to promote the transition from a closed to a

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

176 MAF1 is a repressor of Pol III transcription whose activity is controlled by ph

177 1-dependent response to feeding, the rise of Pol III occupancy before the onset of the night reflects

178 er, our results demonstrate that the role of Pol epsilon in replicative stress sensing is conserved i

179 f protein-coding genes has left the roles of Pol III in organismal physiology relatively unexplored.

180 and approximately 2-fold higher than that of Pol lambda.

181 beta is at least 4-fold higher than that of Pol mu and approximately 2-fold higher than that of Pol

182 eals that Rad26 binds to the DNA upstream of Pol II, where it markedly alters its path.

183 and approximately 2-fold higher than that of Pols mu and lambda, respectively.

184 cted DNA methylation, but does not depend on Pol IV.

185 mote the transition from a closed to an open Pol III pre-initiation complex, a process dependent on t

186 ic cells deficient in Pol kappa, Pol iota or Pol zeta, suggesting the mutual involvement of multiple

187 iffers from B-subunits of either Polalpha or Pol.

188 PIP-seq detected divergently oriented Pol II at both coding and noncoding promoters, as well a

189 of UBF, Ser388 phosphorylated UBF, and other Pol I-related components (POLR1E, TAF1A, and TAF1C) rema

190 tuated within the middle of the BER pathway, Pol beta must efficiently locate its substrates before d

191 anscription factors, PcG proteins and paused Pol II states, these data identify a two-step mechanism

192 ption pausing factor M1BP, containing paused Pol II and enriched with promoter-proximal Polycomb Grou

193 ong support for the residence time of paused Pol II elongation complexes being much shorter than esti

194 ression by controlling the release of paused Pol II in a PAF1-dependent manner.

195 tor 1 (PAF1) modulates the release of paused Pol II into productive elongation.

196 d enhancers attenuates the release of paused Pol II on PAF1 target genes without major interference i

197 P and GAGA factor have high levels of paused Pol II, a unique chromatin signature, and are highly exp

198 uction in PcG binding, the release of paused Pol II, increases in promoter H3K4me3 histone marks and

199 of RNA polymerase II at the promoter (paused Pol II) has emerged as a widespread and conserved mechan

200 We propose that paused Pol II helps prevent new initiation between transcriptio

201 e findings reveal a common core to pervasive Pol II initiation throughout the human genome.

202 s through interaction with S2-phosphorylated Pol II and nascent RNA.

203 es include four members: Polalpha, Poldelta, Pol, and Polzeta, which share common architectural featu

204 ge of the E. coli replicative DNA polymerase Pol IIIcore with the translesion polymerases Pol II and

205 k H3K9me2 and by reduction in RNA polymerase Pol II occupancy.

206 promised more than lagging-strand polymerase Pol delta at low dNTP concentrations in vitro.

207 ster in Saccharomyces cerevisiae polymerase (Pol) delta, the lagging strand DNA polymerase.

208 DNA polymerase (Pol) beta maintains genome fidelity by catalyzing DNA sy

209 of oxidative stress response DNA polymerase (Pol) lambda caused by hyperactive HUWE1 p.R4187C.

210 own of the nuclear-encoded mtDNA polymerase (Pol gamma-alpha), Tamas, produces a more complete block

211 While depletion of polymerase (Pol) eta did not perturb the bypass efficiency of the le

212 ting their capacity to stall RNA polymerase (Pol) II and trigger transcription-coupled nucleotide exc

213 scription through chromatin, RNA polymerase (Pol) II associates with elongation factors (EFs).

214 arboxy-terminal domain (CTD) RNA polymerase (Pol) II formation on the promoters of IRF1, IRF7, and RI

215 ion of gene transcription by RNA polymerase (Pol) III requires the activity of TFIIIB, a complex form

216 helicase and the leading-strand polymerase, Pol epsilon, form a stable assembly.

217 nds by the three replicative DNA polymerases Pol alpha, Pol delta, and Pol epsilon; and canonical mat

218 Pol IIIcore with the translesion polymerases Pol II and Pol IV.

219 ymatic components consisting of polymerases (Pol mu and Pol lambda), a nuclease (the Artemis.DNA-PKcs

220 ks synthesis by replicative DNA polymerases (Pols).

221 primarily replicated by two DNA polymerases, Pol epsilon and Pol delta, that function on the leading

222 two additional multisubunit RNA polymerases, Pol IV and Pol V, which synthesize noncoding RNAs that c

223 l function of the CST complex is its primase-Pol alpha (PP) stimulatory activity.

224 h the Pol alpha N-terminal domain, promoting Pol alpha and delta binding to stalled replication forks

225 upon completing replication, and we propose Pol delta-PCNA collides with the slower CMG, and in the

226 transcription initiation, promoter-proximal Pol II pause release, and transcription termination; how

227 of P-TEFb recruitment and promoter-proximal Pol II pausing.

228 + P587L double variant forms of recombinant Pol gamma.

229 ions, influenced by lesion identity, recruit Pol IV to sites of DNA damage.

230 rapamycin kinase complex 1 (TORC1) regulates Pol III activity, and is also an important determinant o

231 ely studied, using nc886 as a representative Pol III gene.

232 ining Okazaki fragment length by restricting Pol delta progression.

233 RNA Pol II was strongly blocked by a 3d-Napht-A analog but b

234 ogs, into DNA oligonucleotides to assess RNA Pol II transcription elongation in vitro.

235 f DNA alkylation impair transcription by RNA Pol II in cells and with the isolated enzyme and unravel

236 ndently regulates CDK9/phospho-Ser 2 CTD RNA Pol II recruitment to the IRF3-dependent IFN-stimulated

237 These results show how RNA Pol II copes with minor-groove DNA alkylation and establ

238 2-subunit phosphorylated and inactivated RNA Pol I (polymerase I)-associated transcription factor TIF

239 is a higher level of CTD Ser2P modified RNA Pol II near CTCF peaks relative to the Ser5P form in the

240 iption by facilitating the elongation of RNA Pol II and preventing silenced chromatin on the viral ge

241 Ankrd26 promoter and loss of binding of RNA Pol II at the Ankrd26 Transcription Start Site (TSS).

242 2P but increased Ser5P modified forms of RNA Pol II on viral genes.

243 he isolated enzyme and unravel a mode of RNA Pol II stalling that is due to alkylation of DNA in the

244 Here we tested the contributions of the RNA Pol II pre-initiation complex (PIC), mediator and cohesi

245 hibitory activity of SBVDeltaNoLS toward RNA Pol II transcription is impaired.

246 ter gene are increased in both fast and slow Pol II mutant strains and the magnitude of half-life cha

247 ne expression defects for both fast and slow Pol II mutants.

248 wer CMG, and in the absence of a stabilizing Pol delta-CMG interaction, the collision release process

249 m-sized non-coding RNAs (collectively termed Pol III genes).

250 iption is considerably more error-prone than Pols II or V, which may be tolerable in its synthesis of

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

252 r establishing memory in this model but that Pol II itself is not retained as part of the memory mech

253 These results demonstrate that Pol epsilon can act in eukaryotic MMR in vitro.

254 We find that Pol delta bound to DNA is indeed redox-active at physiol

255 ly developed ChIP-nexus method, we find that Pol II pausing inhibits new initiation.

256 We find that Pol IV is strongly enriched near sites of replication on

257 This raises the possibility that Pol III is involved in ageing.

258 These structures reveal that Pol mu binds and incorporates a rNTP with normal active

259 into nucleosome core particles revealed that Pol beta is not processive in the context of a nucleosom

260 These assays revealed that Pol beta scans DNA using a processive hopping mechanism

261 Previous studies show that Pol delta is slow and distributive with CMG on the leadi

262 Our studies show that Pol II pausing is an important contributor to BRCA1-asso

263 Here we show that Pol III limits lifespan downstream of TORC1.

264 We then show that Pol III occupancy of its target genes rises before the o

265 Previously, we showed that Pol II-associated factor 1 (PAF1) modulates the release

266 These results suggest that Pol III transcription is involved in chromatin structure

267 essed chromatin and is a determinant for the Pol III repertoire.

268 eous levels of VSG117 were obtained from the Pol I-transcribed rDNA.

269 s 24 proteins, forming the CMG helicase, the Pol epsilon DNA polymerase, the RFC clamp loader, the PC

270 actively threading the downstream DNA in the Pol II PIC.

271 matin association of many EFs, including the Pol II serine 2 kinases Ctk1 and Bur1 and the histone H3

272 with different conformational states of the Pol I cleft, in addition to the stabilization of either

273 The lack of structures of CSB or the Pol II-CSB complex has hindered our ability to address t

274 Production of snR-DPGs required the Pol II snRNA promoter (PIIsnR), and CPL4RNAi plants show

275 Here, we test the accepted view that the Pol III holoenzyme remains stably associated within the

276 labeled polymerases to demonstrate that the Pol III* complex (holoenzyme lacking the beta2 sliding c

277 h fluorescence microscopy, we found that the Pol III* subassembly frequently disengages from the repl

278 Rad51 directly interacts with the Pol alpha N-terminal domain, promoting Pol alpha and del

279 n of the three states in this study with the Pol II system suggests that a ratchet motion of the Core

280 vered that PR physically associated with the Pol III holoenzyme.

281 zed the roles of translesion synthesis (TLS) Pols in the replication of 3-MeA-damaged DNA in human ce

282 mational change for nucleic acid delivery to Pol alpha and subsequent DNA synthesis.

283 transcription, with M1BP binding leading to Pol II recruitment followed by AbdA targeting, which res

284 o chromatin regions that are in proximity to Pol II and are highly associated with transcripts abunda

285 bits high fidelity transcription, similar to Pol II, suggesting a need for Pol V transcripts to faith

286 ating cell nuclear antigen) binds tightly to Pol delta and recruits it to the lagging strand.

287 crosslink to RNA emerging from transcribing Pol II in the yeast Saccharomyces cerevisiae.

288 ontributes to EF recruitment to transcribing Pol II.

289 ivate gene transcription, themselves undergo Pol II-mediated transcription, but our understanding of

290 Unexpectedly, Pol II transcription of the transgene was required for e

291 owing nt insertion by an as yet unidentified Pol.

292 GED METHYLASE 2 (DRM2) and RNA polymerase V (Pol V), two main actors of RNA-directed DNA methylation,

293 When Pol III genes are hypo-methylated, MYC amplifies their t

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

295 cesses, including base excision repair where Pol beta catalyzes two key enzymatic steps: 5'-dRP lyase

296 While Pol is the most conserved HIV sequence, its association

297 play Pol II promoter-proximal pausing, while Pol II recruitment and Pol II pausing are not correlated

298 t known to rely on Thr4 for association with Pol II.

299 f the PCF11 CID weakens its interaction with Pol II.

300 trimeric HIV-1 gp140 protein or a Gag(ZM96)-Pol-Nef(CN54) polyprotein as Gag-derived virus-like part