ライフサイエンスコーパス: PCNA

1 PCNA enhanced the nucleotide incorporation rate by >10 f

2 PCNA has two structurally similar domains (I and II) lin

3 PCNA inhibition by competing peptides or by T2AA, a smal

4 PCNA interacts with all of these subunits, but only the

5 PCNA is a pivotal component of the replication fork mach

6 ogether, these results reveal that the CAF-1-PCNA nucleosome assembly pathway plays an important role

7 IL-10, PCNA, and insulin expression were increased in the LADA

8 ication (Ku70-Ku80, DNA-PKcs, PARP1, MCM2-7, PCNA, RPA1) and RNA metabolism (RNA helicases, PRP19, p5

9 the C-terminus of pol eta, which contains a PCNA-Interacting Protein motif is required for pol eta t

10 Here, we show that FAM111A, a PCNA-interacting protein, plays an important role in mit

11 This activity requires a PCNA-interacting protein (PIP) motif located within the

12 Here, we report that SDE2, a PCNA-associated protein, plays a key role in maintaining

13 DNA structures did not affect PCNA unloading activity of ATAD5-RLC.

14 ream activity of DNA PKcs, without affecting PCNA ubiquitylation levels in unperturbed cells.

15 This arrangement allows PCNA to thread and stabilize the DNA exiting the catalyt

16 glycosylation following CrP treatment; also, PCNA and vimentin (SMC synthetic marker) expression were

17 Ctf18-RFC is an alternative PCNA loader that links all these processes together by a

18 Although PCNA interacts with the enzymes DNA polymerase delta (Po

19 APE1 interacts with APE2 and PCNA, although PCNA is dispensable for APE1's exonuclease activity.

20 Our results suggest that although PCNA is much more competitive than XPA in binding replic

21 lencing suppressed LPS-induced TNF-alpha and PCNA increases in human cells.

22 S stimulation in vivo, hepatic TNF-alpha and PCNA responses subsided in Nox4-deficient mice compared

23 angiogenic genes (VEGF, bFGF, TNF-alpha and PCNA) were up-regulated as well.

24 In addition, APE1 interacts with APE2 and PCNA, although PCNA is dispensable for APE1's exonucleas

25 n neurogenic niches revealed by the BLBP and PCNA immunostaining.

26 nd decreased MCM2-7 replication helicase and PCNA associated with chromatins.

27 metry, topoisomerases IIalpha and IIbeta and PCNA were noteworthy.

28 luding topoisomerases IIalpha and IIbeta and PCNA, which were found associated with nascent DNA.

29 oliferating cells (assessed by both Ki67 and PCNA) but also express a number of common dental stem ce

30 isolated a complex formed between NEIL1 and PCNA (+/-DNA) using size exclusion chromatography (SEC).

31 Repair factors, PARP1 and PCNA, were immediately recruited to the site of damage,

32 is attenuated by PCNA mutants PCNA-R14E and PCNA-D150E that spontaneously fall off DNA.

33 The introduction of RPA and PCNA influenced PolB and PolD in similar ways, yet provi

34 on and tethers it to the leading strand, and PCNA (proliferating cell nuclear antigen) binds tightly

35 ic data showing the requirement for SUMO and PCNA binding for the SDSA role of Srs2, Srs2 displays a

36 133, and 250 in PCNA as IGF-1R targets, and PCNA phosphorylation was followed by mono- and polyubiqu

37 quently, proliferating cell nuclear antigen (PCNA) activates MutLalpha to nick the error-containing s

38 ication, proliferating cell nuclear antigen (PCNA) adopts a ring-shaped structure to promote processi

39 -induced proliferating cell nuclear antigen (PCNA) and FANCD2 monoubiquitinations (surrogate markers

40 binds to proliferating cell nuclear antigen (PCNA) and functions in genome replication, repair, and r

41 (Pax7), proliferating cell nuclear antigen (PCNA) and nicotinamide phosphoribosyltransferase (Nampt)

42 roteins, Proliferating Cell Nuclear Antigen (PCNA) and Replication Protein A (RPA), which are critica

43 ntaining proliferating cell nuclear antigen (PCNA) and two non-classical DNA polymerases, Rev1 and DN

44 and the proliferating cell nuclear antigen (PCNA) are additional components of the nuclease ensemble

45 ng clamp proliferating cell nuclear antigen (PCNA) are both essential and play critical roles in seve

46 fied the proliferating cell nuclear antigen (PCNA) as a nIGF-1R-binding partner.

47 n factor proliferating cell nuclear antigen (PCNA) can be conjugated to either the small ubiquitinlik

48 eaction: proliferating cell nuclear antigen (PCNA) clamp binding/opening/closure/release, ptDNA bindi

49 A-loaded proliferating cell nuclear antigen (PCNA) for activation.

50 ion with proliferating cell nuclear antigen (PCNA) for nucleosome assembly, participates in the estab

51 Proliferating cell nuclear antigen (PCNA) forms a trimeric ring that encircles duplex DNA an

52 Proliferating cell nuclear antigen (PCNA) is a sliding clamp that acts as a central co-ordin

53 Proliferating cell nuclear antigen (PCNA) lies at the center of the faithful duplication of

54 elies on proliferating cell nuclear antigen (PCNA) monoubiquitylation and is regulated at several lev

55 CDK) and proliferating cell nuclear antigen (PCNA) onto chromatin, as well as initiation and elongati

56 Proliferating cell nuclear antigen (PCNA) recruits Pol delta to the DNA and serves as a proc

57 d to the proliferating cell nuclear antigen (PCNA) replicates the lagging strand and cooperates with

58 ation of proliferating cell nuclear antigen (PCNA) sliding clamps encircling damaged DNA.

59 essed by proliferating cell nuclear antigen (PCNA) staining was also higher.

60 target, proliferating cell nuclear antigen (PCNA) to elicit rapid and robust PCNA degradation and as

61 ation of Proliferating Cell Nuclear Antigen (PCNA) ubiquitylation after UV requires the upstream acti

62 oenzyme, proliferating cell nuclear antigen (PCNA), a homotrimeric DNA sliding clamp and polymerase p

63 bed that proliferating cell nuclear antigen (PCNA), a nuclear scaffolding protein pivotal in DNA synt

64 or human proliferating cell nuclear antigen (PCNA), a small ubiquitin-like modifier (SUMO)-targeted s

65 f Cdc45, proliferating cell nuclear antigen (PCNA), and polymerase delta, but not ORC and MCM protein

66 cts with proliferating cell nuclear antigen (PCNA), Rev1, ubiquitin and ubiquitinated-PCNA and is als

67 n marker proliferating cell nuclear antigen (PCNA), the anti-inflammatory cytokine interleukin (IL) 1

68 tment of proliferating cell nuclear antigen (PCNA), the platform for assembly of the DNA replication

69 Proliferating cell nuclear antigen (PCNA), the processivity factor for DNA replication, play

70 evels of proliferating cell nuclear antigen (PCNA), vascular endothelial growth factor (VEGF), and os

71 BrdU and proliferating cell nuclear antigen (PCNA)-reactive cells showed that, in comparison with the

72 y factor proliferating cell nuclear antigen (PCNA).

73 t of the proliferating cell nuclear antigen (PCNA).

74 eric proliferating cellular nuclear antigen (PCNA).

75 pha, and proliferating cell nuclear antigen (PCNA).

76 i and the proliferating cell nuclear antigen(PCNA) protein have a high level of proximity and are cor

77 Our results provide evidence for an archaeal PCNA 'tool-belt' recruitment model of multienzyme functi

78 DNA polymerase eta, have two architectures: PCNA tool belts and Rev1 bridges.

79 MutLalpha interaction with PCNA, as well as PCNA-dependent activation of MutLalpha endonuclease, PCN

80 suggest that Ctf18-RFC enriches and balances PCNA levels at the replication fork, beyond the needs of

81 observe the complex in a conformation before PCNA opening, with the clamp loader ATPase modules formi

82 HMCES acts at replication forks, binds PCNA and single-stranded DNA, and generates a DNA-protei

83 pa and the PIP motif of yeast Msh6 bind both PCNA and Rev1.

84 ator phenotype of elg1Delta is attenuated by PCNA mutants PCNA-R14E and PCNA-D150E that spontaneously

85 lg1Delta mutator phenotype is exacerbated by PCNA mutants that accumulate on DNA due to enhanced elec

86 ng eukaryotic replication is orchestrated by PCNA ubiquitination.

87 s a genome surveillance protein regulated by PCNA, a DNA clamp and processivity factor at replication

88 Once DNA synthesis has ceased, PCNA must be unloaded.

89 e obtained with the Saccharomyces cerevisiae PCNA sliding clamp, suggesting that KGlu effects are not

90 on unloading of the polymerase sliding clamp PCNA from DNA by Elg1.

91 Here we show that the sliding clamp PCNA is important for crossover-biased resolution.

92 quitylation of the eukaryotic sliding clamp, PCNA, activates a pathway of DNA damage bypass that faci

93 er SUMO1 or SUMO2, but only SUMO2-conjugated PCNA is induced by transcription to facilitate resolutio

94 The number of DCX(+)PCNA(+) cells correlates with functional interactions be

95 The number of DCX(+)PCNA(+) cells is reduced in mild cognitive impairments,

96 umans and down-regulated in mice (e.g. DDB2, PCNA, GADD45A, SESN1, RRM2B, KCNN4, IFI30, and PTPRO).

97 We further define PCNA as a key regulator of ZRANB3 function, which recrui

98 leting replication, and we propose Pol delta-PCNA collides with the slower CMG, and in the absence of

99 However, Saccharomyces cerevisiae Pol delta-PCNA is a rapid and processive enzyme, suggesting that C

100 Msh6 (or Msh2-Msh3), Exo1, RPA, RFC-Delta1N, PCNA, and Pol epsilon was found to catalyze an MMR react

101 Msh6 (or Msh2-Msh3), Exo1, RPA, RFC-Delta1N, PCNA, and Pol epsilon was found to catalyze both short-p

102 Here, we show the distinct PCNA loading or unloading activity of each clamp loader.

103 ucture of the human processive Pol delta-DNA-PCNA complex in the absence and presence of FEN1.

104 sociation and formation of a 1:1:1 NEIL1-DNA-PCNA(monomer) complex.

105 Thus, dynamic PCNA complexes coordinate Okazaki fragment synthesis and

106 1 by Srs2 helicase is required for efficient PCNA loading and restoration of resected DNA As a result

107 maturation, which interferes with efficient PCNA unloading by ATAD5 and subsequent nucleosome deposi

108 umulate on DNA due to enhanced electrostatic PCNA-DNA interactions.

109 endent activation of MutLalpha endonuclease, PCNA- and DNA-dependent activation of MutLalpha ATPase,

110 ring 5' end processing and that LigI engages PCNA at the DNA nick generated by FEN1 and Pol delta.

111 NA path through the CMG helicase-Pol epsilon-PCNA clamp.

112 thesis together with its processivity factor PCNA.

113 one or in the presence of accessory factors (PCNA and RPA) indicates that translesion synthesis occur

114 s are needed to determine possible roles for PCNA and other host proteins detected.IMPORTANCE Poxviru

115 icament lies ahead for the replication fork, PCNA is there to orchestrate the events necessary to han

116 itive than XPA in binding replication forks, PCNA sequestration by progerin may shift the equilibrium

117 In its monoubiquitylated form, PCNA recruits a set of damage-tolerant DNA polymerases f

118 ree" RPA inhibits monoubiquitination of free PCNA by directly interacting with Rad18.

119 tes the rapid dissociation of pol delta from PCNA on stalling at a DNA lesion.

120 al DNA into CMG to exit of daughter DNA from PCNA.

121 Furthermore, PCNA localizes to prospective crossover sites along syna

122 CT116 (HCT116-OxR) cells and that gammaH2AX, PCNA, and FANCD2 monoubiquitinations are induced by oxal

123 findings provide molecular insights into how PCNA is released from chromatin to finalize DNA replicat

124 However, PCNA is also ubiquitinated during normal S-phase progres

125 We show here that human PCNA and MutLalpha interact specifically but weakly in s

126 and NMR studies, has revealed how the human PCNA clamp slides on DNA.

127 lymphocytes by double immunohistochemistry (PCNA-staining) and flow cytometry (BrdU incorporation) r

128 ation of Thr(6) or Tyr(8) on UNG2 can impede PCNA binding without affecting UNG2 catalytic activity o

129 r mutation of Tyr-60, Tyr-133, or Tyr-250 in PCNA abrogated its ubiquitination.

130 icated tyrosine residues 60, 133, and 250 in PCNA as IGF-1R targets, and PCNA phosphorylation was fol

131 tranded DNA formation, leading to defects in PCNA-dependent DNA damage bypass and stalled fork recove

132 en combined with Cac1 mutations deficient in PCNA binding.

133 y employing 293T and RPE1 cells deficient in PCNA ubiquitination, generated through CRISPR/Cas9 gene

134 ns for the plasticity of the binding site in PCNA and reveals how a disease mutation selectively alte

135 estabilizes Rad18 and compromises UV-induced PCNA mono-ubiquitylation and Pol eta recruitment to stal

136 ink this phenotype to AKT ability to inhibit PCNA ubiquitylation, since the targeted knockdown of PCN

137 sh6 mismatch recognition complex through its PCNA-interacting peptide motif, causing accumulation of

138 sites (Thr(6) and Tyr(8)) located within its PCNA-interacting motif (PIP-box).

139 Following ligation, PCNA and LigI remain on the DNA, indicating that Pol del

140 RFC loaded PCNA through two intermediate states on DNA, separated b

141 r ptDNA as the correct substrate for loading PCNA.

142 r C (RFC), a heteropentamer of RFC1-5, loads PCNA onto DNA during replication and repair.

143 onical Rfc1-RFC complex preferentially loads PCNA onto the lagging strand, which is crucial for DNA r

144 Ctf18-RFC loads PCNA with a slight preference for the leading strand, wh

145 ortant functional interactions that maintain PCNA orientation during synthesis.

146 marker (BLBP) and cell proliferation marker (PCNA).

147 uring efficient Okazaki fragment maturation, PCNA-ubiquitination protects fork integrity and promotes

148 tering analysis confirmed the NEIL1 mediated PCNA trimer dissociation and formation of a 1:1:1 NEIL1-

149 Elg1 complex is critical for efficient MMR: PCNA needs to be on DNA long enough to enable MMR, but i

150 nd various post-translational modifications, PCNA has far-reaching impacts on a myriad of cellular fu

151 peting peptides or by T2AA, a small-molecule PCNA inhibitor, decreased NADPH oxidase activation in vi

152 an in vitro assay to quantitatively monitor PCNA monoubiquitination under in vivo scenarios.

153 er show that gammaH2AX and monoubiquitinated PCNA and FANCD2 are constitutively up-regulated in oxali

154 ared to unmodified PCNA or monoubiquitinated PCNA.

155 upon its association with monoubiquitylated PCNA, rendering it susceptible to extraction from DNA da

156 mutation lies near the binding site for most PCNA-interacting proteins.

157 We show that ESCO2 contains multiple PCNA-interaction motifs in its N terminus, each of which

158 We propose that multiple PCNA-interaction motifs embedded in a largely flexible a

159 e of elg1Delta is attenuated by PCNA mutants PCNA-R14E and PCNA-D150E that spontaneously fall off DNA

160 ification and functional analysis of a novel PCNA interacting protein NreA that is conserved in the a

161 rmed DNA-Pol delta complex in the absence of PCNA was 40 s-1.

162 oichiometries by Pol delta in the absence of PCNA, using electrophoretic mobility shift assays, fluor

163 nloader complex, causes over-accumulation of PCNA on DNA and also increases mutation rate, but it has

164 In vitro MS analysis of PCNA co-incubated with the IGF-1R kinase indicated tyros

165 ing synthesis is carried out by a complex of PCNA, Pol delta, FEN1 and LigI.

166 regions by physically blocking diffusion of PCNA along ssDNA, and this activity was required for eff

167 te of damage, though the local enrichment of PCNA persisted longer than that of PARP1.

168 tative RT-PCR to determine the expression of PCNA and Bax/Bcl-2.

169 e IL-33-positive cells had low expression of PCNA.

170 incorporation rate, identifying the face of PCNA that is important for the acceleration of catalysis

171 The formation of PCNA tool belts and Rev1 bridges and the ability of thes

172 DNA Polymerase delta with different forms of PCNA.

173 ere Rad6/Rad18 and a significant fraction of PCNA reside.

174 ific immunostaining and real-time imaging of PCNA expressing apical progenitors revealed that at midc

175 val kinase AKT leads to strong impairment of PCNA ubiquitylation.

176 Independently of PCNA binding, Srs2 also displaces Rad51 from nascent str

177 ed screening assay to identify inhibitors of PCNA ubiquitylation, a key post-translational modificati

178 quitylation, since the targeted knockdown of PCNA E3-ligase (RAD18) and a non-ubiquitylable (PCNA K16

179 ated that the interdomain-connecting loop of PCNA interacted directly with the phox homology (PX) dom

180 forks, concurrent with a significant loss of PCNA at the forks, whereas PCNA efficiently bound to pro

181 Moreover, concomitant loss of PCNA-ubiquitination and the BRCA pathway results in incr

182 Loss of PCNA-ubiquitination results in DNA2-dependent but MRE11-

183 required for efficient monoubiquitination of PCNA on DNA.

184 ay selectively promote monoubiquitination of PCNA on long RPA-coated ssDNA.

185 Mutations of PCNA residues involved in recruiting CAF-1 to the chroma

186 Subsequently, nodes of PCNA that incorporated deoxynucleotide analogs were obse

187 inity to the classical PIP-binding pocket of PCNA via a highly atypical PIP box located at the p12 N

188 talytic rates in the absence and presence of PCNA were determined at millisecond time resolution usin

189 ng protein, is involved in the regulation of PCNA monoubiquitination and interacts directly with Rad1

190 work identifies AKT as a novel regulator of PCNA ubiquitylation and provides the proof-of-concept of

191 Here we show that timely removal of PCNA from DNA by the Elg1 complex is important to preven

192 In order to learn how the retention of PCNA on DNA might interfere with normal DNA metabolism,

193 Progerin sequestration of PCNA promotes replication fork collapse and mislocalizat

194 motif of EndoQ and the toroidal structure of PCNA are critical for the stimulation of the endonucleas

195 lly, we present the co-crystal structures of PCNA with two specific motifs in ZRANB3: the PIP box and

196 n of lysine residues at the inner surface of PCNA is induced by DNA lesions.

197 The catalytic core sits on top of PCNA in an open configuration while the regulatory subun

198 are activated by the ubiquitylation (ub) of PCNA through components of the RAD6-RAD18 pathway, where

199 rgistically triggered mono-ubiquitination of PCNA and apoptosis in a RAD18-dependent manner.

200 Although premature unloading of PCNA generally increases mutation rate, the mutator phen

201 roximately 1:1 stoichiometry that depends on PCNA interaction with the C-terminal endonuclease domain

202 vity, irrespective of its attachment site on PCNA.

203 ay crystallography-based analyses of the p12-PCNA interaction, which takes part in the modulation of

204 hat IGF-1R interacts with and phosphorylates PCNA in human embryonic stem cells and other cell lines.

205 tioned off to the side of the catalytic Pol3-PCNA-DNA axis.

206 case ZRANB3, shown to bind polyubiquitinated PCNA.

207 y and its interaction with polyubiquitinated PCNA, pinpointing ZRANB3 as a key effector of error-free

208 though known effectors of polyubiquitylated PCNA are not strictly linkage-selective.

209 cally engineered mimics of polyubiquitylated PCNA, we have now examined the properties of the ubiquit

210 kage-selective receptor of polyubiquitylated PCNA.

211 acting preferentially with polyubiquitylated PCNA, the molecular function of the chain and the releva

212 ATAD5-RLC possesses the potent PCNA unloading activity.

213 tin ligase RAD18 and the replication protein PCNA.

214 rsial how RFC and RLCs cooperate to regulate PCNA loading and unloading.

215 Thus, acetylation regulates PCNA sliding on DNA in the presence of DNA damage, favor

216 ed fork reversal in mammalian cells requires PCNA ubiquitination, UBC13, and K63-linked polyubiquitin

217 RPA restricted the resident PCNAs to the upstream duplex regions by physically block

218 XPA or progerin each significantly restored PCNA at replication forks.

219 In elg1Delta, over-retained PCNA hyper-recruits the Msh2-Msh6 mismatch recognition c

220 asymmetric distribution of MutSgamma and RFC-PCNA on meiotic recombination intermediates may drive bi

221 Finally, the MutLgamma-MutSgamma-EXO1-RFC-PCNA nuclease ensemble preferentially cleaves DNA with H

222 as many similarities to a previous yeast RFC:PCNA crystal structure, suggesting that eukaryotic clamp

223 ar antigen (PCNA) to elicit rapid and robust PCNA degradation and associated effects on DNA synthesis

224 The p21's PCNA interacting region (PIR), and not its CDK binding d

225 sis from Finasteride treated patients showed PCNA expression in BECs was highly correlated to the lev

226 TLS and TS depend on site-specific PCNA K164 monoubiquitination and polyubiquitination, res

227 In addition to specific PCNA and polymerase interactions (PIP site), we have now

228 Upon genotoxic stress, PCNA ubiquitination allows for replication of damaged DN

229 inctive doughnut-shaped molecular structure, PCNA was originally studied for its role in stimulating

230 tin-conjugating enzyme UBE2D3 with substrate PCNA), and endogenous proteins interacting with thioredo

231 es SUMO2-PCNA conjugation but inhibits SUMO1-PCNA formation.

232 t on both transcription and RECQ5, and SUMO2-PCNA level correlates with TRIM28 expression.

233 TRIM28 as the E3 ligase that catalyzes SUMO2-PCNA conjugation.

234 hat provides substrate specificity for SUMO2-PCNA conjugation in response to TRC remains unknown.

235 I)-interacting protein RECQ5, promotes SUMO2-PCNA conjugation but inhibits SUMO1-PCNA formation.

236 oops over unextended D-loops when SUMOylated PCNA is present, compared to unmodified PCNA or monoubiq

237 Our data suggest that targeting PCNA in inflammatory neutrophils holds promise as a mult

238 s may serve as a flexible scaffold to tether PCNA and RPA at the replication fork, and that post-tran

239 These findings add to growing evidence that PCNA can bind a diverse range of protein sequences that

240 Stokes radii measured by SEC hinted that PCNA in complex with NEIL1 (+/-DNA) was no longer a trim

241 However, we now know that PCNA does much more than promote processive DNA synthesi

242 We posit that PCNA molecules trapped on DNA interfere with the correct

243 We propose that PCNA and ATP-dependency serve as a multi-layered regulat

244 Here, we show that PCNA also stimulates the catalytic rate of Saccharomyces

245 In vitro assays with human enzymes show that PCNA and its loader RFC are sufficient to activate the M

246 We herein showed that PCNA associated with p47phox, a key subunit of NADPH oxi

247 Our results suggest that PCNA retention controlled by the Elg1 complex is critica

248 These findings suggest that PCNA unloading by Elg1 is necessary to limit Fbh1 and Sr

249 Epistasis analysis suggests that PCNA over-accumulation on DNA interferes with both MMR a

250 with primed DNA, an incoming ddTTP, and the PCNA clamp.

251 e the apurinic endonuclease activity and the PCNA-binding domain of Ape2 (APEX2), but not Ape1 (APEX1

252 nines relay critical information between the PCNA-binding, DNA-binding, and ATPase sites at all steps

253 an intact trypsin-like protease domain, the PCNA interaction, and the DNA-binding domain that is nec

254 mediated clamp and DNA interface enables the PCNA clamp to "waterskate" along the duplex with minimum

255 In humans, the PCNA-associated recombination inhibitor (PARI) protein h

256 tion proteins such as Fen1 could inhibit the PCNA unloading activity of Elg1-RLC, a yeast homolog of

257 ovide important structural insights into the PCNA-APIM interaction, and reveal unexpected similaritie

258 on DNA polymerase, the RFC clamp loader, the PCNA sliding clamp, and the RPA single-stranded DNA bind

259 Because of the heterotrimeric nature of the PCNA clamp in some archaea, there is potential to occupy

260 py also demonstrated the dissociation of the PCNA homotrimer in the presence of NEIL1 and DNA, while

261 gets lysine 20 at the sliding surface of the PCNA ring in vitro and in vivo in response to DNA damage

262 cations function at the outer surface of the PCNA ring to favor DNA damage bypass.

263 dly, Pol delta binds only one subunit of the PCNA trimer.

264 Loss of Elg1, the major subunit of the PCNA unloader complex, causes over-accumulation of PCNA

265 en protomers in the crystal structure of the PCNA-K20ac ring.

266 the UNG2 N-terminus disrupt formation of the PCNA-UNG2-RPA protein complex.

267 this recruitment through mutagenesis of the PCNA/Pol30 polymerase clamp or deleting specific error-p

268 t-replication repair pathway members, or the PCNA modification sites involved in regulation of this p

269 This PCNA sequestration likely exposed ds-ssDNA junctions at

270 Pol delta is anchored to one of the three PCNA monomers through the C-terminal domain of the catal

271 ly replication polymerase (YB site) bound to PCNA and DNA from Sulfolobus solfataricus.

272 e report the structure of human RFC bound to PCNA by cryogenic electron microscopy to an overall reso

273 The X-ray crystal structure of TIP bound to PCNA reveals that TIP binds to the canonical PIP interac

274 w that in the absence of Srs2 recruitment to PCNA or in helicase-deficient mutants, breakage at a CAG

275 ATAD5-RLC could unload ubiquitinated PCNA.

276 en (PCNA), Rev1, ubiquitin and ubiquitinated-PCNA and is also ubiquitinated itself.

277 A E3-ligase (RAD18) and a non-ubiquitylable (PCNA K164R) knock-in model recapitulate the observed SL

278 domain, helps recruit FAN1 to ubiquitylated PCNA accumulated at stalled forks.

279 ities and its interaction with ubiquitylated PCNA may offer therapeutic opportunities for treatment o

280 t FAN1 contains a previously-uncharacterized PCNA interacting peptide (PIP) motif that, together with

281 Our data also suggests that unmodified UNG2, PCNA, and RPA can form a ternary protein complex.

282 surements, we reveal that ATAD5-RLC unloaded PCNA through one intermediate state before ATP hydrolysi

283 ated PCNA is present, compared to unmodified PCNA or monoubiquitinated PCNA.

284 gnificant loss of PCNA at the forks, whereas PCNA efficiently bound to progerin.

285 Both LigI and FEN1 associate with PCNA-Pol delta during gap-filling synthesis, suggesting

286 pol delta maintains a loose association with PCNA while replicating DNA.

287 polymerase Poleta that also colocalized with PCNA.

288 es at the replication forks, in complex with PCNA and the nascent DNA, where it regulates DNA synthes

289 RNA expression is positively correlated with PCNA, APE1, XRCC1, PARP1, Chk1, and Chk2 across these 6

290 in sister chromatid cohesion correlates with PCNA loading but is separable from its role in the repli

291 g to curtail the interaction of Pol eta with PCNA at damaged DNA to prevent harmful mutagenesis.

292 ains in which MutLgamma cannot interact with PCNA present defects in forming crossovers.

293 We conclude that Srs2 interaction with PCNA allows the helicase activity to unwind fork-blockin

294 in the nucleus enhanced its interaction with PCNA in squamous cell carcinoma of the head and neck (SC

295 In cells, TRIM28 interaction with PCNA on human chromatin is dependent on both transcripti

296 or abolish human MutLalpha interaction with PCNA, as well as PCNA-dependent activation of MutLalpha

297 of DNA replication, through interaction with PCNA.

298 azaki fragment synthesis and processing with PCNA and LigI forming a terminal structure of two linked

299 ays to explore the interactions of UNG2 with PCNA and RPA and to determine the effects of two UNG2 ph

300 pared to wild-type, a growth-defective yeast PCNA mutant (DD41,42AA) showed substantially less stimul