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1 PCNA has two structurally similar domains (I and II) lin
2 PCNA is a highly conserved sliding clamp protein essenti
3 PCNA is a master regulator of DNA replication and S-phas
4 PCNA is a pivotal component of the replication fork mach
6 y) and short interfering RNA (interleukin-8, PCNA, and Bax), as a validation of effective and functio
8 r synthesis during recombination events in a PCNA interaction-dependent way but independently of its
9 artan (also known as DVC1 and C1orf124) is a PCNA-interacting protein implicated in translesion synth
10 i-recombination function but it also plays a PCNA-independent pro-recombination role, probably by sti
11 All proteins that bind to PCNA do so via a PCNA-interacting peptide (PIP) motif that binds near the
12 tion signals including ERK1/2, p-90RSK, Akt, PCNA, and Ki-67, and a reduction in apoptotic factors su
13 glycosylation following CrP treatment; also, PCNA and vimentin (SMC synthetic marker) expression were
15 oliferation markers (Ki-67, p-Erk, p-Akt and PCNA); (3) decreased apoptosis markers, such as cleaved
17 S stimulation in vivo, hepatic TNF-alpha and PCNA responses subsided in Nox4-deficient mice compared
21 conserved interaction mode between FANCM and PCNA during replication stress, and suggest that this in
28 isolated a complex formed between NEIL1 and PCNA (+/-DNA) using size exclusion chromatography (SEC).
31 on and tethers it to the leading strand, and PCNA (proliferating cell nuclear antigen) binds tightly
32 ic data showing the requirement for SUMO and PCNA binding for the SDSA role of Srs2, Srs2 displays a
33 133, and 250 in PCNA as IGF-1R targets, and PCNA phosphorylation was followed by mono- and polyubiqu
36 ication, proliferating cell nuclear antigen (PCNA) adopts a ring-shaped structure to promote processi
38 -induced proliferating cell nuclear antigen (PCNA) and FANCD2 monoubiquitinations (surrogate markers
39 level of proliferating cell nuclear antigen (PCNA) and minichromosome maintenance 4 (MCM4) proteins w
40 (Pax7), proliferating cell nuclear antigen (PCNA) and nicotinamide phosphoribosyltransferase (Nampt)
41 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
45 NA clamp proliferating cell nuclear antigen (PCNA) associates with the C-terminal domain of Exo1 and
46 eaction: proliferating cell nuclear antigen (PCNA) clamp binding/opening/closure/release, ptDNA bindi
47 gulating proliferating cell nuclear antigen (PCNA) expression and ribosomal RNA (rRNA) synthesis in T
51 Ki67 and proliferating cell nuclear antigen (PCNA) immunofluorescence, we determined the duration of
56 repair, proliferating cell nuclear antigen (PCNA) loading onto DNA (PCNA(DNA)) triggers the interact
57 -induced proliferating cell nuclear antigen (PCNA) monoubiquitination in Poleta-proficient but not in
59 CDK) and proliferating cell nuclear antigen (PCNA) onto chromatin, as well as initiation and elongati
60 ng clamp proliferating cell nuclear antigen (PCNA) plays a vital role in a number of DNA repair pathw
61 ECQ5 and proliferating cell nuclear antigen (PCNA) promotes RAD18-dependent PCNA ubiquitination and t
64 cts with proliferating cell nuclear antigen (PCNA) via a highly conserved PIP box motif within the ki
65 itinated Proliferating Cell Nuclear Antigen (PCNA), a marker of stalled replication forks, interacts
66 act with proliferating cell nuclear antigen (PCNA), an essential co-factor for DNA polymerases in bot
67 f Cdc45, proliferating cell nuclear antigen (PCNA), and polymerase delta, but not ORC and MCM protein
69 2-Msh3), proliferating cell nuclear antigen (PCNA), and replication factor C (RFC) and a reconstitute
71 tment of proliferating cell nuclear antigen (PCNA), the platform for assembly of the DNA replication
73 but not proliferating cell nuclear antigen (PCNA)-interacting motif (PIM), leads to increased cell d
81 itors of proliferating cell nuclear antigen (PCNA)/PCNA interacting protein box (PIP-Box) interaction
82 such as proliferating cell nuclear antigen (PCNA); however, the exact mechanism of PCNA activation i
83 Our results provide evidence for an archaeal PCNA 'tool-belt' recruitment model of multienzyme functi
85 regulated sites on known DDR players such as PCNA and identify previously unknown DDR targets such as
86 MutLalpha interaction with PCNA, as well as PCNA-dependent activation of MutLalpha endonuclease, PCN
88 d a SWI/SNF domain facilitating DNA-binding, PCNA-polyubiquitin-ligase, and dsDNA-translocase activit
95 that Elg1 unloads the DNA replication clamp PCNA from DNA, we tested whether PCNA overexpression wou
97 it, Mcm4, and the replication sliding clamp, PCNA, between different stages of the cell cycle and bet
98 cal marker where interaction with beta-clamp/PCNA could distinguish parent/daughter strand identity.
100 with the DNA replication machinery component PCNA and promotes replication of DNA lesions and common
103 ctions are mediated by one or more conserved PCNA-interacting protein (PIP) motifs that bind in a hyd
106 leting replication, and we propose Pol delta-PCNA collides with the slower CMG, and in the absence of
107 However, Saccharomyces cerevisiae Pol delta-PCNA is a rapid and processive enzyme, suggesting that C
110 Msh6 (or Msh2-Msh3), Exo1, RPA, RFC-Delta1N, PCNA, and Pol epsilon was found to catalyze an MMR react
111 Msh6 (or Msh2-Msh3), Exo1, RPA, RFC-Delta1N, PCNA, and Pol epsilon was found to catalyze both short-p
112 lear antigen (PCNA) promotes RAD18-dependent PCNA ubiquitination and the helicase activity of RECQ5 p
113 ell nuclear antigen (PCNA) loading onto DNA (PCNA(DNA)) triggers the interaction between CRL4(CDT2) a
115 1 by Srs2 helicase is required for efficient PCNA loading and restoration of resected DNA As a result
116 endent activation of MutLalpha endonuclease, PCNA- and DNA-dependent activation of MutLalpha ATPase,
119 els of Pdx-1 (insulin transcription factor), PCNA (a marker of cell proliferation), and LC3 (a marker
120 reduced alphaSMA immunoreactivity and fewer PCNA (+) nuclei among alphaSMA (+) cells (P < 0.008).
124 RAD51, but not BRCA2, is also required for PCNA monoubiquitination in response to HU, suggesting th
125 portant for ATP binding is also required for PCNA poly-ubiquitination and recombination-based lesion
126 IP1 and RAD18, the E3 ligase responsible for PCNA monoubiquitination, are specifically required for A
127 These results reveal a central role for PCNA in the Exo1-independent MMR pathway and suggest tha
128 s are needed to determine possible roles for PCNA and other host proteins detected.IMPORTANCE Poxviru
129 icament lies ahead for the replication fork, PCNA is there to orchestrate the events necessary to han
130 itive than XPA in binding replication forks, PCNA sequestration by progerin may shift the equilibrium
132 CT116 (HCT116-OxR) cells and that gammaH2AX, PCNA, and FANCD2 monoubiquitinations are induced by oxal
135 ngle point mutation, Ser228Ile, in the human PCNA gene was recently identified to cause a disease who
137 lymphocytes by double immunohistochemistry (PCNA-staining) and flow cytometry (BrdU incorporation) r
138 ation of Thr(6) or Tyr(8) on UNG2 can impede PCNA binding without affecting UNG2 catalytic activity o
140 icated tyrosine residues 60, 133, and 250 in PCNA as IGF-1R targets, and PCNA phosphorylation was fol
142 further support a role for Bub1 and LANA in PCNA-mediated cellular DNA replication processes as well
143 Due to this fundamental role, mutations in PCNA that profoundly impair protein function would be in
144 tomatically classifying cell cycle phases in PCNA-immunolabeled cells from single time point images,
145 t FANCD2 and RAD51 have an important role in PCNA monoubiquitination and TLS in a FANCD2 monoubiquiti
146 ns for the plasticity of the binding site in PCNA and reveals how a disease mutation selectively alte
147 findings reveal a modulatory role of USP7 in PCNA ubiquitination-mediated stress-tolerance pathways b
148 estabilizes Rad18 and compromises UV-induced PCNA mono-ubiquitylation and Pol eta recruitment to stal
150 Rad5 enzymatic domains concertedly influence PCNA modification, and unveil their discrete contributio
151 chromatin colocalization but did not inhibit PCNA monoubiquitination, suggesting that T2AA hinders in
152 tein, called TIP, binds to PCNA and inhibits PCNA-dependent activities although it does not contain a
153 with the Elg1 complex and down-regulate its PCNA-unloading function to promote the G1/S transition.
156 pathway and suggest that Msh2-Msh6 localizes PCNA to repair sites after mispair recognition to activa
158 tering analysis confirmed the NEIL1 mediated PCNA trimer dissociation and formation of a 1:1:1 NEIL1-
159 The Rad5 ubiquitin ligase activity mediates PCNA poly-ubiquitination and subsequently recombination-
160 nd various post-translational modifications, PCNA has far-reaching impacts on a myriad of cellular fu
162 er show that gammaH2AX and monoubiquitinated PCNA and FANCD2 are constitutively up-regulated in oxali
167 A, with or without Msh2-Msh6 (or Msh2-Msh3), PCNA, and RFC but did not require nicking of the substra
169 ification and functional analysis of a novel PCNA interacting protein NreA that is conserved in the a
170 UVA laser, H2O2, and at sites of sub-nuclear PCNA foci, suggesting that poly (ADP-ribose) promotes XR
178 induced caspase 3 activity and expression of PCNA and Ki67, but activation of the Akt survival pathwa
187 f Enok reduced the chromatin-bound levels of PCNA in both S2 cells and early embryos, suggesting that
188 esults indeed reveal that elevated levels of PCNA rescue pds5-1 temperature sensitivity and cohesion
189 ion within the interdomain connector loop of PCNA, and much of the regulation is a result of the inhe
190 forks, concurrent with a significant loss of PCNA at the forks, whereas PCNA efficiently bound to pro
193 eview, we focus on the monoubiquitination of PCNA by Rad6/Rad18 and summarize the current knowledge o
195 Together, our findings detail a mutation of PCNA in humans associated with a neurodegenerative pheno
197 ase) based on the characteristic patterns of PCNA distribution, is feasible for both confocal and wid
199 show that c-Abl and Y211 phosphorylation of PCNA is an important axis downstream of Ron, which is re
202 in a hydrophobic pocket on the front side of PCNA as well as by conserved Rev1-interacting region (RI
203 motif of EndoQ and the toroidal structure of PCNA are critical for the stimulation of the endonucleas
206 lly, we present the co-crystal structures of PCNA with two specific motifs in ZRANB3: the PIP box and
208 are activated by the ubiquitylation (ub) of PCNA through components of the RAD6-RAD18 pathway, where
210 roximately 1:1 stoichiometry that depends on PCNA interaction with the C-terminal endonuclease domain
212 clamp, proliferating cell nuclear antigen or PCNA, is a ring-shaped protein complex that surrounds DN
213 plication processivity factor (beta-clamp or PCNA) activate the latent MutL endonuclease to nick the
214 of proliferating cell nuclear antigen (PCNA)/PCNA interacting protein box (PIP-Box) interactions, inc
215 discovered that, beginning in late S phase, PCNA(DNA) is no longer sufficient to trigger CRL4(CDT2)-
216 hat IGF-1R interacts with and phosphorylates PCNA in human embryonic stem cells and other cell lines.
217 ivity, which in turn directly phosphorylates PCNA at Y211 and leads to an increased level of chromati
219 enhancing the processivity of the polymerase PCNA is an allosteric modulator of other Pol delta activ
221 y and its interaction with polyubiquitinated PCNA, pinpointing ZRANB3 as a key effector of error-free
223 es (PARP1, MSH2, Ku, DNA-PKcs, MCM proteins, PCNA and DNA Pol delta) and in protein metabolic process
224 roper balance between the anti-recombination PCNA-bound and pro-recombination pools of Srs2 is crucia
227 ed fork reversal in mammalian cells requires PCNA ubiquitination, UBC13, and K63-linked polyubiquitin
230 -induced telomere synthesis requires the RFC-PCNA-Pol delta axis, but is independent of other canonic
233 sis from Finasteride treated patients showed PCNA expression in BECs was highly correlated to the lev
236 inctive doughnut-shaped molecular structure, PCNA was originally studied for its role in stimulating
238 tin-conjugating enzyme UBE2D3 with substrate PCNA), and endogenous proteins interacting with thioredo
239 ; it not only mediates interaction with SUMO-PCNA to promote the anti-recombination function but it a
240 oops over unextended D-loops when SUMOylated PCNA is present, compared to unmodified PCNA or monoubiq
241 s the inhibition of ribosomal RNA synthesis, PCNA expression, and T-cell activation induced by MPA, s
242 s may serve as a flexible scaffold to tether PCNA and RPA at the replication fork, and that post-tran
243 Stokes radii measured by SEC hinted that PCNA in complex with NEIL1 (+/-DNA) was no longer a trim
246 s, in vitro and in vivo analysis showed that PCNA unloading is delayed in the absence of nucleosome a
247 nines relay critical information between the PCNA-binding, DNA-binding, and ATPase sites at all steps
250 ovide important structural insights into the PCNA-APIM interaction, and reveal unexpected similaritie
251 on DNA polymerase, the RFC clamp loader, the PCNA sliding clamp, and the RPA single-stranded DNA bind
252 Because of the heterotrimeric nature of the PCNA clamp in some archaea, there is potential to occupy
253 py also demonstrated the dissociation of the PCNA homotrimer in the presence of NEIL1 and DNA, while
254 gets lysine 20 at the sliding surface of the PCNA ring in vitro and in vivo in response to DNA damage
256 tering (SAXS) confirms the disruption of the PCNA trimer upon addition of the TIP protein in solution
259 nrecognized contribution of the motif to the PCNA and ubiquitination enzyme interaction, and not due
261 tionship between domains I and II within the PCNA monomer such that the trimeric ring structure is br
268 The X-ray crystal structure of TIP bound to PCNA reveals that TIP binds to the canonical PIP interac
269 tive evidence that the binding of pol eta to PCNA and the ensuing TLS are both independent of PCNA ub
270 w that in the absence of Srs2 recruitment to PCNA or in helicase-deficient mutants, breakage at a CAG
271 TLS involves the conjugation of ubiquitin to PCNA clamps encircling damaged DNA and the role of this
272 y the alcohol, coupled to a proton transfer (PCNA: proton-coupled nucleophilic attack) and a subseque
273 e variant bound to peptides derived from two PCNA partner proteins reveal that the binding pocket can
274 y-accepted model purports that ubiquitinated PCNA recruits TLS polymerases such as pol eta to sites o
275 e observed increased levels of ubiquitylated PCNA and significantly lower mutation frequency in the t
277 ities and its interaction with ubiquitylated PCNA may offer therapeutic opportunities for treatment o
278 t FAN1 contains a previously-uncharacterized PCNA interacting peptide (PIP) motif that, together with
282 ation clamp PCNA from DNA, we tested whether PCNA overexpression would similarly rescue pds5-1 mutant
287 how that LANA is able to form a complex with PCNA, a critical protein for viral DNA replication.
291 e SIRV2 proteins were found to interact with PCNA, providing insights into the recruitment of host re
292 l replication in S phase and interacted with PCNA to promote its monoubiquitination in response to UV
294 in the nucleus enhanced its interaction with PCNA in squamous cell carcinoma of the head and neck (SC
295 or abolish human MutLalpha interaction with PCNA, as well as PCNA-dependent activation of MutLalpha
297 plication forks that directly interacts with PCNA via a conserved PCNA-interacting peptide (PIP) box
298 rase carries out processive replication with PCNA in vitro; however, in yeast, it requires an increas
299 TDG that disrupt the interaction of TDG with PCNA or change critical basic residues essential for the
300 ays to explore the interactions of UNG2 with PCNA and RPA and to determine the effects of two UNG2 ph
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