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1 s and elucidate the interplay between HR and translesion DNA synthesis.
2  polymerases during replication, repair, and translesion DNA synthesis.
3  the Y family of DNA polymerases involved in translesion DNA synthesis.
4 genome integrity as well as participating in translesion DNA synthesis.
5 vily on hydrogen-bonding interactions during translesion DNA synthesis.
6  in both a DNA damage checkpoint control and translesion DNA synthesis.
7 genome integrity as well as participating in translesion DNA synthesis.
8 te in a DNA damage checkpoint control and in translesion DNA synthesis.
9 ination in response to UV-induced damage for translesion DNA synthesis.
10 equires specialized polymerases that perform translesion DNA synthesis.
11  that PARP10 binding to PCNA is required for translesion DNA synthesis.
12 ro-8-oxo-2'-deoxyguanosine (8-oxo-dG) during translesion DNA synthesis.
13  zeta (Pol zeta) and Rev1 are key players in translesion DNA synthesis.
14 , including T2 amino alcohol (T2AA), inhibit translesion DNA synthesis.
15 amily DNA polymerases play a crucial role in translesion DNA synthesis.
16 atch repair, nucleotide excision repair, and translesion DNA synthesis.
17 ward loop to enhance PCNA ubiquitylation and translesion DNA synthesis.
18 of accessory proteins retained on DNA during translesion DNA synthesis.
19 oid and induced expression of genes encoding translesion DNA synthesis.
20 A provides a novel biochemical tool to study translesion DNA synthesis.
21 ons coordinates homologous recombination and translesion DNA synthesis.
22 cA nucleoprotein filament (RecA*), catalyses translesion DNA synthesis.
23 A/FANC pathway, homologous recombination, or translesion DNA synthesis.
24 accounting for polymerase "switching" during translesion DNA synthesis.
25 rmation of the 8-oxo-dG template base during translesion DNA synthesis.
26 s involved in the tolerance of DNA damage by translesion DNA synthesis.
27           To probe the mechanism for in vivo translesion DNA synthesis across this adduct, in vitro p
28 ryonic viability and development through the translesion DNA synthesis activity of Polzeta preserving
29                               In addition to translesion DNA synthesis activity, MacDinB-1 synthesize
30 way is believed to be the major mechanism of translesion DNA synthesis and base damage-induced mutage
31 evant platinum-based drugs by promoting both translesion DNA synthesis and DNA repair.
32  the Y-family of DNA polymerases involved in translesion DNA synthesis and genome mutagenesis.
33 rily conserved Y family members that perform translesion DNA synthesis and have low fidelity, we desc
34 ily of bypass polymerases is responsible for translesion DNA synthesis and includes the human polymer
35 NA polymerase zeta (Polzeta) participates in translesion DNA synthesis and is involved in the generat
36 erase eta (pol eta), an enzyme that performs translesion DNA synthesis and may participate in somatic
37 erences argue against a unified mechanism of translesion DNA synthesis and suggest that polymerases e
38 ucleotide of the ICL, followed by incisions, translesion DNA synthesis, and extension of the nascent
39 epair of ICLs requires sequential incisions, translesion DNA synthesis, and homologous recombination,
40  Mismatched cisplatin adducts could arise by translesion DNA synthesis, and improved repair of such a
41       Polymerase eta (PolH) is necessary for translesion DNA synthesis, and PolH deficiency predispos
42               Nucleotide excision repair and translesion DNA synthesis are two processes that operate
43  of concept for the coordinate inhibition of translesion DNA synthesis as a strategy to improve chemo
44 ve polymerases involved in DNA repair and/or translesion DNA synthesis as anticancer agents are discu
45 hat BRCA1 plays a critical role in promoting translesion DNA synthesis as well as DNA template switch
46 e II appears to be required for the observed translesion DNA synthesis because essentially similar re
47 rthermore, 5-NapITP is a chain terminator of translesion DNA synthesis because the DNA polymerase is
48  the Klenow fragment follows the "A-rule" of translesion DNA synthesis by preferentially incorporatin
49 ur new structures depicting several steps of translesion DNA synthesis by RB69 gp43 exo-, employing a
50 se may play a critical role during mutagenic translesion DNA synthesis bypassing a template AP site i
51  the assessment of the mutagenic profiles of translesion DNA synthesis catalyzed by any error-prone D
52 of metal ion substitution on the dynamics of translesion DNA synthesis catalyzed by the bacteriophage
53 the rate of the conformational change during translesion DNA synthesis depends on pi-electron density
54 cis on a damaged template strand obstructing translesion DNA synthesis despite the absolute requireme
55 sults suggest that PolN might play a role in translesion DNA synthesis during ICL repair in human cel
56 he Escherichia coli Klenow fragment performs translesion DNA synthesis during the misreplication of a
57 orporation fidelity, mismatch extension, and translesion DNA synthesis efficiencies were determined u
58  DNA processing (error-free) to low-fidelity translesion DNA synthesis (error-prone) at DNA damage si
59  particularly pol eta, may contribute to the translesion DNA synthesis events observed for 1,N(6)-eth
60  measured include fidelity and efficiency of translesion DNA synthesis, excision repair, and recombin
61 ure-function analyses for the checkpoint and translesion DNA synthesis functions of the umuDC gene pr
62      Several mutant forms of PCNA that block translesion DNA synthesis have been identified in geneti
63  understand the role of Poleta in error-free translesion DNA synthesis, here we examine the ability o
64 rase switching recently suggested during the translesion DNA synthesis, implies the multiple function
65 ein interactions specific for Rev1's role in translesion DNA synthesis in human cells, and I2 acts as
66           In order to characterize mutagenic translesion DNA synthesis in UVM-induced Escherichia col
67     The close parallels in the efficiency of translesion DNA synthesis in vitro and in vivo for the f
68 monstrate the ability to selectively inhibit translesion DNA synthesis in vitro.
69 s capable of both error-free and error-prone translesion DNA synthesis in vitro.
70 e identify a function of PAF, a component of translesion DNA synthesis, in modulating Wnt signaling.
71                           It involves either translesion DNA synthesis initiated by proliferating cel
72                                              Translesion DNA synthesis is an essential process that h
73                                              Translesion DNA synthesis is an important branch of the
74 D30, thereby suggesting that Rad30-dependent translesion DNA synthesis is conserved within the eukary
75 e dynamic behavior of DNA polymerases during translesion DNA synthesis is dependent upon the nature o
76 on have direct implications for low-fidelity translesion DNA synthesis, most of which is found to be
77  have been used to study polymerase-mediated translesion DNA synthesis of abasic sites and TT dimers,
78       Some of these polymerases perform such translesion DNA synthesis of specific types of damage wi
79  PolH to translocate to replication foci for translesion DNA synthesis of UV-induced DNA lesions.
80 how that NDP kinase mutants are dependent on translesion DNA synthesis, often a mutagenic form of DNA
81                 T2AA significantly inhibited translesion DNA synthesis on a cisplatin-cross-linked te
82 approach, we examined the effect of impaired translesion DNA synthesis on cisplatin response in aggre
83                                Nevertheless, translesion DNA synthesis opposite 8-oxoguanine was obse
84         Pol theta has the ability to conduct translesion DNA synthesis opposite an AP site or thymine
85 decade that specialized DNA polymerases for "translesion DNA synthesis" or "TLS" were identified and
86 xide, consistent with a role for DinB(Pa) in translesion DNA synthesis over N2-dG adducts.
87   Because pol beta has been shown to perform translesion DNA synthesis past cisplatin (CP)- and oxali
88 gesting their catalytically limited roles in translesion DNA synthesis past deaminated, oxidized base
89 and kappa, which have been shown to catalyze translesion DNA synthesis past several DNA lesions.
90  both nucleolytic incisions near the ICL and translesion DNA synthesis past the lesion.
91 hosphates on DNA polymerases when performing translesion DNA synthesis past the pro-mutagenic DNA add
92 llow us to conveniently screen regulators of translesion DNA synthesis pathway and monitor environmen
93 g., REV1, REV3L) involved in the error-prone translesion DNA synthesis pathway can sensitize intrinsi
94 e, the authors present the structures of the translesion DNA synthesis polymerase Rev1 in complex wit
95 is would preserve the substrate for the REV1 translesion DNA synthesis polymerase to incorporate cyto
96 it of DNA polymerase zeta (Polzeta), 1 of 10 translesion DNA synthesis polymerases known in mammals.
97 rs to recruit and coordinate replicative and translesion DNA synthesis polymerases to ensure genome i
98 A, animal cell mitochondria lack specialized translesion DNA synthesis polymerases to tolerate these
99   At the molecular level, the enhancement in translesion DNA synthesis reflects a substantial increas
100                                              Translesion DNA synthesis represents the ability of a DN
101                                              Translesion DNA synthesis represents the ability of a DN
102 seamlessly coordinate both high fidelity and translesion DNA synthesis requires a means to regulate r
103 ity (DNA pol V) that facilitates error-prone translesion DNA synthesis (SOS mutagenesis).
104 inks (ICLs) are repaired by mechanisms using translesion DNA synthesis that is regulated by monoubiqu
105                                              Translesion DNA synthesis, the ability of a DNA polymera
106          Due to the critical role of PolH in translesion DNA synthesis, the activity of PolH is tight
107 titude in promoting efficient and error-free translesion DNA synthesis through the diverse array of b
108  irradiation, DNA polymerases specialized in translesion DNA synthesis (TLS) aid DNA replication.
109                                              Translesion DNA synthesis (TLS) allows bypass of DNA les
110 DNA polymerase V, which participates in both translesion DNA synthesis (TLS) and a DNA damage checkpo
111 which repair is initiated by NER followed by translesion DNA synthesis (TLS) and completed through an
112 served Y family enzyme that is implicated in translesion DNA synthesis (TLS) but whose cellular funct
113                                              Translesion DNA synthesis (TLS) can use specialized DNA
114                                              Translesion DNA synthesis (TLS) during S-phase uses spec
115 switch from accurate DNA repair to mutagenic translesion DNA synthesis (TLS) during the SOS response
116 ored biallelic inactivating mutations of the translesion DNA synthesis (TLS) gene REV7 (also known as
117                                         Most translesion DNA synthesis (TLS) in Escherichia coli is d
118 tion in DNA polymerase V- (pol V-) dependent translesion DNA synthesis (TLS) in vivo.
119 zeta (REV3 and REV7) play important roles in translesion DNA synthesis (TLS) in which DNA replication
120                                              Translesion DNA synthesis (TLS) is a process whereby spe
121                                              Translesion DNA synthesis (TLS) is the ability of DNA po
122 ions encountered on the template strand, and translesion DNA synthesis (TLS) is used to rescue progre
123                                              Translesion DNA synthesis (TLS) of damaged DNA templates
124 -family DNA polymerase capable of catalyzing translesion DNA synthesis (TLS) on certain DNA lesions,
125 s are converted to dsDNA with an appropriate translesion DNA synthesis (TLS) polymerase, followed by
126 l three kingdoms of life possess specialized translesion DNA synthesis (TLS) polymerases (Pols) that
127                We propose that NusA recruits translesion DNA synthesis (TLS) polymerases to RNA polym
128 t include mismatch repair (MMR) proteins and translesion DNA synthesis (TLS) polymerases.
129 es the cooperative actions of at least three translesion DNA synthesis (TLS) polymerases: Poleta, REV
130 used attention on the umuD(+)C(+)-dependent, translesion DNA synthesis (TLS) process that is responsi
131  Saccharomyces cerevisiae, Rev1 functions in translesion DNA synthesis (TLS) together with polymerase
132                                           In translesion DNA synthesis (TLS), a specialized TLS pol i
133 pathways such as nucleotide-excision repair, translesion DNA synthesis (TLS), and homologous recombin
134 r processes, including nucleolytic incision, translesion DNA synthesis (TLS), and homologous recombin
135        The two main tolerance strategies are translesion DNA synthesis (TLS), in which low-fidelity D
136 gene products, all implicated in error-prone translesion DNA synthesis (TLS), mediate mutagenesis in
137                                           In translesion DNA synthesis (TLS), specialized DNA polymer
138 l of attention due to the roles they play in translesion DNA synthesis (TLS), the potentially mutagen
139    Given the critical role of pol eta during translesion DNA synthesis (TLS), these findings unveil a
140 bute to the bypassing of DNA lesions, termed translesion DNA synthesis (TLS).
141 ng that CSCs may have intrinsically enhanced translesion DNA synthesis (TLS).
142 s cope with replication-blocking lesions via translesion DNA synthesis (TLS).
143 cialized low fidelity polymerases to perform translesion DNA synthesis (TLS).
144 haracterized for their ability to facilitate translesion DNA synthesis (TLS).
145 nal modification essential for DNA repair by translesion DNA synthesis (TLS).
146 nit and Rev7 accessory subunit, in promoting translesion DNA synthesis (TLS).
147 lerance to DNA damage by replicative bypass [translesion DNA synthesis (TLS)].
148 he replicative bypass of base damage in DNA (translesion DNA synthesis [TLS]) is a ubiquitous mechani
149 fore resorting to mutagenic pathways such as translesion DNA synthesis to bypass these impediments to
150                                       During translesion DNA synthesis, Ug was bypassed more efficien
151                The mechanism and dynamics of translesion DNA synthesis were evaluated using primer/te
152 NA damage are the consequence of error-prone translesion DNA synthesis, which could be responsible fo
153 V serve dual roles by facilitating efficient translesion DNA synthesis while simultaneously introduci

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