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1 a human enzyme able to recognize and process abasic and oxidized ribonucleotides embedded in DNA.
2 mixture of 2'-deoxy, 2'-fluoro, 2'-O-methyl, abasic and/or ribonucleotides, is a representative oligo
3                                              Abasic (AP) lesions are the most frequent type of damage
4 e of DNA is a common event that generates an abasic (Ap) site (1).
5 on of DNA deoxyribose generates the oxidized abasic (AP) site 2-deoxyribonolactone (dL).
6 tly reported that the aldehyde residue of an abasic (Ap) site in duplex DNA can generate an interstra
7 s of a base in DNA leading to creation of an abasic (AP) site leaving a deoxyribose residue in the st
8                     Replacement of oxoG with abasic (AP) site rescued the activity, and calculations
9 pe of interstrand DNA-DNA cross-link between abasic (Ap) sites and 2'-deoxyadenosine (dA) residues wa
10                                              Abasic (AP) sites and strand breaks are frequently occur
11                                              Abasic (Ap) sites are common lesions in genomic DNA that
12                                          DNA abasic (AP) sites are one of the most frequent lesions i
13                                              Abasic (AP) sites are potent blocks to DNA and RNA polym
14                                              Abasic (AP) sites are the most common lesions arising in
15 nd repairs most nonbulky lesions, uracil and abasic (AP) sites in DNA.
16  indicates that PARP1 binds to DNA at nicks, abasic (AP) sites, and ends as a monomer.
17 oxanthine, and etheno bases from DNA to form abasic (AP) sites.
18 res of Nei enzymes unliganded or bound to an abasic (apurinic or apyrimidinic) site, until now there
19 ate cytotoxic double strand breaks (DSB) and abasic (apurinic/apyrimidinic (AP)) sites in DNA.
20 8-oxo-G) from DNA and then nicks the nascent abasic (apurinic/apyrimidinic) site by beta-elimination.
21                                              Abasic (apurinic/apyrimidinic) sites are among the most
22 itro that POLD3 promotes extension beyond an abasic by the Poldelta holoenzyme suggesting that while
23 AG and AlkA catalyze reactions between bound abasic DNA and small, primary alcohols to form novel DNA
24 rstanding of the chemistry and enzymology of abasic DNA largely relies upon the study of AP sites in
25 cal uracil search, contribute to binding the abasic DNA product and help present the DNA product to A
26 ure revealed TDG (catalytic domain) bound to abasic DNA product in a 2:1 complex, one subunit at the
27 nding modes of Mug between its substrate and abasic DNA product using both band shift and fluorescenc
28 ibute substantially to the binding of TDG to abasic DNA product, and it cannot account for the slow p
29 a single uracil, giving the complex with the abasic DNA product.
30 nthine in vitro is limited by release of the abasic DNA product.
31  glycosylase II (AlkA) bind tightly to their abasic DNA products, potentially protecting these reacti
32 dination of BER activities would protect the abasic DNA repair intermediate and ensure its correct pr
33 E1) is the predominant enzyme for processing abasic DNA sites in human cells.
34 abnormal interaction of R237C and G241R with abasic DNA substrates, but is not simply due to a DNA bi
35 p2 and Tdp2-DNA complexes with alkylated and abasic DNA that unveil a dynamic Tdp2 active site lid an
36 the DNA-O-glycosides are converted back into abasic DNA upon being incubated with AAG or AlkA in the
37      Biochemical studies showed TDG can bind abasic DNA with 1:1 or 2:1 stoichiometry, but the dissoc
38 sed base from its tight product complex with abasic DNA, contrary to previous reports.
39 DG forms a tight enzyme-product complex with abasic DNA, which severely impedes enzymatic turnover.
40 ted one of our unnatural DNAs in stabilizing abasic DNA.
41 ifier (SUMO) proteins weakens its binding to abasic DNA.
42                            Several different abasic duplexes achieve potent and selective inhibition,
43 on to the functional activation of the major abasic endonuclease in mammalian base excision repair (B
44 yrimidinic endonuclease 1 (APE1) is the main abasic endonuclease in the base excision repair (BER) pa
45  be recognized by uracil DNA glycosylase and abasic endonuclease to produce single-strand breaks.
46 estion with uracil DNA glycosylase (UNG) and abasic endonuclease.
47 nit binds very tightly to G . U mispairs and abasic (G . AP) sites, and somewhat less tightly G . T m
48 BER machinery of repair may be influenced by abasic-induced energetic alterations in the properties o
49                                 The oxidized abasic lesion 5'-(2-phosphoryl-1,4-dioxobutane) (DOB) is
50                                 The oxidized abasic lesion 5'-(2-phosphoryl-1,4-dioxobutane) (DOB) is
51  the fewest mutations in the vicinity of the abasic lesion and inserting dAMP with a frequency of 67%
52 v1 in ternary complex with DNA containing an abasic lesion and with dCTP as the incoming nucleotide.
53 , among the enzymes, hPoleta has the highest abasic lesion bypass efficiency.
54 ggest that hPoleta is best suited to perform abasic lesion bypass in vivo.
55 uencing assays to determine the sequences of abasic lesion bypass products synthesized by human Y-fam
56     To provide complete mutation spectra for abasic lesion bypass, we employed short oligonucleotide
57 ic bond, the ability of Rev1 to stabilize an abasic lesion in its active site and employ a surrogate
58 e reveals a mechanism of synthesis across an abasic lesion that differs from that in other polymerase
59          This enzyme inserts a C opposite an abasic lesion with much greater catalytic efficiency tha
60                                         Such abasic lesion-induced energetic enhancement of slipped/l
61 -16.8 min) in NCPs is shorter than any other abasic lesion.
62    We further demonstrate that destabilizing abasic lesions alter the loop distributions so as to fav
63 nitiating removal of mutagenic and cytotoxic abasic lesions as part of the base excision repair (BER)
64 1) is responsible for the initial removal of abasic lesions as part of the base excision repair pathw
65 t(50)(bypass)) required to bypass 50% of the abasic lesions encountered by hPoleta, hPoliota and hPol
66 ed observations in the literature concerning abasic lesions that are not repaired efficiently.
67         In addition, clusters of two or more abasic lesions within one to two turns of DNA, a hallmar
68 ly sensitive to 3'-OH base mispairs and 3' N:abasic lesions, which elicited 1000- to >20000-fold decr
69 erant of 5'-phosphate base mispairs and 5' N:abasic lesions.
70 ns flanking the G4 have been connected by an abasic linker to form G4 clamps, varying both linker len
71  RNA with 4-thiouridine, 4-deoxyuridine, and abasic modifications and G378/379 with 2-aminopurine, N7
72 d the effects of the 5'-terminal hydroxyl or abasic nucleotide on Ago2 cleavage activity and binding
73 residues 427-580) bound to DNA containing an abasic nucleotide paired with guanine, providing a glimp
74           The combination of single-atom and abasic nucleotide substitutions provides a powerful stra
75 e RNAs with either a 5'-terminal hydroxyl or abasic nucleotide.
76 th DNAs containing alkylated, mismatched and abasic nucleotides.
77       The human AP endonuclease Ape1 acts on abasic or 3'-blocking DNA lesions such as those generate
78 ated nucleotide damage, including base loss (abasic or apurinic/apyrimidinic (AP) sites).
79 ducts from DNA such as phosphoglycolates and abasic or apurinic/apyrimidinic (AP) sites.
80 lbeta), and different BER DNA intermediates (abasic or gapped DNA).
81                 Whether RNase H2 may process abasic or oxidized rNMPs incorporated in DNA is unknown.
82 fication rates for free TDG and TDG bound to abasic or undamaged DNA.
83 sential intermediates by overcoming slow TDG-abasic product dissociation during active DNA demethylat
84 uation in other glycosylases, release of the abasic product is faster than N-glycosidic bond cleavage
85          As with other DNA glycosylases, the abasic product is potentially more harmful than the init
86 xt of duplex DNA, insertion of high-affinity abasic product sites between two uracil lesions serves t
87                  The presence of intervening abasic product sites mimics the situation where hUNG act
88 ost human glycosylases bind tightly to their abasic product.
89 heses for abasic substitutions and show that abasic RNA duplexes allele-selectively inhibit both muta
90 tively modified depurinated/depyrimidinated (abasic) RNA.
91  that human RNase H2 is unable to process an abasic rNMP (rAP site) or a ribose 8oxoG (r8oxoG) site e
92 t and inserting preferably an A opposite the abasic site (A rule).
93 oguanine DNA glycosylase (OGG1), yielding an abasic site (AP).
94                             The C4'-oxidized abasic site (C4-AP) is a commonly formed DNA lesion, whi
95 s-link (ICL) resulting from the C4'-oxidized abasic site (C4-AP) is a unique clustered lesion compris
96 4-dioxobutane) (DOB) and the C4-hydroxylated abasic site (C4-AP), are formed reversibly.
97 ch is the first structure of any Nei with an abasic site analog.
98 wo oxidatively derived lesions as well as an abasic site analogue by the replicative DNA polymerase f
99 e effect of two spontaneous DNA lesions, the abasic site and 8-oxoguanine, on the transition from dup
100 ssion of intermediate products, including an abasic site and a single strand break, before the origin
101             Thus, dATP insertion opposite an abasic site and dATP misinsertions have common features.
102 product in a 2:1 complex, one subunit at the abasic site and the other bound to undamaged DNA.
103 was observed between the phosphate 5' to the abasic site and water H-bonded to N1 and N6 of A and N1
104 s Endonulcease Q (EndoQ), recognizes uracil, abasic site and xanthine, as well as hypoxanthine, and c
105                                           An abasic site at the G or T positions is cleaved by the en
106                 This effectively produces an abasic site because the template pocket is devoid of an
107 anner to other lyases, Ku nicks DNA 3' of an abasic site by a mechanism involving a Schiff-base coval
108 ass a single cyclobutane pyrimidine dimer or abasic site by translesion synthesis in the absence of s
109                  It is not known whether the abasic site bypass activity is an intrinsic property of
110 eplication, it may help Poldelta to complete abasic site bypass independently of canonical TLS polyme
111 sly that hpol eta is a major pol involved in abasic site bypass.
112 that the DNA between the 5' terminus and the abasic site can also be retained in junctions formed by
113  flanking Ku70 K31 in expanding the range of abasic site contexts that can be used as substrate was a
114 owed this activity is important for excising abasic site damage from ends.
115 es, metal ions, and active site features for abasic site endonucleases.
116  ssDNA breaks generated in cells lacking the abasic site endonucleases.
117 pends on uracil excision, which generates an abasic site for strand breakage.
118                                              Abasic site formation thermally destabilizes the duplex
119  including a lyase reaction that removes the abasic site from DNA following incision of its 5'-phosph
120 primary unhooking mechanism for psoralen and abasic site ICLs.
121 ne nucleobase and the aldehyde residue of an abasic site in duplex DNA.
122 erentially inserts an adenine opposite to an abasic site in RNA to create a quantitative polymerase c
123 ntermediate resulting from 5'-incision of an abasic site in the hairpin loop.
124 dition of each of the four nucleobases to an abasic site in the middle of the PNA strand.
125 t the polymerase stalls upon encountering an abasic site in the template strand, indicating that, lik
126 ropriate pyrimidine was positioned 5' to the abasic site in the template.
127 KlenTaq structure bound to DNA containing an abasic site indicates that binding of the nucleotide tri
128               Another strategic siting of an abasic site induces directed loop migration toward denat
129 on by replacement of the i+2 residue with an abasic site inhibits Pol II activity to the same degree
130 often considered to proceed through a common abasic site intermediate, emerging evidence indicates th
131                                     Detailed abasic site investigation elucidates the electrical impa
132 ency of nucleotide incorporation opposite an abasic site is controlled by energies associated with nu
133                                The resulting abasic site is further processed by apurinic/apyrimidini
134                                   Because an abasic site is highly mutagenic, it is critical that the
135                   Notably, the effect of the abasic site is nearly doubled when heated from room temp
136                             The C4'-oxidized abasic site is produced in DNA by a variety of oxidizing
137                                 The oxidized abasic site is removed in its entirety from the DNA and
138 estricted to substrates where excision of an abasic site is required for ligation, a degree of specif
139 w here that this activity is greatest if the abasic site is within a short 5' overhang, when this act
140  Like that of a previous study of bistranded abasic site lesion, the aim of this investigation was to
141                  Transport yield through the abasic site monolayer strongly increases with temperatur
142                             At 5' nucleobase-abasic site nicks, DraRnl prefers to ligate when the nuc
143 oxidation products: the 2-deoxyribonolactone abasic site of 1'-oxidation and the nucleoside 5'-aldehy
144              Here we report the effect of an abasic site on the rate and yield of charge transport th
145 ated nucleotide damage, including base loss (abasic site or 5'-dRP/AP sites).
146 cleotide, 8-oxodGTP, as well as bypass of an abasic site or 8-oxoG DNA template lesion in different c
147 bles translesion synthesis across a template abasic site or a cyclobutane thymidine dimer.
148  unhooked DNA fragments containing either an abasic site or a psoralen-thymine monoadduct.
149 bstitution of G12 of NHEIII(1) with a single abasic site or a single 8-oxoguanine prevented formation
150                           The presence of an abasic site or furan within a DNA duplex, electrophoreti
151  removing Tg to give an intermediate with an abasic site or single-strand break.
152 cating rapid exchange of AAG and APE1 at the abasic site produced by the AAG reaction.
153 netics of base repair reactions involving an abasic site product.
154   It therefore provides a new perspective on abasic site protection and the findings are discussed in
155  Taking advantage of the high resolution for abasic site recognition, the rate of uracil-DNA glycosyl
156 onuclease of the Nth/MutY family involved in abasic site removal during base excision repair.
157 imer was accurate, whereas replication of an abasic site resulted in mainly -1 frameshifts.
158          The most common lesion in DNA is an abasic site resulting from glycolytic cleavage of a base
159 ) bound to a 10-mer DNA duplex containing an abasic site resulting from the cleavage of a uracil base
160  with adenosine and, separately, opposite an abasic site show that there is almost no fluorescence in
161 interactions allow transient exposure of the abasic site so that it can be captured by APE1.
162 nds approximately 10-fold more tightly to an abasic site than to a hypoxanthine lesion site.
163 varying sizes was removed by OGG1 leaving an abasic site that was subsequently 5'-incised by AP endon
164 ty, B35DNAP was able to successfully perform abasic site TLS without template realignment and inserti
165 tic parameters for incorporation opposite an abasic site to interrogate the contributions of pi-elect
166 penultimate base pairs (PBs) adjacent to the abasic site using all 16 possible combinations.
167 incorporation for incoming dNTPs opposite an abasic site varied between 2- and 210-fold depending on
168                                           An abasic site was introduced at the 3' G of the HRE.
169 ss-link resulting from the reaction of a DNA abasic site with a guanine residue on the opposing stran
170 ase I, incorporates a nucleotide opposite an abasic site with efficiencies of A > G > T > C.
171 ly shorter than the estimated lifetime of an abasic site within a cell, suggesting that the observed
172                     The presence of a single abasic site within dsDNA that is in proximity to the lat
173 cleotide is efficiently inserted opposite an abasic site, a commonly formed and potentially mutagenic
174 ect nucleotides during the replication of an abasic site, a non-instructional DNA lesion.
175 n of 3-Eth-5-NITP is highly selective for an abasic site, and occurs even in the presence of a 50-fol
176 pass efficiencies on templates containing an abasic site, but another mutant, D316N/D515A, showed a l
177 serted and bonded in the primer opposite the abasic site, but it did not pair with a 5' T in the temp
178 rolyzable analog of dATP or dGTP opposite an abasic site, H-bonding was observed between the phosphat
179 inant AMP insertion, which also occurs at an abasic site, is unaffected by the identity of the 5'-tem
180 exes containing 5,6-dihydrouracil, a natural abasic site, its tetrahydrofuran analog, and undamaged d
181 nine opposite unsubstituted cytosine, (Me)C, abasic site, or unnatural nucleobase analogs.
182 base and then cleave the DNA backbone at the abasic site, resulting in a gap that is then filled with
183 te of transport is largely unaffected by the abasic site, showing Arrhenius-type behavior with an act
184 t the presence within the G4 structure of an abasic site, the most common lesion spontaneously genera
185 lge loop domain of a guanosine residue by an abasic site, the universal BER intermediate, increases t
186 a model in which APE1 displaces AAG from the abasic site, thereby coordinating the first two steps of
187 ytosine and incise the sugar backbone at the abasic site, thus initiating a base excision repair path
188 ond, converting 2'-deoxyuridine in DNA to an abasic site, was continuously monitored by electrophoret
189 of dNTPs when a DNA polymerase encounters an abasic site, we varied the penultimate base pairs (PBs)
190 e wild-type inserted an adenine opposite the abasic site, whereas these enzymes inserted cytosine and
191 otides, but not ribonucleotides, opposite an abasic site, with kinetic preference for dATP as the sub
192 sites are at least partly resistant to other abasic site-cleaving activities as well.
193 E1 for Polbeta is higher in the complex with abasic site-containing DNA than after the APE1-catalyzed
194 aevis has been shown to cleave psoralen- and abasic site-induced ICLs in Xenopus egg extracts.
195 UV irradiation and a significant decrease in abasic site-induced mutagenesis in the immunoglobulin lo
196 ying a thymidine dimer than to those with an abasic site.
197 RuvC product than those carrying a synthetic abasic site.
198 site during nucleotide selection opposite an abasic site.
199 tion of a non-natural nucleotide opposite an abasic site.
200 d by as little as two paired bases 5' of the abasic site.
201 eaving the phosphodiester backbone 5' to the abasic site.
202 nnot perform translesion synthesis across an abasic site.
203 ivity that incises the DNA backbone 5' to an abasic site.
204  groups are extended when paired opposite an abasic site.
205 a Schiff-base covalent intermediate with the abasic site.
206  to create frameshift mutations opposite the abasic site.
207  and APE1 enables APE1 to replace AAG at the abasic site.
208 for the replication of the non-instructional abasic site.
209 ng dAMP with a frequency of 67% opposite the abasic site.
210 sivity, impaired primer extension beyond the abasic site.
211 onformation, base-substitution fidelity, and abasic-site translesion synthesis.
212 ficantly reduced AP endonuclease activity on abasic-site-containing oligonucleotide substrates, a res
213 L) constitutes a sensing zone for individual abasic sites (and furan analogs) in double-stranded DNA
214 ond of the bases to give potentially harmful abasic sites (AP-sites).
215 ty are avoided by deoxyuridine conversion to abasic sites ahead of nascent lagging strand DNA synthes
216  variety of three-lesion clusters containing abasic sites and 8-oxo-7, 8-dihydroguanine to investigat
217 ng that UVA produces a significant amount of abasic sites and cyclobutane pyrimidine dimers (CPDs).
218  bypass of other common DNA lesions, such as abasic sites and cyclobutane thymine dimers.
219 and necrosis; indeed, steady-state levels of abasic sites and nuclear PAR polymers were significantly
220              Experiments with DNA containing abasic sites and polyethylene glycol spacers show that t
221                                              Abasic sites and single base bulges are thermodynamicall
222  Here we discuss the binding properties with abasic sites and single base bulges of Rh(bpy)(2)(chrysi
223                           The recognition of abasic sites and single base bulges with bulky metalloin
224 ty and the ability to insert and extend past abasic sites and thymine glycol lesions.
225  and can read through damaged bases, such as abasic sites and thymine photo-dimers.
226              Pol V carries out TLS to bypass abasic sites and thymine-thymine dimers resulting from U
227 merase-mediated translesion DNA synthesis of abasic sites and TT dimers, while other probes have been
228                                              Abasic sites are chemically labile, but naked DNA contai
229         At single-strand breaks, 5'-terminal abasic sites are excised by the 5'-deoxyribose-5-phospha
230                                              Abasic sites are ubiquitous DNA lesions that are mutagen
231 EC3A-expressing cells resulted in a surge of abasic sites at replication forks, revealing an ATR-medi
232 nique type of replication stress by inducing abasic sites at replication forks.
233 e repair process by recognizing intermediary abasic sites cleaving the phosphodiester backbone 5' to
234 s N3-methyladenine, as well as bypassing the abasic sites generated after Mag1 removes N3-methyladeni
235 Nth and MutM can perform strand incisions at abasic sites in addition to NApe.
236 e-dependent increases in the accumulation of abasic sites in cells at levels that correlate with thei
237                                              Abasic sites in DNA are prevalent as both naturally form
238                 Because of the importance of abasic sites in genetic damage, most research has involv
239                        X-ray structures with abasic sites in oligonucleotides have been reported for
240        The inability to enzymatically cleave abasic sites in single-stranded telomere regions would b
241 ain is capable of highly efficient bypass of abasic sites in the absence of the helicase-like or cent
242 nt human Poldelta holoenzyme performs TLS of abasic sites in vitro much more efficiently than the wil
243 ainly responsible for repairing oxidized and abasic sites into DNA.
244 s the fact that DNA polymerase can bypass dA/abasic sites more efficiently than other dN/abasic sites
245 containing extrahelical fluorescein adducts, abasic sites nor a cyclobutane pyrimidine dimer, regardl
246 roach in which individual bases are added to abasic sites of a peptide nucleic acid (PNA).
247 ional affinity toward DNA targets containing abasic sites opposite of the modification site (DeltaT(m
248 brogates the ability of the enzyme to bypass abasic sites or thymine glycol lesions.
249             In a number of cellular studies, abasic sites preferentially code for dATP insertion (the
250 radation of mtDNA and that strand breaks and abasic sites prevail over mutagenic base lesions in ROS-
251    Recently, it was discovered that oxidized abasic sites react with the opposing strand of DNA to pr
252 ctural effects of multiple tetrahydrofuranyl abasic sites replacing loop adenines (A/AP) and tetrad g
253 , in vitro end joining experiments show that abasic sites significantly embedded in double-stranded D
254                                     Oxidized abasic sites such as 2-deoxyribonolactone (L) are produc
255                       Recently, DNA oxidized abasic sites that are produced by potent antitumor agent
256                                The repair of abasic sites that arise in DNA from hydrolytic depurinat
257 aged DNA bases to generate potentially toxic abasic sites that in turn generate highly toxic DNA stra
258  activity of hPMC2 is required for repair of abasic sites that result from estrogen-induced DNA damag
259                      An oligo RNA containing abasic sites that were derivatized with ARP was pulled d
260                                 The surge of abasic sites upon ATR inhibition associated with increas
261 ose structures were inspired by the oxidized abasic sites was synthesized and screened for the abilit
262        This tight binding could help protect abasic sites when the adaptive response to DNA alkylatio
263 nd to uracil-containing substrates but binds abasic sites with a Kd of <1.4 mum.
264                            Cisplatin induces abasic sites with a reduced accumulation in uracil DNA g
265 hat Rh(bpy)(2)(chrysi)(3+) selectively binds abasic sites with affinities of 1-4 x 10(6) M(-1); speci
266 s between 2'-deoxyadenosine and the oxidized abasic sites, 5'-(2-phosphoryl-1,4-dioxobutane) (DOB) an
267  incisions (a prerequisite for CSR) at these abasic sites, a direct test of the requirement for APE1
268 rations including 3'-phosphoglycolate and 3'-abasic sites, and exhibits 3'-nucleosidase activity indi
269 ons, such as single and multiple mismatches, abasic sites, and single nucleotide insertions.
270 es (>/= 20 bp) that additionally may contain abasic sites, cross-links, or miscoding lesions are acqu
271 e that hpol eta, a major copying enzyme with abasic sites, follows a purine rule, which can also lead
272 , suggests that Rh(bpy)(2)(chrysi)(3+) binds abasic sites, like mismatches, through insertion of the
273  variety of damage, such as the formation of abasic sites, pyrimidine dimers, alkylation adducts, or
274 e nucleobase to the backbone in DNA leads to abasic sites, the most frequent lesion under physiologic
275 le mismatches, multiple mismatches, and even abasic sites, whereas RecA and Rad51 are not.
276         Apurinic/apyrimidinic (AP) sites, or abasic sites, which are a common type of endogenous DNA
277 f dUs by uracil DNA glycosylase (UNG) yields abasic sites, which are excised by apurinic/apyrimidinic
278  most likely by removing uracils to generate abasic sites.
279 city of a DNA methylating agent that creates abasic sites.
280 /abasic sites more efficiently than other dN/abasic sites.
281  UDG present within this holoenzyme, leaving abasic sites.
282 t these are converted into non-instructional abasic sites.
283 ed as CPDs, are true CPDs; the other 40% are abasic sites.
284 ratus capable of repairing damaged bases and abasic sites.
285 mutants, enhancing dA incorporation opposite abasic sites.
286 plication in vivo and, when required, TLS of abasic sites.
287 yield base modifications, strand breaks, and abasic sites; have a propensity to adopt non-canonical D
288 vestigated whether apurinic/apyrimidinic (AP/abasic) sites were more frequent in regions of DNA repli
289 r processing apurinic/apyrimidinic (known as abasic) sites, is also involved in the generation of sma
290 he RNAi protein argonaute 2, even though the abasic substitution disrupts the catalytic cleavage of R
291           We describe flexible syntheses for abasic substitutions and show that abasic RNA duplexes a
292                     These findings introduce abasic substitutions as a tool for tailoring RNA duplexe
293               Here, we examine the effect of abasic substitutions on RNAi and allele-selective gene s
294              Here we combine single-atom and abasic substitutions to probe functions of conserved nuc
295                                              Abasic substitutions within DNA or RNA are tools for eva
296 le information is available on the impact of abasic substitutions within RNA or on RNA interference (
297 lycosidic bond and leaves the C1' hydrolyzed abasic sugar in the flipped state.
298 the beta rather than the alpha anomer of the abasic sugar, which might stabilize the enzyme-product c
299 ers 3'-OH adenosine when sealing opposite an abasic template site.
300 junction, sites where the flexibility of the abasic "universal hinge" relaxes unfavorable interaction

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