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1 nzymatic activity in repair of abasic sites (AP endonuclease).
2 turn corresponds to a decreased abundance of AP endonuclease.
3 the 5' side of the deoxyribose phosphate by AP endonuclease.
4 in from yeast and show that it is a class II AP endonuclease.
5 emove the 5' sugar-phosphate residue left by AP endonuclease.
6 notion that yeast contains only one major 5'-AP endonuclease.
7 itors of a critical DNA repair enzyme, human AP endonuclease.
8 ecognition of bistranded AP lesions by human AP endonuclease.
9 RP residues that remain after cleavage by 5'-AP endonuclease.
10 n of bistranded abasic site lesions by human AP endonuclease.
11 nts following incision of the abasic site by AP endonuclease.
12 ic/apyrimidinic (AP) site intermediate by an AP endonuclease.
13 significantly stimulated by the presence of AP-endonuclease.
14 that are toxic if they are not processed by AP endonucleases.
15 homologous to the exonuclease III family of AP endonucleases.
16 critical elements in targeted recognition by AP endonucleases.
17 n/Escherichia coli exonuclease III family of AP endonucleases.
18 N-terminus show only low homology with other AP endonucleases.
19 stored by addition of apurinic/apyrimidinic (AP) endonuclease.
20 d by reactive oxygen species are repaired by AP-endonucleases.
21 DG) and mitochondrial apurinic/apyrimidinic (AP) endonucleases.
22 ons is carried out by apurinic/apyrimidinic (AP) endonucleases.
23 ons and resembles the apurinic/apyrimidinic (AP) endonucleases.
24 erential oxidative deamination in vitro, and AP endonuclease 1 (APE1) can cleave the resulting ICL DN
27 dent and that this activity co-purifies with AP endonuclease 1 (APE1) over phosphocellulose and gel f
29 , we further provide the first evidence that AP endonuclease 1 (APE1) prevented TNR expansions via it
30 ystallographic studies reveal loops in human AP endonuclease 1 (APE1) that interact with the major an
31 The follow-on base excision repair enzyme, AP endonuclease 1 (APE1), stimulates the turnover of TDG
33 at the appropriate time in development when AP endonuclease 1 (Apex), the upstream protein in BER, i
35 5'-flanking T:G mispair; this reduces OGG1, AP endonuclease 1, and DNA polymerase beta activities.
37 sic site that was subsequently 5'-incised by AP endonuclease 1, introducing a single-strand breakage
38 P site with either endonuclease III or human AP endonuclease 1, strongly inhibit excision of 8-oxoG b
39 s to AP sites inhibits the activity of human AP endonuclease 1, which is as a valid anticancer drug t
42 erexpression of human apurinic/apyrimidinic (AP) endonuclease 1 (APE1/Ref-1), a key enzyme in the DNA
43 glycosylase 1 (OGG1), apurinic/apyrimidinic (AP) endonuclease 1, DNA polymerase beta, and DNA ligases
44 ubstrate specificity, lack of stimulation by AP-endonuclease 1 (APE1) and anomalous DNA binding confo
48 tect both uracil DNA N-glycosylase (UNG) and AP-endonuclease 1 (APE1) within few nanograms of nuclear
49 re particles using the known repair enzymes, AP-endonuclease 1, DNA polymerase beta and DNA ligase II
51 se excision repair (homologs of XPF, XPC and AP-endonuclease-1), and repair of double-stranded DNA br
53 ision repair protein, Apurinic/apyrimidinic (AP) endonuclease 2 (APE2, APN2, or APEX2), is required f
55 air enzyme whose nuclease activities include AP-endonuclease, 3'-exonuclease, 3'-phosphodiesterase an
56 omology to the gene encoding the major human AP endonuclease, a component of the highly conserved DNA
60 tivity of an E.coli mutant deficient for the AP endonuclease activities associated with exonuclease I
63 etabolism, decreases the efficiency of human AP endonuclease activity and that this effect is mostly
64 ver, glutathione-agarose was able to deplete AP endonuclease activity from GST-PO fusion protein prep
67 uced with Ape1/ref-1 exhibited 2-fold higher AP endonuclease activity in the oligonucleotide cleavage
68 hin NExo that is responsible for its lack of AP endonuclease activity is also important for its 3'-ph
69 n interactions of Ape1, we conclude that the AP endonuclease activity is essential for cellular viabi
72 tion of Asp-210 by Asn or Ala eliminates the AP endonuclease activity of HAP1, while substitution by
74 titution of alanine for Asn212 abolished the AP endonuclease activity of purified recombinant HAP1 pr
75 of the carboxyl terminus does not affect the AP endonuclease activity of the protein, but this protei
77 nylated APE1 displayed significantly reduced AP endonuclease activity on abasic-site-containing oligo
78 the base excision repair pathway, exhibiting AP endonuclease activity that incises the DNA backbone 5
80 As a means of confirming that the source of AP endonuclease activity was in fact due to PO, glutathi
81 were generally not altered in rho(0) cells, AP endonuclease activity was substantially reduced in nu
83 P1 and Ref-1) accounts for >95% of the total AP endonuclease activity, and is essential for the prote
84 ly been shown to be independent of Apn1-like AP endonuclease activity, and the main reason for the MM
94 -independent class II apurinic/apyrimidinic (AP) endonuclease activity and represents greater than 90
98 me initiating repair of AP sites is the Ape1 AP endonuclease (also called Apex or Hap1), which also f
99 ave weak dRP lyase activity and to stimulate AP endonuclease and FEN1 activities on BER substrates.
101 al lysates with pure uracil DNA glycosylase, AP endonuclease and/or the catalytic subunit of polymera
102 oli strain defective for the major 5'-acting AP endonucleases and the fusions purified using glutathi
103 NA glycosylase (UDG), apurinic/apyrimidinic (AP) endonuclease and DNA ligase I, pol iota can use its
104 e1 is the major human apurinic/apyrimidinic (AP) endonuclease and initiates repair of abasic sites by
106 sms are equipped with apurinic/apyrimidinic (AP) endonucleases and 3'-nucleases that initiate repair.
108 revealed that the expression of RecA, SmnA (AP endonuclease), and Nth (endonuclease) were down-regul
111 s ability to interact directly both with the AP endonuclease (APE) and with DNA polymerase beta (pol
112 sed on studies in Escherichia coli, in which AP endonuclease (APE) removes all 3' blocking groups (in
113 sites in DNA is through the participation of AP endonuclease (APE), which initiates the removal of ba
119 We examined substrate binding by the human AP endonuclease, Ape protein (also called Hap1, Apex or
124 4 as an N-terminally truncated form of human AP endonuclease (Ape1) lacking residues 1-35 (delta35-Ap
126 the presence of a comparable amount of human AP endonuclease (APE1) the specific activity of OGG1 was
127 ntaining duplex is a substrate for the human AP endonuclease (APE1), an enzyme that cleaves an apurin
128 t repairs AP sites in mammalian cells is the AP endonuclease (APE1), which functions through the base
129 using murine homolog of MutY (Myh) and human AP endonuclease (Ape1), which shares 94% amino acid iden
134 hosphodeoxyribose (dRP) moiety, generated by AP-endonuclease (APE1), is removed by the lyase activity
139 epair and between the apurinic/apyrimidinic (AP) endonuclease, Ape1, and the 8-oxoguanine DNA glycosy
140 B and the major human apurinic/apyrimidinic (AP) endonuclease, APE1, physically and functionally inte
142 myces cerevisiae, the apurinic/apyrimidinic (AP) endonucleases Apn1 and Apn2 act as alternative pathw
143 g, Nth, and NTH1) and apurinic/apyrimidinic (AP) endonucleases (Apn1, APE1, and Nfo), the analysis of
144 oth cases, expression of the unrelated yeast AP endonuclease, Apn1, largely restored resistance.
148 ation of oxidized bases must be processed by AP endonucleases before they compromise cell integrity.
149 ing" of the AP site-containing DNA strand by AP endonuclease, beta-pol performs DNA synthesis prior t
152 the first to demonstrate the inducibility of AP-endonuclease by a human class I carcinogen associated
153 OGG1's activity in vitro in the presence of AP-endonuclease by reducing its affinity for the abasic
156 ses caused a 7- to 18-fold mutator effect in AP endonuclease-deficient (deltaapn1) yeast, which depen
165 hese data suggest that following incision by AP endonuclease, DNA Pol beta recognizes and binds to th
167 sion repair pathway (uracil DNA glycosylase, AP endonuclease, DNA polymerase beta, and an NAD+-depend
169 the lysate contained uracil DNA glycosylase, AP endonuclease, DNA polymerase, flap endonuclease, and
170 ER proteins required for PCNA-dependent BER (AP endonuclease, DNA polymerases delta, beta and DNA lig
171 that is slower than the respective rates of AP endonuclease, DNA synthesis, and ligation, suggesting
172 III, lambda exonuclease, RNase H, RNase HII, AP endonuclease, duplex-specific nuclease, DNase I, or T
176 mutans expresses an inducible, class II-like AP endonuclease, encoded by the smx gene, that exhibits
179 re we report that the apurinic/apyrimidinic (AP) endonucleases--Escherichia coli Xth and human APE1--
181 studies are described using Escherichia coli AP endonucleases, exonuclease III and endonuclease IV.
182 bacterial Nfo represent the two conserved 5' AP endonuclease families in the biosphere; they both rec
183 ain homologous to the apurinic/apyrimidinic (AP) endonuclease family and shows nicking in vitro with
184 etype for a conserved apurinic/apyrimidinic (AP) endonuclease family that primes DNA repair synthesis
185 iled structural and biochemical study of the AP endonuclease from Neisseria meningitidis that has all
187 an E.coli mutant lacking the major 5'-acting AP endonucleases from sensitivity to an alkylating agent
195 ant frequencies in spermatogenic cell types, AP endonuclease heterozygous (Apex(+/-)) knockout mice w
204 ues are eliminated by apurinic/apyrimidinic (AP) endonucleases in the nucleotide incision repair path
205 permutating B cells, whereas APE1, the major AP-endonuclease in faithful base excision repair, does n
206 he DNA repair enzyme, apurinic/apyrimidinic (AP)-endonuclease, in isolated mesothelial cells, the pro
208 Smx is likely the primary, if not the sole, AP endonuclease induced during growth at low pH values.
209 3' side following incision at its 5' side by AP endonuclease is a prerequisite to completion of these
210 ial phosphorylation sites, recombinant human AP endonuclease is weakly phosphorylated in vitro (4% at
211 is property of the exonuclease III family of AP endonucleases is remarkably conserved from Archaea to
213 5 and 2.5 microg/cm2 significantly increased AP-endonuclease mRNA and protein levels as well as enzym
214 g BER in single and multiple glycosylase and AP-endonuclease mutants confirmed that Mag1 is the major
216 s in DNA repair: one is a typical Neisserial AP endonuclease (NApe), whereas the other is a specialis
218 processing of these noncoding lesions by the AP endonucleases Nfo, ExoA, and Nth contribute to the pr
222 and characterised two apurinic/apyrimidinic (AP) endonuclease paralogues in the human pathogen Neisse
223 ocess of damaged bases, apurinic-apyrimidic (AP) endonucleases play an essential role in enabling the
225 reviously, we showed that when the zebrafish AP endonuclease protein (ZAP1) level is knocked down, em
226 ble-nucleotide flipping and sharp bending by AP endonucleases provide exquisite damage specificity wh
227 e of action used by both human and bacterial AP endonucleases raises important questions regarding th
228 The magnesium dependence of steady-state AP endonuclease reactions was sigmoidal for both wild-ty
232 f AP sites with six purified human proteins: AP endonuclease, replication factor C, PCNA, flap endonu
233 he AP site has been previously 5'-incised by AP endonuclease, resulting in a 5' 2-deoxyribose 5-phosp
234 irectly test whether a genetic diminution of AP endonuclease results in increased spontaneous mutant
235 omer of the carbocyclic abasic site by human AP endonuclease showed that the enzyme recognizes both c
236 sion of the S. mutans apurinic/apyrimidinic (AP) endonuclease, Smx, in Escherichia coli; initial char
237 inic/apyrimidinic (AP) sites is initiated by AP endonucleases, such as the human Ape1 protein (also c
239 the incision of DNA at an abasic site by an AP endonuclease, they all lack the ability for the subse
240 itochondrial class II apurinic/apyrimidinic (AP) endonuclease to cleave the DNA backbone on the 5' si
241 ycosylase activity by apurinic/apyrimidinic (AP) endonuclease using murine homolog of MutY (Myh) and
242 nfocal scanning laser microscopy showed that AP-endonuclease was primarily localized in the nucleus b
243 ifunctional glycosylase/AP lyases as well as AP endonuclease, were significantly higher in cerebellar
245 : oxidative Polbeta-DPC depended on the Ape1 AP endonuclease, which generates the Polbeta lyase subst
246 by repair initiated by 'class II' apurinic (AP) endonucleases, which cleave immediately 5'to abasic
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