4.2.99.18: DNA-(apurinic or apyrimidinic site) lyase
This is an abbreviated version!
For detailed information about DNA-(apurinic or apyrimidinic site) lyase, go to the full flat file.
Reaction
the C-O-P bond 3' to the apurinic or apyrimidinic site in DNA is broken by a beta-elimination reaction, leaving a 3'-terminal unsaturated sugar and a product with a terminal 5'-phosphate
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Synonyms
8-oxoG DNA glycosylase, abasic (AP)-endonuclease, abasic endonuclease, AdAPE1/Ref-1, Af0371, Afogg enzyme, ALKBH1, AP 1, AP DNA endonuclease 1, AP Dnase, AP endo, AP endonuclease, AP endonuclease 1, AP endonuclease Ape1, AP endonuclease Class I, AP endonuclease I, AP endonuclease VI, AP lyase, AP site-DNA 5'-phosphomonoester-lyase, AP-endonuclease, AP-endonuclease 1, AP-endonuclease 2, AP-endonuclease/3'-5'exodeoxyribonuclease, AP-lyase, Ap1, Ap2, Ape, APE-1, APE/Ref-1, APE1, APE1/Ref-1, Ape1L, Ape2, APEN, APEX nuclease, APEX1, APLM, APN, APN-1, APN1, apurinic DNA endonuclease, apurinic endodeoxyribonuclease, apurinic endonuclease, apurinic endonuclease 1, apurinic-apyrimidinic DNA endonuclease, apurinic-apyrimidinic endodeoxyribonuclease, apurinic-apyrimidinic endonuclease, apurinic-apyrimidinic endonuclease 1, apurinic-apyrimidinic endonuclease I, apurinic/apyrimidic endonuclease 1, apurinic/Apyrimidinic (AP) endonuclease 1, apurinic/apyrimidinic AP endonuclease, apurinic/apyrimidinic DNA endonuclease 1, apurinic/apyrimidinic endonuclease, apurinic/apyrimidinic endonuclease 1, apurinic/apyrimidinic endonuclease 1/redox factor-1, apurinic/apyrimidinic endonuclease 2, apurinic/apyrimidinic endonuclease APE1, apurinic/apyrimidinic endonuclease-1, apurinic/apyrimidinic endonuclease-1/Redox factor-1, apurinic/apyrimidinic endonuclease/redox effector factor-1, Apurinic/apyrimidinic endonuclease1/redox factor 1, apurinic/apyrimidinic endonuclease1/redox factor-1, apurinic/apyrimidinic lyase, apurinic/apyrimidinic site lyase, apurinic/apyrimidinic specific endonuclease, apurinic/apyrimidinic-endonuclease, apyrimidinic endonuclease, archaeal GO glycosylase, BAP1, class II AP endonuclease LMAP, class II apurinic/apyrimidinic(AP)-endonuclease, class-II AP-endonuclease, deoxyribonuclease (apurinic or apyrimidinic), DNA lyase, DNA polymerase X, DNA-(apurinic or apyrimidinic site) lyase, E. coli endonuclease III, EC 3.1.25.2, EcoNth, Endo III, endodeoxyribonuclease, endodeoxyribonuclease III, EndoIV, endonuclease III, endonuclease IV, endonuclease VI, endonuclease VIII, Escherichia coli endonuclease III, EXO-3, ExoA, ExoA type AP endonuclease, ExoIII, HAP-1, HAP1, HAP1h, hAPE, hAPE1, hNTH, hNTH1, hOgg1 protein, HpXth, human apurinic/apyrimidinic endonuclease, human apurinic/apyrimidinic endonuclease 1, Kae1, KsgA, LplExo, Micrococcus luteus UV endonuclease, MJ0724, mjOgg, MMH, More, mtAPE, MtbXthA, multi-functional apyrimidinic endonuclease1/redox factor-1, N-glycosylase AP lyase, N-glycosylase apurinic/apyrimidinic lyase, NapE, Nei, Nfo, Ntg1, Ntg1p, Ntg2, Ntg2p, Nth, NTH1, nuclease SmnA, nuclease, apurinic endodeoxyribo-, nuclease, apurinic-apyrimidinic endodeoxyribo-, nuclease, endodeoxyribo-, III, Ogg2, oxoG DNA glycosylase, Pa-AGOG, Pa-AGOG DNA glycosylase, PAE2237, PaKae1, PALF, pE296R, PF0258, phage-T4 UV endonuclease, redox effector factor 1, redox factor-1, redox factor-1:Ref-1, Ref-1, REF-1 protein, Ref1, SisExoIII, Smx nuclease, TvoExo, UL30, UV endo V, UV endonuclease, UV endonuclease V, X-ray endonuclease III, XTH, xthA, ZAP1, zApe
ECTree
Specific Activity
Specific Activity on EC 4.2.99.18 - DNA-(apurinic or apyrimidinic site) lyase
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0.0000015
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age-dependent modulation of APE activity in mouse liver organelles, 4-months, mitochondria
0.0000196
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age-dependent modulation of APE activity in mouse liver organelles, 10-months, total extract
0.0000232
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age-dependent modulation of APE activity in mouse liver organelles, 20-months, total extract
0.0000236
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age-dependent modulation of APE activity in mouse liver organelles, 4-months, total extract
0.000038
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age-dependent modulation of APE activity in mouse liver organelles, 4-months, nuclear
0.0000485
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age-dependent modulation of APE activity in mouse liver organelles, 10-months, nuclear
0.000072
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age-dependent modulation of APE activity in mouse liver organelles, 20-months, nuclear
0.0000096
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age-dependent modulation of APE activity in mouse liver organelles, 10-months, mitochondria
0.0000096
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age-dependent modulation of APE activity in mouse liver organelles, 20-months, mitochondria
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cells lacking Nfo and ExoA are around 1.2times more susceptible to H2O2 treatment than cells of the parental strain
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compared to wild-type spores, nfo and exoA spores exhibit slower outgrowth, although they exhibit essentially identical rates of germination when germination is judged by determining the decrease in the OD600 of spore cultures shortly after addition of spores to germination medium
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germination rate of spores lacking both Nfo and ExoA is similar to that of wild-type spores, but the return to vegetative growth (outgrowth) is significantly slower for the nfo exoA spores
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The absence of Nfo and ExoA in uvrA and recA spores resulted in a slow-outgrowth phenotype
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the mutation frequency in outgrown nfo exoA spores is 10fold higher than that in outgrown wild-type spores treated with H2O2
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the outgrowth of spores lacking the enzyme is slowed, and the spores have an elevated mutation frequency, suggesting that these enzymes repair DNA lesions induced by oxidative stress during spore germination and outgrowth.
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T58C zApe has near wild-type human Ape1 redox activity in the transactivation assay
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Activity is determined with phage T4 AP DNA endonuclease assay agrees with divalent metal (Mn2+ and Zn2+) content measured for purified His-tagged Endo IV wild-type and mutant proteins, except for E261Q and to a lesser extent E145Q, which are adjacent in the active site. Mutations of the first-shell metal-ion binding residues resulted in mild (10fold reduction activity, H109N and D179N), severe (100-2600fold reduction in activity, H69N, H182N, D229N, H216N and H231N) or complete loss (E145Q, E261Q) of catalytic activity in both the T4 AP-DNA endonuclease assay and the AP-oligonucleotide cleavage assay
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10 mM Mg2+, all Cys mutants except those with C99S mutation are at least as active as the wild-type APE1
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750 nM substrate and 100 nM enzyme and a reaction time of 3 h is sufficient to convert most, if not all, of the Rp stereoisomer substrate DNA into product
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activity of Cys99 mutants is comparable to that of the wild-type in 0.5 or 2mM Mg2+, while only the Cys99 mutants are strongly inhibited at 5 mM and higher Mg2+ concentration
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APE-1 expression in tissues from Helicobacter pylori-infected subjects is significantly increased compared to that in tissues from subjects after successful eradication therapy
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APE/Ref-1 accounts for 95% of the total apurinic/apyrimidinic endonuclease activity and is essential for the protection of cells against the toxic effects of several classes of DNA-damaging agents
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APE/Ref-1 is involved in the regulation of metastatic potential in melanoma cells
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APE/Ref-1 is very sensitive to redox-status alterations. ROS regulates its activity and expression on both transcriptional and posttranscriptional levels
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Ape1 has only slightly more robust activity on the partial DNA-DNA duplex than on the comparable DNA/RNA duplex.
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Ape1/Ref-1 increases the expression of glial cell-derived neurotropic factor receptor alpha1 (GFRalpha1), a key receptor for glial cell-derived neurotropic factor (GDNF). Expression of Ape1/Ref- 1 leads to an increase in the GDNF responsiveness in human fibroblast. Ape1/Ref-1 induced GFRalpha1 transcription through enhances binding of NF-kappaB complexes to the GFRalpha1 promoter.
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By adding of purified Y-box-binding protein-1 to the nuclease reaction containing 0.2 microg of TAP-hNTH1 (minimum of protein required to see cleavage of the DNA duplex), there is an 12fold increase in cleavage activity
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Cell-based analysis of redox activity for hApe1 Cys-mutants using an in vitro EMSA redox assay in which reduction of the trancription factor AP-1 by hApe1 results in a shifted band. Only C65A hApe1 is found to be redox inactive.
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creation of three-strand substrates provided a 2- to 2.5fold increase in the specific activity of Ape1 over the partial duplex with the abasic lesion positioned at the ssDNA-dsDNA junction (54Fendbubble18-18DNA)
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Cys99 in hAPE1 as a critical residue modulating function for ensuring optimum activity
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decreased levels of AP endonuclease activity (smaller amount of cleaved 14-mer products and greater amount of uncleaved 26-mer oligonucleotides) are observed in both H460 and H69 cells that express high levels of endogenous Bcl2 as compared with the other cell lines that express undetectable levels of Bcl2
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expression of endogenous Bcl2 is associated with decreased APE1 endonuclease activity in various human lung cancer cells
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GFRalpha1 levels correlates proportionally with Ape1/Ref-1 in cancer cells
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in neuronal cells, the Ape1/Ref-1-mediated increase in GDNF responsiveness not only stimulated neurite outgrowth but also protected the cells from beta-amyloid peptide and oxidative stress
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Increased expression of APE/Ref-1 protein in nucleus of different human melanoma cell lines
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involvement of APE/Ref-1 in the process of inflammation
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Mutation D70A has decreased AP incision activity
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no activity is detected using a probe without 8-oxoguanine residue demonstrating the specificity of hNTH1 for oxidized DNA duplex
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oxidized APE/Ref-1 lacks endonuclease activity
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substrates with either a purine (G) or a pyrimidine (C) positioned opposite the AP site and two purines flanking the abasic site shows that Ape1 incision activity under optimal reaction conditions is two to threefold higher with the GFT-CCA, CFA-GCT, and CFT-GGA arrangements relative to GFA-CCT
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TAP-hNTH1 expressing cells transfected with a small interference RNA specific to hNTH1 show decreased protein levels and nuclease activities toward the radioactive duplex 8-oxoguanine
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the enzyme is responsible for eliminating as many as 105 potentially mutagenic and genotoxic lesions from the genome of each cell every day
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the knockdown of endogenous Ape1/Ref-1 in pancreatic cancer cells markedly suppresses GFRalpha1 expression and invasion in response to GNDF, while overexpression of GFRalpha1 restores invasion
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the MCF7-eluted TAP-hNTH1 protein exhibits nuclease activities on a radioactive duplex containing 8-oxoguanine residues
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The necessity of APE1 for cellular survival and its frequent overexpression in tumor cells strongly suggest a fundamental role of this protein in preventing cell death and in controlling cellular proliferation.
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The nucleotide incision repair (NIR) activity of APE1 provides an alternative and complementary repair pathway to BER
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The regulatory functions of the different APE1 activities can be fine-tuned and implemented via three different mechanisms: increase in APE1 level after transcriptional activation, relocalization of APE1 from the cytoplasm to the nucleus, and modulation of the posttranslational modifications of APE1, such as acetylation and phosphorylation.
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The specific activity is significantly increased in the case of the D70A mutant enzyme. Upon incubation at 37°C, 5 nM of purified APE1 mutant D70A remove most of the 3'-phosphoglycolate residues in 10 min, while the same enzyme amounts of APE1 converts only around 60% and 50% of the substrate into the corresponding 3'-OH form.
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Y-box-binding protein-1 binds specifically to the auto-inhibitory domain of hNTH1 to stimulating its activity
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Y-box-binding protein-1 strongly stimulates in vitro the activity of hNTH1 toward DNA duplex probes containing oxidized bases, lesions prone to be present in cisplatin treated cells
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Mutation A138D has decreased AP incision activity
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upon incubation at 37°C, 5 nM of LMAP protein remove most of the 3'-PG residues in 10 min, while the LMAP mutant A138D converts only around 50% of the substrate into the corresponding 3'-OH form
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APE1 exonuclease activity
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APE1 is most efficiently (5% yield) modified by DNA substrate bearing the 5'-pF group (DNAFAP-pF), which flanks a nick. This DNA structure is a model of a short-patch BER intermediate or a long-patch BER product and is an analog of the product of endonuclease or substrate of the exonuclease APE1 activity
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genomic instability increased in the livers of 1-month-old methionine adenosyltransferase 1a knock-out mice, compared with wild-type mice, whereas Apex1 mRNA and protein levels are reduced by 20% and 50%, in knock-out mice of all ages
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in mouse cultured hepatocytes, APEX1 protein levels decrease by 40% despite the increase in mRNA levels, and treatment with 2 mmol/L S-adenosylmethionine is able to completely prevent it
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the redox activity of APE/Ref-1 is regulated by chemical reduction and oxidation in vitro
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mRNA levels of APE/Ref-1 decrease 43.36% and increase 31.75% in acute spinal cord injury and spinal cord injury plus embryonic neural stem cells therapy groups, respectively in acute study groups and decrease 31.97% and increase 65.13% in chronic spinal cord injury and spinal cord injury plus embryonic neural stem cells therapy groups in chronic study groups, when compared to the sham. After embryonic neural stem cells therapy, in both acute and chronic spinal cord injury groups APE/Ref-1 levels significantly improve.
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overexpression of Ape1 reduces cisplatin-induced apoptosis in sensory neuronal cell cultures
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specific activity in the picomolar range