3.2.2.23 A288V naturally occuring polymorphism, the mutant displays opposite-base specificity similar to that of wild-type OGG1, activity, substrate specificity and kinetics compared to the wild-type enzyme, overview 708484 3.2.2.23 D322N naturally occuring polymorphism, the mutant is 2.3fold more specific for the correct opposite base than the wild-type enzyme, activity, substrate specificity and kinetics compared to the wild-type enzyme 708484 3.2.2.23 E131R loss of activity 750392 3.2.2.23 E173Q no enzymic activity, E173 may play a crucial role in forming the active site pocket 667594 3.2.2.23 E2Q no enzymic activity, interactions with G167 and Y170 are interupted 667594 3.2.2.23 E3Q crystallization data 680361 3.2.2.23 E3Q inactive. Mutant binds DNA duplexes containing spiroiminodihydantoin or guanidinohydantoin about 1000fold more tightly over corresponding duplexes containing 8-oxoguanine 678318 3.2.2.23 E77S in wild-type, 8-oxoguanine is bound via E77 in syn conformation. In mutant E77S, which reflects the sequence of the Escherichia coli enzyme, 8-oxoguanine is preferentially bound in the anti conformation 678139 3.2.2.23 F110A the mutation affects the enzyme activity, especially in the case of oxoG/C substrate, in the second and third reaction steps 710030 3.2.2.23 F110W the mutation affects the enzyme activity, especially in the case of oxoG/C substrate, in the second and third reaction steps 710030 3.2.2.23 F111A the mutant displays a significant increase in the average diffusion constant compared to the wild-type protein with no enzymatic activity on DNA containing 8-oxoguanine residues opposite cytosine. The mutant has little or no ability to form a Schiff base with 8-oxoguanine residues opposite cytosine or 5,6-dihydrouracil opposite guanine compared to wild type enzyme 716394 3.2.2.23 H71A severely compromised in turnover of oligonucleotides with 8-oxoguanosine opposie cytosine, but show turnover rates comparable to wild-type on abasic-site containing DNA 678197 3.2.2.23 H89A selective diminition of the rate of excision of 8-oxoguanine 669289 3.2.2.23 H89A/R109A about 10fold increase in KM-value 669289 3.2.2.23 K155A effect of mutation on specificity, mutant with very low activity, kinetic study 646944 3.2.2.23 K155A mutant enzyme with decreased N-glycosylase and increased AP lyase activity, it dissociates prematurely from the covalent enzyme-DNA complex leading to a higher turnover number for DNA containing an AP site 646946 3.2.2.23 K155A mutant with 50fold decreased activity with 7-hydro-8-oxoguanine-DNA as substrate, only 3-4fold decreased activity with 7-methylformamidopyrimidine-DNA, increased AP lyase activity 646945 3.2.2.23 K155A mutant with reduced 8-oxoguanine-DNA but unchanged Fapy-DNA glycosylase activity -, 646950 3.2.2.23 K217T selective reduction of the ability to excise 8-oxoguanine from DNA 669289 3.2.2.23 K57A mutant with about 15% of wild-type activity in both N-glycosylase and AP lyase activity 646946 3.2.2.23 K57G effect of mutation on specificity, mutant removes FapyAde and FapyGua with reduced activity compared to wild-type Fpg, kinetic study 646944 3.2.2.23 K57G mutant has dramatically reduced 7,8-dihydro-8-oxoguanine-DNA glycosylase activity and is poorly effective in formation of Schiff base complex with 8-oxoG/C, little effect on 2,6-diamino-4-hydroxy-5-N-methylformamidopyrimidine-DNA glycosylase activity, no effect on DNA nicking activity at abasic sites -, 646950 3.2.2.23 K57G study of the effect of the mutation on the structure dynamics, mutant with decreased 8-hydroxyguanine-DNA glycosylase activity -, 646943 3.2.2.23 K57R effect of mutation on specificity, mutant removes FapyAde and FapyGua with reduced activity compared to wild-type Fpg, kinetic study 646944 3.2.2.23 K57R slight effect of mutation on 7,8-dihydro-8-oxoguanine-DNA glycosylase activity, no effect on 2,6-diamino-4-hydroxy-5-N-methylformamidopyrimidine-DNA glycosylase activity and on DNA nicking activity at abasic sites -, 646950 3.2.2.23 additional information expression in Chinese hamster ovary cells results in decrease of the levels of oxypurine clustered damages while those of oxypyrimidine clusters and abasic clusters are unchanged. Growth rates of cells are increased and the level of spontaneous background mutants in the hypoxanthine guanine phosphoribosyl transferase gene is decreased 679529 3.2.2.23 additional information expression of enzyme in human cells from patients belonging to Cockayne syndrome complementation groups A and B completely corrects the repair deficiency in both CS-A and CS-B cells. The sensitivity of CS-B cells to elevated concentrations of potassium bromate is not compensated by expression of enzyme 679970 3.2.2.23 additional information expression of enzyme-green fluorescent protein fusion protein in human bladder cells. Cells expressing the fusion protein repair 8-oxoguanine and abasic sites at accelerated rates and are resistant to the oxidizing carcinogen potassium bromate 680213 3.2.2.23 additional information gene disruption mutants exhibits an enhanced mutator phenotype and susceptibility to hydrogen peroxide as well as a remarkable increase in accumulation of A to G (or T to C) mutations. Exposure of the mutant to sub-lethal level of hydrogen peroxide results in a major shift toward C to G (or G to C) mutations 679465 3.2.2.23 additional information monitoring of spontaneous revertants in a background in which a T/G replacement inactivates the lacZ gene, in strains possessing and lacking Fpg activity. In strains without enzymic activity grown on glucose medium, the proportion of revertants increases over a 5-day period. In contrast, in strains with enzymic activity, revertants appear primarily during the first 2-3 days after plating, few new revertants appear in the following days 682050 3.2.2.23 additional information mutant Fpg protein with NH2-terminal modifications -, 646932 3.2.2.23 additional information study on the polymorphism 23A to G in the DNA repair gene XPA. Presence of the A allele is associated with higher levels of DNA damage as well as with higher activity of the OGG1 8-oxoguanidine DNA glycosylase. In individuals with the A allele, OGG1 repair activity also increases with age 682047 3.2.2.23 additional information the content of 2,6-diamino-4-hydroxy-5-formamidopyrimidine derived guanine is increased in some but not all tissues of Neil1-/- mice -, 708311 3.2.2.23 additional information the gene shows several polymorphisms in vivo 708484 3.2.2.23 N168D 0.2% of wild-type activity 751732 3.2.2.23 N168Q 9.5% of wild-type activity 751732 3.2.2.23 P2E completely inactive mutant: no 2,6-diamino-4-hydroxy-5-N-methylformamidopyrimidine DNA/7,8-dihydro-8-oxoguanine-DNA glycosylase activity or cleavage of DNA containing AP sites 646954 3.2.2.23 P2E effect of mutation on specificity, inactive mutant, kinetic study 646944 3.2.2.23 P2E study of the effect of the mutation on the structure dynamics, mutation causes complete loss of DNA glycosylase/beta-lyase activity and induces a conformational change leading to a more rigid globular structure than wild-type, K57G and P2G Fpg -, 646943 3.2.2.23 P2G effect of mutation on specificity, mutant with very low activity, kinetic study 646944 3.2.2.23 P2G mutant with 10% of wild-type 2,6-diamino-4-hydroxy-5-N-methylformamidopyrimidine DNA glycosylase activity and barely detectable 7,8-dihydro-8-oxoguanine-DNA glycosylase activity, no cleavage of DNA containing AP sites 646954 3.2.2.23 P2G study of the effect of the mutation on the structure dynamics, mutant with complete loss of beta-lyase and partial loss of DNA glycosylase activity -, 646943 3.2.2.23 P2T mutant with 10% of wild-type 2,6-diamino-4-hydroxy-5-N-methylformamidopyrimidine DNA glycosylase activity and barely detectable 7,8-dihydro-8-oxoguanine-DNA glycosylase activity, no cleavage of DNA containing AP sites 646954 3.2.2.23 Q234R mutant retains activity 750392 3.2.2.23 Q234R/R244E mutant retains activity 750392 3.2.2.23 R108A R108 is a major determinant of opposite-base specificity 669289 3.2.2.23 R108K 1.9% of wild-type activity 751732 3.2.2.23 R108L 0.3% of wild-type activity 751732 3.2.2.23 R108Q 0.3% of wild-type activity 751732 3.2.2.23 R109A binding of enzyme to damaged DNA is almost abolished 669289 3.2.2.23 R244E mutant retains activity 750392 3.2.2.23 R258A 0.4% of wild-type activity 751732 3.2.2.23 R258K 0.3% of wild-type activity 751732 3.2.2.23 R258Q 6.2% of wild-type activity 751732 3.2.2.23 R54E loss of activity 750392 3.2.2.23 R54E/E131R loss of activity 750392 3.2.2.23 S1245C naturally occuring polymorphism. No correlation between mutation and gastric cancer 682051 3.2.2.23 S208A mutation has no effect, in both wild-type and S208 A residue Tyr170 quickly reorients to form an alternative set of hydrogen bonds 750392 3.2.2.23 S231E naturally occuring polymorphism, kinetics compared to the wild-type enzyme, overview 708484 3.2.2.23 S231E/S232E naturally occuring polymorphism, kinetics compared to the wild-type enzyme, overview 708484 3.2.2.23 S232E naturally occuring polymorphism, kinetics compared to the wild-type enzyme, overview 708484 3.2.2.23 S280E naturally occuring polymorphism, kinetics compared to the wild-type enzyme, overview 708484 3.2.2.23 S326C naturally occuring polymorphism, the mutant displays opposite-base specificity similar to that of wild-type OGG1. The mutant efficiently excises 8-oxoGua from oligodeoxynucleotides and 2,6-diamino-4-hydroxy-5-formamidopyrimidine from gamma-irradiated DNA, but excises 8-oxoG rather inefficiently from gamma-irradiated DNA 708484 3.2.2.23 S326E naturally occuring polymorphism, kinetics compared to the wild-type enzyme, overview 708484 3.2.2.23 Y170F mutation decreases Fpg binding but does not fully inactivate the protein 750392