Base-excision repair of oxidative DNA damage

No abstract is available for this paper.

• Publication year

  2007

• Venue

  Nature

• Publication date

  2007-06-21

• Fields of study

  Biology, Medicine, Chemistry

• Identifiers
  DOI 10.1038/nature05978PMID 17581577PMCID PMC2896554
• External record

  Open on Semantic Scholar

• Source metadata

  Semantic Scholar, PubMed

• No claims are published for this paper.

• No concepts are published for this paper.

• The substrate specificity of MutY for hyperoxidized guanine lesions in vivo.

  2007cited by this paper
• MUTYH-associated polyposis--from defect in base excision repair to clinical genetic testing.

  2007cited by this paper
• Functional characterization of human MutY homolog (hMYH) missense mutation (R231L) that is linked with hMYH-associated polyposis.

  2007cited by this paper
• The intricate structural chemistry of base excision repair machinery: implications for DNA damage recognition, removal, and repair.

  2007cited by this paper
• Structural Characterization of Human 8-Oxoguanine DNA Glycosylase Variants Bearing Active Site Mutations*

  2007cited by this paper
• The metabolic syndrome resulting from a knockout of the NEIL1 DNA glycosylase.

  2006cited by this paper
• Mechanisms of formation, genotoxicity, and mutation of guanine oxidation products.

  2006cited by this paper
• A nucleobase lesion remodels the interaction of its normal neighbor in a DNA glycosylase complex

  2006cited by this paper
• Cancer genetics: colorectal cancer as a model

  2006cited by this paper
• Recommendations for the care of individuals with an inherited predisposition to Lynch syndrome: a systematic review.

  2006cited by this paper
• Structure of a DNA Glycosylase Searching for Lesions

  2006cited by this paper
• Association of MUTYH and colorectal cancer

  2006cited by this paper
• Microsatellite instability in colorectal cancer

  2006cited by this paper
• Roles of base excision repair subpathways in correcting oxidized abasic sites in DNA

  2006cited by this paper
• A base-excision DNA-repair protein finds intrahelical lesion bases by fast sliding in contact with DNA.

  2006cited by this paper
• A role for iron-sulfur clusters in DNA repair.

  2005cited by this paper
• The genetics of FAP and FAP-like syndromes

  2005cited by this paper
• Nei deficient Escherichia coli are sensitive to chromate and accumulate the oxidized guanine lesion spiroiminodihydantoin.

  2005cited by this paper
• [Base excision repair].

  2005cited by this paper
• Insight into the roles of tyrosine 82 and glycine 253 in the Escherichia coli adenine glycosylase MutY.

  2005cited by this paper
• Structure of a repair enzyme interrogating undamaged DNA elucidates recognition of damaged DNA

  2005cited by this paper
• Functional characterization of two human MutY homolog (hMYH) missense mutations (R227W and V232F) that lie within the putative hMSH6 binding domain and are associated with hMYH polyposis

  2005cited by this paper
• Induction of the Human Oxidized Base-specific DNA Glycosylase NEIL1 by Reactive Oxygen Species*

  2005cited by this paper
• Genetics of hereditary colorectal cancer.

  2005cited by this paper
• DNA base damage recognition and removal: new twists and grooves.

  2005cited by this paper
• Insight into the functional consequences of hMYH variants associated with colorectal cancer: distinct differences in the adenine glycosylase activity and the response to AP endonucleases of Y150C and G365D murine MYH.

  2005cited by this paper
• Establishing the background level of base oxidation in human lymphocyte DNA: results of an interlaboratory validation study

  2005cited by this paper
• Germline susceptibility to colorectal cancer due to base-excision repair gene defects.

  2005cited by this paper
• Recognition of the oxidized lesions spiroiminodihydantoin and guanidinohydantoin in DNA by the mammalian base excision repair glycosylases NEIL1 and NEIL2.

  2005cited by this paper
• MutYH (MYH) and colorectal cancer.

  2005cited by this paper
• A novel functionally deficient MYH variant in individuals with colorectal adenomatous polyposis

  2005cited by this paper
• Hereditary colorectal cancer syndromes

  2005cited by this paper
• Is prophylactic colectomy indicated in patients with MYH‐associated polyposis?

  2005cited by this paper
• Structural basis for removal of adenine mispaired with 8-oxoguanine by MutY adenine DNA glycosylase

  2004cited by this paper
• Inactivating mutations of the human base excision repair gene NEIL1 in gastric cancer.

  2004cited by this paper
• Deficiencies in mouse Myh and Ogg1 result in tumor predisposition and G to T mutations in codon 12 of the K-ras oncogene in lung tumors.

  2004cited by this paper
• The crystal structure of human endonuclease VIII-like 1 (NEIL1) reveals a zincless finger motif required for glycosylase activity.

  2004cited by this paper
• Accumulation of the Oxidative Base Lesion 8-Hydroxyguanine in DNA of Tumor-Prone Mice Defective in Both the Myh and Ogg1 DNA Glycosylases

  2004cited by this paper
• The role of oxidative stress in carcinogenesis.

  2004cited by this paper
• Base excision repair.

  2004cited by this paper
• Myh Deficiency Enhances Intestinal Tumorigenesis in Multiple Intestinal Neoplasia (ApcMin/+) Mice

  2004cited by this paper
• Differential Specificity of Human and Escherichia coli Endonuclease III and VIII Homologues for Oxidative Base Lesions*

  2004cited by this paper
• DNA glycosylase recognition and catalysis.

  2004cited by this paper
• High frequency of MYH gene mutations in a subset of patients with familial adenomatous polyposis.

  2004cited by this paper
• Colorectal cancer and inherited mutations in base-excision repair.

  2004cited by this paper
• Identification of critical residues required for the mutation avoidance function of human MutY (hMYH) and implications in colorectal cancer.

  2004cited by this paper
• Inroads into base excision repair II. The discovery of DNA glycosylases. "An N-glycosidase from Escherichia coli that releases free uracil from DNA containing deaminated cytosine residues," Proc. Nat. Acad. Sci. USA, 1974.

  2004cited by this paper
• Site-specific DNA damage recognition by enzyme-induced base flipping.

  2004cited by this paper
• The multiple colorectal adenoma phenotype and MYH, a base excision repair gene.

  2004cited by this paper
• Comprehensive analysis of the contribution of germline MYH variation to early‐onset colorectal cancer

  2004cited by this paper
• Germline MUTYH (MYH) mutations in Portuguese individuals with multiple colorectal adenomas

  2004cited by this paper
• MUTYH prevents OGG1 or APEX1 from inappropriately processing its substrate or reaction product with its C-terminal domain.

  2004cited by this paper
• Recognition of an unnatural difluorophenyl nucleotide by uracil DNA glycosylase.

  2004cited by this paper
• Repair and genetic consequences of endogenous DNA base damage in mammalian cells.

  2004cited by this paper
• Prevalence of the Y165C, G382D and 1395delGGA germline mutations of the MYH gene in Italian patients with adenomatous polyposis coli and colorectal adenomas

  2004cited by this paper
• Error-prone replication of oxidatively damaged DNA by a high-fidelity DNA polymerase

  2004cited by this paper
• MUTYH prevents OGG 1 or APEX 1 from inappropriately processing its substrate or reaction product with its C-terminal domain

  2004cited by this paper
• Autosomal recessive colorectal adenomatous polyposis due to inherited mutations of MYH.

  2003cited by this paper
• Effect of the oxidized guanosine lesions spiroiminodihydantoin and guanidinohydantoin on proofreading by Escherichia coli DNA polymerase I (Klenow fragment) in different sequence contexts.

  2003cited by this paper
• MYH polyposis: A new autosomal recessive form of familial adenomatous polyposis due to defective base excision repair-reappraisal of genetic risk and family management

  2003cited by this paper
• DNA damage and repair

  2003cited by this paper
• Repair of Oxidized Bases in DNA Bubble Structures by Human DNA Glycosylases NEIL1 and NEIL2*

  2003cited by this paper
• DNA Lesion Recognition by the Bacterial Repair Enzyme MutM*

  2003cited by this paper
• Carcinogenesis in MYH-associated polyposis follows a distinct genetic pathway.

  2003cited by this paper
• Mutator Phenotype of MUTYH-null Mouse Embryonic Stem Cells*

  2003cited by this paper
• Structure of DNA polymerase beta with the mutagenic DNA lesion 8-oxodeoxyguanine reveals structural insights into its coding potential.

  2003cited by this paper
• The hydantoin lesions formed from oxidation of 7,8-dihydro-8-oxoguanine are potent sources of replication errors in vivo.

  2003cited by this paper
• The enigma of endonuclease VIII.

  2003cited by this paper
• Recognition and removal of oxidized guanines in duplex DNA by the base excision repair enzymes hOGG1, yOGG1, and yOGG2.

  2003cited by this paper
• Insight into the functional consequences of inherited variants of the hMYH adenine glycosylase associated with colorectal cancer: complementation assays with hMYH variants and pre-steady-state kinetics of the corresponding mutated E.coli enzymes.

  2003cited by this paper
• Repair of DNA containing Fapy.dG and its beta-C-nucleoside analogue by formamidopyrimidine DNA glycosylase and MutY.

  2003cited by this paper
• The novel DNA glycosylase, NEIL1, protects mammalian cells from radiation-mediated cell death.

  2003cited by this paper
• Tobacco smoke carcinogens, DNA damage and p53 mutations in smoking-associated cancers

  2002cited by this paper
• Identification and Characterization of a Novel Human DNA Glycosylase for Repair of Cytosine-derived Lesions*

  2002cited by this paper
• Flipping Duplex DNA Inside Out

  2002cited by this paper
• Human DNA glycosylases of the bacterial Fpg/MutM superfamily: an alternative pathway for the repair of 8-oxoguanine and other oxidation products in DNA.

  2002cited by this paper
• Structure and potential mutagenicity of new hydantoin products from guanosine and 8-oxo-7,8-dihydroguanine oxidation by transition metals.

  2002cited by this paper
• Global genome repair of 8-oxoG in hamster cells requires a functional CSB gene product

  2002cited by this paper
• A novel human DNA glycosylase that removes oxidative DNA damage and is homologous to Escherichia coli endonuclease VIII.

  2002cited by this paper
• Spiroiminodihydantoin is a major product in the photooxidation of 2'-deoxyguanosine by the triplet states and oxyl radicals generated from hydroxyacetophenone photolysis and dioxetane thermolysis.

  2002cited by this paper
• In vitro nucleotide misinsertion opposite the oxidized guanosine lesions spiroiminodihydantoin and guanidinohydantoin and DNA synthesis past the lesions using Escherichia coli DNA polymerase I (Klenow fragment).

  2002cited by this paper
• Identification and characterization of a human DNA glycosylase for repair of modified bases in oxidatively damaged DNA

  2002cited by this paper
• A global DNA repair mechanism involving the Cockayne syndrome B (CSB) gene product can prevent the in vivo accumulation of endogenous oxidative DNA base damage

  2002cited by this paper
• Inherited variants of MYH associated with somatic G:C→T:A mutations in colorectal tumors

  2002cited by this paper
• Spiroiminodihydantoin is the major product of the 8-oxo-7,8-dihydroguanosine reaction with peroxynitrite in the presence of thiols and guanosine photooxidation by methylene blue.

  2001cited by this paper
• Characterization of hydantoin products from one-electron oxidation of 8-oxo-7,8-dihydroguanosine in a nucleoside model.

  2001cited by this paper
• Age-related and tissue-specific accumulation of oxidative DNA base damage in 7,8-dihydro-8-oxoguanine-DNA glycosylase (Ogg1) deficient mice.

  2001cited by this paper
• The ABC of APC.

  2001cited by this paper
• The pH-dependent role of superoxide in riboflavin-catalyzed photooxidation of 8-oxo-7,8-dihydroguanosine.

  2001cited by this paper
• Repair of hydantoins, one electron oxidation product of 8-oxoguanine, by DNA glycosylases of Escherichia coli.

  2001cited by this paper
• Efficient recognition of substrates and substrate analogs by the adenine glycosylase MutY requires the C-terminal domain.

  2001cited by this paper
• Removal of hydantoin products of 8-oxoguanine oxidation by the Escherichia coli DNA repair enzyme, FPG.

  2000cited by this paper
• Lessons learned from structural results on uracil-DNA glycosylase.

  2000cited by this paper
• Characterization of spiroiminodihydantoin as a product of one-electron oxidation of 8-Oxo-7,8-dihydroguanosine.

  2000cited by this paper
• Structural basis for recognition and repair of the endogenous mutagen 8-oxoguanine in DNA

  2000cited by this paper
• Accumulation of premutagenic DNA lesions in mice defective in removal of oxidative base damage.

  1999cited by this paper
• The C-terminal domain of the adenine-DNA glycosylase MutY confers specificity for 8-oxoguanine.adenine mispairs and may have evolved from MutT, an 8-oxo-dGTPase.

  1999cited by this paper
• Chemistry of Glycosylases and Endonucleases Involved in Base-Excision Repair.

  1998cited by this paper
• Oxidative Nucleobase Modifications Leading to Strand Scission.

  1998cited by this paper
• MutY catalytic core, mutant and bound adenine structures define specificity for DNA repair enzyme superfamily

  1998cited by this paper

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