David M Wilson

Summary

Affiliation: National Institutes of Health
Country: USA

Publications

  1. pmc Functional assessment of population and tumor-associated APE1 protein variants
    Jennifer L Illuzzi
    Laboratory of Molecular Gerontology, National Institute on Aging, National Institutes of Health, Baltimore, Maryland, United States of America
    PLoS ONE 8:e65922. 2013
  2. pmc Identification and characterization of inhibitors of human apurinic/apyrimidinic endonuclease APE1
    Anton Simeonov
    NIH Chemical Genomics Center, National Human Genome Research Institute, NIH, Bethesda, MD, USA
    PLoS ONE 4:e5740. 2009
  3. pmc Functional capacity of XRCC1 protein variants identified in DNA repair-deficient Chinese hamster ovary cell lines and the human population
    Brian R Berquist
    Laboratory of Molecular Gerontology, National Institute on Aging, NIH, Baltimore, MD 21224, USA
    Nucleic Acids Res 38:5023-35. 2010
  4. pmc XRCC1 haploinsufficiency in mice has little effect on aging, but adversely modifies exposure-dependent susceptibility
    Daniel R McNeill
    Laboratory of Molecular Gerontology, National Institute on Aging, National Institutes of Health, IRP, Biomedical Research Center, Baltimore, MD 21224, USA
    Nucleic Acids Res 39:7992-8004. 2011
  5. pmc Diverse small molecule inhibitors of human apurinic/apyrimidinic endonuclease APE1 identified from a screen of a large public collection
    Dorjbal Dorjsuren
    NIH Chemical Genomics Center, National Center for Advancing Translational Sciences, National Institutes of Health, Bethesda, Maryland, United States of America
    PLoS ONE 7:e47974. 2012
  6. ncbi request reprint Base excision repair: contribution to tumorigenesis and target in anticancer treatment paradigms
    J L Illuzzi
    Laboratory of Molecular Gerontology, National Institute on Aging, National Institutes of Health, Baltimore, MD 21224, USA
    Curr Med Chem 19:3922-36. 2012
  7. pmc Variation in base excision repair capacity
    David M Wilson
    Laboratory of Molecular Gerontology, National Institute on Aging, National Institutes of Health, Baltimore, MD 21224, United States
    Mutat Res 711:100-12. 2011
  8. pmc Small molecule inhibitors of DNA repair nuclease activities of APE1
    David M Wilson
    Laboratory of Molecular Gerontology, Biomedical Research Center, National Institute on Aging, NIH, IRP, 251 Bayview Boulevard, Baltimore, MD 21224, USA
    Cell Mol Life Sci 67:3621-31. 2010
  9. pmc A novel link to base excision repair?
    David M Wilson
    Laboratory of Molecular Gerontology, National Institute on Aging, National Institutes of Health, Baltimore, MD 21224, USA
    Trends Biochem Sci 35:247-52. 2010
  10. ncbi request reprint XRCC1 down-regulation in human cells leads to DNA-damaging agent hypersensitivity, elevated sister chromatid exchange, and reduced survival of BRCA2 mutant cells
    Jinshui Fan
    Laboratory of Molecular Gerontology, National Institute on Aging, Baltimore, Maryland, USA
    Environ Mol Mutagen 48:491-500. 2007

Collaborators

Detail Information

Publications61

  1. pmc Functional assessment of population and tumor-associated APE1 protein variants
    Jennifer L Illuzzi
    Laboratory of Molecular Gerontology, National Institute on Aging, National Institutes of Health, Baltimore, Maryland, United States of America
    PLoS ONE 8:e65922. 2013
    ..Our results indicate that APE1 missense mutations are seemingly rare and that the cancer-associated R237C variant may represent a reduced-function susceptibility allele...
  2. pmc Identification and characterization of inhibitors of human apurinic/apyrimidinic endonuclease APE1
    Anton Simeonov
    NIH Chemical Genomics Center, National Human Genome Research Institute, NIH, Bethesda, MD, USA
    PLoS ONE 4:e5740. 2009
    ..The studies herein report on the identification of novel, small molecule APE1-targeted bioactive inhibitor probes, which represent initial chemotypes towards the development of potential pharmaceuticals...
  3. pmc Functional capacity of XRCC1 protein variants identified in DNA repair-deficient Chinese hamster ovary cell lines and the human population
    Brian R Berquist
    Laboratory of Molecular Gerontology, National Institute on Aging, NIH, Baltimore, MD 21224, USA
    Nucleic Acids Res 38:5023-35. 2010
    ....
  4. pmc XRCC1 haploinsufficiency in mice has little effect on aging, but adversely modifies exposure-dependent susceptibility
    Daniel R McNeill
    Laboratory of Molecular Gerontology, National Institute on Aging, National Institutes of Health, IRP, Biomedical Research Center, Baltimore, MD 21224, USA
    Nucleic Acids Res 39:7992-8004. 2011
    ....
  5. pmc Diverse small molecule inhibitors of human apurinic/apyrimidinic endonuclease APE1 identified from a screen of a large public collection
    Dorjbal Dorjsuren
    NIH Chemical Genomics Center, National Center for Advancing Translational Sciences, National Institutes of Health, Bethesda, Maryland, United States of America
    PLoS ONE 7:e47974. 2012
    ..To our knowledge, this represents the largest-scale HTS to identify inhibitors of APE1, and provides a key first step in the development of novel agents targeting BER for cancer treatment...
  6. ncbi request reprint Base excision repair: contribution to tumorigenesis and target in anticancer treatment paradigms
    J L Illuzzi
    Laboratory of Molecular Gerontology, National Institute on Aging, National Institutes of Health, Baltimore, MD 21224, USA
    Curr Med Chem 19:3922-36. 2012
    ..In this review, the repair mechanisms, as well as the links to cancer progression and treatment, of three key proteins that function in the base excision repair pathway, i.e. APE1, POLβ, and FEN1, are discussed...
  7. pmc Variation in base excision repair capacity
    David M Wilson
    Laboratory of Molecular Gerontology, National Institute on Aging, National Institutes of Health, Baltimore, MD 21224, United States
    Mutat Res 711:100-12. 2011
    ..We also discuss studies that associate BER deficiency with disease risk and the current state of BER capacity measurement assays...
  8. pmc Small molecule inhibitors of DNA repair nuclease activities of APE1
    David M Wilson
    Laboratory of Molecular Gerontology, Biomedical Research Center, National Institute on Aging, NIH, IRP, 251 Bayview Boulevard, Baltimore, MD 21224, USA
    Cell Mol Life Sci 67:3621-31. 2010
    ..In this review, we summarize the current state of the efforts to design potent and selective inhibitors against APE1 AP site incision activity...
  9. pmc A novel link to base excision repair?
    David M Wilson
    Laboratory of Molecular Gerontology, National Institute on Aging, National Institutes of Health, Baltimore, MD 21224, USA
    Trends Biochem Sci 35:247-52. 2010
    ..Recent work, coupled with a much earlier report, now suggest an emerging link between proteins of the base excision repair pathway and crosslink processing...
  10. ncbi request reprint XRCC1 down-regulation in human cells leads to DNA-damaging agent hypersensitivity, elevated sister chromatid exchange, and reduced survival of BRCA2 mutant cells
    Jinshui Fan
    Laboratory of Molecular Gerontology, National Institute on Aging, Baltimore, Maryland, USA
    Environ Mol Mutagen 48:491-500. 2007
    ....
  11. doi request reprint Modulation of DNA base excision repair during neuronal differentiation
    Peter Sykora
    Laboratory of Molecular Gerontology, National Institute on Aging National Institutes of Health, Baltimore, MD, USA
    Neurobiol Aging 34:1717-27. 2013
    ..Thus, because of their higher BER capacity, proliferative neural progenitor cells are more efficient at repairing DNA damage compared with their neuronally differentiated progeny...
  12. pmc The interaction between polynucleotide kinase phosphatase and the DNA repair protein XRCC1 is critical for repair of DNA alkylation damage and stable association at DNA damage sites
    Julie Della-Maria
    Radiation Oncology Research Laboratory, Department of Radiation Oncology and The Marlene and Stewart Greenebaum Cancer Center, University of Maryland School of Medicine, Baltimore, Maryland 21201, USA
    J Biol Chem 287:39233-44. 2012
    ..Together our results reveal novel roles for the interaction between PNKP and XRCC1 in the retention of XRCC1 at DNA damage sites and in DNA alkylation damage repair...
  13. pmc The Werner syndrome protein operates in base excision repair and cooperates with DNA polymerase beta
    Jeanine A Harrigan
    Laboratory of Molecular Gerontology, National Institute on Aging, NIH, Baltimore, MD, USA
    Nucleic Acids Res 34:745-54. 2006
    ..These findings demonstrate that WRN plays a direct role in the repair of methylation-induced DNA damage, and suggest a role for both WRN helicase and exonuclease activities together with pol beta during LP BER...
  14. pmc Cockayne syndrome group B protein promotes mitochondrial DNA stability by supporting the DNA repair association with the mitochondrial membrane
    Maria D Aamann
    Laboratory of Molecular Gerontology, National Institute on Aging, NIH, 5600 Nathan Shock Dr, Baltimore, MD 21224, USA
    FASEB J 24:2334-46. 2010
    ....
  15. pmc Cockayne syndrome B protein stimulates apurinic endonuclease 1 activity and protects against agents that introduce base excision repair intermediates
    Heng Kuan Wong
    Laboratory of Molecular Gerontology, National Institute on Aging, NIH, 5600 Nathan Shock Drive, Baltimore, MD 21224, USA
    Nucleic Acids Res 35:4103-13. 2007
    ..Moreover, human fibroblasts defective in CSB were found to be hypersensitive to both methyl methanesulfonate (MMS) and 5-hydroxymethyl-2'-deoxyuridine, agents that introduce base excision repair (BER) DNA substrates/intermediates...
  16. pmc Human RECQL5 participates in the removal of endogenous DNA damage
    Takashi Tadokoro
    Laboratory of Molecular Gerontology, National Institute on Aging, Baltimore, MD 21224, USA
    Mol Biol Cell 23:4273-85. 2012
    ....
  17. pmc WRN exonuclease activity is blocked by DNA termini harboring 3' obstructive groups
    Jeanine A Harrigan
    Laboratory of Molecular Gerontology, National Institute on Aging, National Institutes of Health, Baltimore, MD 21224, United States
    Mech Ageing Dev 128:259-66. 2007
    ....
  18. ncbi request reprint A dominant-negative form of the major human abasic endonuclease enhances cellular sensitivity to laboratory and clinical DNA-damaging agents
    Daniel R McNeill
    Laboratory of Molecular Gerontology, National Institute on Aging, NIH, Baltimore, MD 21224, USA
    Mol Cancer Res 5:61-70. 2007
    ....
  19. pmc XRCC1 protects against the lethality of induced oxidative DNA damage in nondividing neural cells
    Avanti Kulkarni
    Laboratory of Molecular Gerontology, National Institute of Aging NIA National Institutes of Health NIH, 251 Bayview Boulevard, Suite 100, Baltimore, MD 21224, USA
    Nucleic Acids Res 36:5111-21. 2008
    ..The cumulative results implicate XRCC1, and more broadly SSBR, in the protection of nondividing neuronal cells from the genotoxic consequences of oxidative stress...
  20. pmc Synthesis, biological evaluation, and structure-activity relationships of a novel class of apurinic/apyrimidinic endonuclease 1 inhibitors
    Ganesha Rai
    NIH Chemical Genomics Center, National Center for Advancing Translational Sciences, National Institutes of Health, Bethesda, Maryland 20892 3370, USA
    J Med Chem 55:3101-12. 2012
    ..Moreover, this class of compounds possesses a generally favorable in vitro ADME profile, along with good exposure levels in plasma and brain following intraperitoneal dosing (30 mg/kg body weight) in mice...
  21. ncbi request reprint XRCC1 and DNA polymerase beta interaction contributes to cellular alkylating-agent resistance and single-strand break repair
    Heng Kuan Wong
    Laboratory of Molecular Gerontology, National Institute on Aging, 5600 Nathan Shock Drive, Baltimore, Maryland 21224, USA
    J Cell Biochem 95:794-804. 2005
    ..Our data favor a model where the interaction of XRCC1 with POLbeta contributes to efficient DNA repair in vivo, whereas its interactions with target DNA is biologically less relevant...
  22. pmc Human Cockayne syndrome B protein reciprocally communicates with mitochondrial proteins and promotes transcriptional elongation
    Brian R Berquist
    Laboratory of Molecular Gerontology, National Institute on Aging, National Institutes of Health, 251 Bayview Boulevard, Baltimore, MD 21224, USA
    Nucleic Acids Res 40:8392-405. 2012
    ..These observations provide strong evidence for the importance of CSB in maintaining mitochondrial function and argue that the pathologies associated with CS are in part, a direct result of the roles that CSB plays in mitochondria...
  23. pmc Cockayne syndrome group B protein prevents the accumulation of damaged mitochondria by promoting mitochondrial autophagy
    Morten Scheibye-Knudsen
    Laboratory of Molecular Gerontology, National Institute on Aging, National Institutes of Health, Baltimore, MD 21224, USA
    J Exp Med 209:855-69. 2012
    ..Our data imply that CSB acts as an mtDNA damage sensor, inducing mitochondrial autophagy in response to stress, and that pharmacological modulators of autophagy are potential treatment options for this accelerated aging phenotype...
  24. pmc XRCC1 suppresses somatic hypermutation and promotes alternative nonhomologous end joining in Igh genes
    Huseyin Saribasak
    Laboratory of Molecular Biology and Immunology, National Institute on Aging, National Institutes of Health, Baltimore, MD 21224, USA
    J Exp Med 208:2209-16. 2011
    ..Our results imply that AID-induced single-strand breaks in Igh variable and switch regions become substrates simultaneously for BER and mutagenesis pathways...
  25. pmc The excitatory neurotransmitter glutamate stimulates DNA repair to increase neuronal resiliency
    Jenq Lin Yang
    Laboratory of Molecular Gerontology, National Institute on Aging Intramural Research Program, Baltimore, MD, USA
    Mech Ageing Dev 132:405-11. 2011
    ..We conclude that glutamate signaling involves an adaptive cellular stress response pathway that enhances DNA repair capability, thereby protecting neurons against injury and disease...
  26. pmc APE1 incision activity at abasic sites in tandem repeat sequences
    Mengxia Li
    Laboratory of Molecular Gerontology, National Institute on Aging Intramural Research Program, National Institutes of Health, 251 Bayview Boulevard, Baltimore, MD 21224, USA
    J Mol Biol 426:2183-98. 2014
    ....
  27. pmc Impairment of APE1 function enhances cellular sensitivity to clinically relevant alkylators and antimetabolites
    Daniel R McNeill
    Biomedical Research Center, National Institute on Aging, NIH, Baltimore, MD 21224, USA
    Mol Cancer Res 7:897-906. 2009
    ..Our data suggest that APE1, and BER more broadly, is a potential target for inactivation in anticancer treatment paradigms that involve select alkylating agents or antimetabolites...
  28. ncbi request reprint Mitochondrial DNA, base excision repair and neurodegeneration
    Nadja C de Souza-Pinto
    Laboratory of Molecular Gerontology, National Institute on Aging, NIH, Baltimore, MD 21224, USA
    DNA Repair (Amst) 7:1098-109. 2008
    ....
  29. ncbi request reprint Lead promotes abasic site accumulation and co-mutagenesis in mammalian cells by inhibiting the major abasic endonuclease Ape1
    Daniel R McNeill
    Laboratory of Molecular Gerontology, GRC, National Institute on Aging, IRP, NIH, Baltimore, Maryland 21224 6825, USA
    Mol Carcinog 46:91-9. 2007
    ..Our studies in total indicate that Ape1 is a member of an emerging group of DNA surveillance proteins that are inhibited by environmental heavy metals, and suggest an underlying mechanism by which lead promotes co-carcinogenesis...
  30. pmc NEIL1 responds and binds to psoralen-induced DNA interstrand crosslinks
    Daniel R McNeill
    Laboratory of Molecular Gerontology, Biomedical Research Center, NIA, National Institutes of Health, Baltimore, Maryland 21224, USA
    J Biol Chem 288:12426-36. 2013
    ..Our results indicate that NEIL1 recognizes specifically and distinctly interstrand crosslinks in DNA, and can obstruct the efficient removal of lethal crosslink adducts...
  31. pmc Characterization of abasic endonuclease activity of human Ape1 on alternative substrates, as well as effects of ATP and sequence context on AP site incision
    Brian R Berquist
    Unit of Structure and Function in Base Excision Repair, Laboratory of Molecular Gerontology, National Institute on Aging, National Institutes of Health, 5600 Nathan Shock Drive, Baltimore, MD 21224, USA
    J Mol Biol 379:17-27. 2008
    ....
  32. ncbi request reprint Telomere repeat binding factor 2 interacts with base excision repair proteins and stimulates DNA synthesis by DNA polymerase beta
    Meltem Muftuoglu
    Laboratory of Molecular Gerontology, National Institute on Aging, NIH, Baltimore, Maryland, USA
    Cancer Res 66:113-24. 2006
    ..Potential roles of TRF2 in cooperation with BER proteins for DNA repair pathways at telomeres, as well as other genomic regions, are discussed...
  33. ncbi request reprint DNA damage levels and biochemical repair capacities associated with XRCC1 deficiency
    Heng Kuan Wong
    Laboratory of Molecular Gerontology, National Institute on Aging, National Institutes of Health, 5600 Nathan Shock Drive, Baltimore, Maryland 21224, USA
    Biochemistry 44:14335-43. 2005
    ....
  34. pmc S-glutathionylation of cysteine 99 in the APE1 protein impairs abasic endonuclease activity
    Yun Jeong Kim
    Laboratory of Molecular Gerontology, Biomedical Research Center, National Institute on Aging, National Institutes of Health, Baltimore, MD 21224, USA
    J Mol Biol 414:313-26. 2011
    ..This modification is reversible by reducing agents, which restore APE1 incision function. Our studies describe a novel posttranslational modification of APE1 that regulates the DNA repair function of the protein...
  35. pmc Base excision repair in the mammalian brain: implication for age related neurodegeneration
    Peter Sykora
    Laboratory of Molecular Gerontology, National Institute on Aging Intramural Research Program, 251 Bayview Boulevard, Suite 100, Baltimore, MD 21224, United States
    Mech Ageing Dev 134:440-8. 2013
    ..The BER response may have particular relevance for the onset and progression of many neurodegenerative diseases associated with an increase in oxidative stress including Alzheimer's. ..
  36. pmc XRCC1 co-localizes and physically interacts with PCNA
    Jinshui Fan
    Laboratory of Molecular Gerontology, National Institute on Aging, 5600 Nathan Shock Drive, Baltimore, MD 21224, USA
    Nucleic Acids Res 32:2193-201. 2004
    ..The current evidence suggests a model where XRCC1 is sequestered via its interaction with PCNA to sites of DNA replication factories to facilitate efficient SSBR in S phase...
  37. ncbi request reprint Werner syndrome protein 1367 variants and disposition towards coronary artery disease in Caucasian patients
    Vilhelm A Bohr
    Laboratory of Molecular Gerontology, National Institute on Aging, National Institutes of Health, 5600 Nathan Shock Dr, Baltimore, MD 21224, USA
    Mech Ageing Dev 125:491-6. 2004
    ..There was no indication that the R allele was protective against CAD. We conclude that the C/R polymorphism does not affect enzyme function or localization and does not influence CAD incidence in the BLSA cohort...
  38. doi request reprint Repair of persistent strand breaks in the mitochondrial genome
    Peter Sykora
    NIH Biomedical Research Center, 251 Bayview Boulevard, Baltimore, MD 21224, USA
    Mech Ageing Dev 133:169-75. 2012
    ..These significant advances in mitochondrial DNA repair may open new avenues in the management and treatment of a number of neurological disorders associated with mitochondrial dysfunction, and will be reviewed in further detail herein...
  39. pmc Direct and indirect roles of RECQL4 in modulating base excision repair capacity
    Shepherd H Schurman
    Laboratory of Molecular Gerontology, National Institute on Aging, NIH, Baltimore, MD 21224, USA
    Hum Mol Genet 18:3470-83. 2009
    ..The data herein support a model in which RECQL4 regulates both directly and indirectly base excision repair capacity...
  40. pmc Complementary non-radioactive assays for investigation of human flap endonuclease 1 activity
    Dorjbal Dorjsuren
    NIH Chemical Genomics Center, National Human Genome Research Institute, National Institutes of Health, Bethesda, MD 20892 3370, USA
    Nucleic Acids Res 39:e11. 2011
    ..59 and 0.93 µM, respectively). The availability of these simple complementary assays obviates the need for undesirable radiotracer-based assays and should facilitate efforts to develop novel inhibitors for this key biological target...
  41. pmc Overview of base excision repair biochemistry
    Yun Jeong Kim
    Laboratory of Molecular Gerontology, Biomedical Research Center, National Institute on Aging, National Institutes of Health, Baltimore, MD 21224, USA
    Curr Mol Pharmacol 5:3-13. 2012
    ..g. temozolomide), nucleoside analogs (e.g. 5-fluorouracil), and ionizing radiation. The molecular details of BER and the contribution of the pathway to therapeutic agent resistance are reviewed herein...
  42. pmc Nucleic acid binding activity of human Cockayne syndrome B protein and identification of Ca(2+) as a novel metal cofactor
    Brian R Berquist
    Laboratory of Molecular Gerontology, National Institute on Aging, National Institutes of Health, Baltimore, MD 21224, USA
    J Mol Biol 391:820-32. 2009
    ....
  43. pmc Aprataxin localizes to mitochondria and preserves mitochondrial function
    Peter Sykora
    Laboratory of Molecular Gerontology, National Institute on Aging, National Institutes of Health, Baltimore, MD 21224, USA
    Proc Natl Acad Sci U S A 108:7437-42. 2011
    ..Moreover, mtDNA, not nuclear DNA, was found to have higher levels of background DNA damage on aprataxin knockdown, suggesting a direct role for the enzyme in mtDNA processing...
  44. pmc The involvement of DNA-damage and -repair defects in neurological dysfunction
    Avanti Kulkarni
    Laboratory of Molecular Gerontology, National Institute of Aging, National Institutes of Health, Baltimore, MD 21224, USA
    Am J Hum Genet 82:539-66. 2008
    ..Finally, the review touches upon the role of oxidative stress, a leading precursor to DNA damage, in the development of certain neurodegenerative pathologies, such as Alzheimer's and Parkinson's...
  45. pmc Inhibition of Ape1 nuclease activity by lead, iron, and cadmium
    Daniel R McNeill
    Laboratory of Molecular Gerontology, Gerontology Research Center, National Institute on Aging, Intramural Research Program, National Institutes of Health, Department of Health and Human Services, Baltimore, Maryland 21224 6825, USA
    Environ Health Perspect 112:799-804. 2004
    ..Our results are the first to identify a potential DNA repair enzyme target for lead and suggest a means by which these prevalent environmental metals may elicit their deleterious effects...
  46. ncbi request reprint The mechanics of base excision repair, and its relationship to aging and disease
    David M Wilson
    Laboratory of Molecular Gerontology, National Institute on Aging NIH, Baltimore, MD 21224, USA
    DNA Repair (Amst) 6:544-59. 2007
    ..In this review, we outline the basic mechanics of the BER process, and describe the potential association of this pathway with aging and age-related disease, namely cancer and neurodegeneration...
  47. pmc A real-time fluorescence method for enzymatic characterization of specialized human DNA polymerases
    Dorjbal Dorjsuren
    NIH Chemical Genomics Center, National Human Genome Research Institute, National Institutes of Health, Bethesda, MD 20892 3370, USA
    Nucleic Acids Res 37:e128. 2009
    ..The fluorogenic method presented here should facilitate mechanistic and inhibitor investigations of these polymerases and is also applicable to the study of highly processive replicative polymerases...
  48. ncbi request reprint Nucleotide sequence and DNA secondary structure, as well as replication protein A, modulate the single-stranded abasic endonuclease activity of APE1
    Jinshui Fan
    Laboratory of Molecular Gerontology, NIA, National Institutes of Health, Baltimore, MD 21224, USA
    J Biol Chem 281:3889-98. 2006
    ..The data herein suggested a model whereby RPA selectively suppresses the nontemplated ss cleavage activity of Ape1 in vivo, particularly at sites of ongoing replication/recombination, by coating the ssDNA...
  49. ncbi request reprint Molecular mechanisms of sister-chromatid exchange
    David M Wilson
    Laboratory of Molecular Gerontology, National Institute on Aging, NIH, 5600 Nathan Shock Drive, Baltimore, MD 21224, USA
    Mutat Res 616:11-23. 2007
    ..A more general overview of the cellular processes and key protein "effectors" that regulate the manifestation of SCE is also presented...
  50. pmc Oxidative damage in telomeric DNA disrupts recognition by TRF1 and TRF2
    Patricia L Opresko
    Laboratory of Molecular Gerontology, National Institute on Aging NIH, Baltimore, MD 21224, USA
    Nucleic Acids Res 33:1230-9. 2005
    ..These studies indicate that oxidative DNA damage may exert deleterious effects on telomeres by disrupting the association of telomere-maintenance proteins TRF1 and TRF2...
  51. ncbi request reprint Ape1 abasic endonuclease activity is regulated by magnesium and potassium concentrations and is robust on alternative DNA structures
    David M Wilson
    Laboratory of Molecular Gerontology, GRC, National Institute on Aging, IRP, NIH, 5600 Nathan Shock Drive, Baltimore, MD 21224 6825, USA
    J Mol Biol 345:1003-14. 2005
    ....
  52. pmc DNA repair mechanisms in dividing and non-dividing cells
    Teruaki Iyama
    Laboratory of Molecular Gerontology, National Institute on Aging, National Institutes of Health, 251 Bayview Boulevard, Baltimore, MD 21224, USA
    DNA Repair (Amst) 12:620-36. 2013
    ..We describe herein the molecular mechanisms of the different DNA repair pathways, and review their roles in non-dividing and dividing cells, with an eye toward how these pathways may regulate the development of neurological disease. ..
  53. ncbi request reprint Protein-protein interactions and posttranslational modifications in mammalian base excision repair
    Jinshui Fan
    Laboratory of Molecular Gerontology, GRC, National Institute on Aging, IRP, NIH, 5600 Nathan Shock Drive, Baltimore, MD 21224 6825, USA
    Free Radic Biol Med 38:1121-38. 2005
    ..In this review, we summarize the current state of the emerging complexities of mammalian BER, focusing on the growing number of reported protein-protein interactions and posttranslational modifications...
  54. pmc DNA damage, DNA repair, ageing and age-related disease
    David M Wilson
    Laboratory of Molecular Gerontology, National Institute on Aging, National Institutes of Health, 5600 Nathan Shock Drive, Baltimore, MD 21224, USA
    Mech Ageing Dev 129:349-52. 2008
  55. ncbi request reprint Neurodegeneration: nicked to death
    David M Wilson
    Laboratory of Molecular Gerontology, National Institute on Aging Intramural Research Program, Baltimore, Maryland, USA
    Curr Biol 17:R55-8. 2007
    ..A recent study demonstrates that aprataxin is critical for the processing of obstructive DNA termini, suggesting a broader role for DNA single-strand break repair in neurodegenerative disease...
  56. ncbi request reprint Repair mechanisms for oxidative DNA damage
    David M Wilson
    Laboratory of Molecular Gerontology, GRC, National Institute on Aging, IRP, NIH, 5600 Nathan Shock Drive, Baltimore, MD 21224 6825, USA
    Front Biosci 8:d963-81. 2003
    ....
  57. pmc Identification and quantification of DNA repair protein apurinic/apyrimidinic endonuclease 1 (APE1) in human cells by liquid chromatography/isotope-dilution tandem mass spectrometry
    Guldal Kirkali
    Biomolecular Measurement Division, National Institute of Standards and Technology, Gaithersburg, Maryland, United States of America
    PLoS ONE 8:e69894. 2013
    ..The results describe a novel approach for the accurate measurement of wild-type and variant forms of hAPE1 in vivo, and ultimately for defining the role of this protein in disease development and treatment responses. ..
  58. ncbi request reprint Properties of and substrate determinants for the exonuclease activity of human apurinic endonuclease Ape1
    David M Wilson
    Laboratory of Molecular Gerontology, GRC, National Institute on Aging, IRP NIH, 5600 Nathan Shock Drive, Baltimore, MD 21224 6825, USA
    J Mol Biol 330:1027-37. 2003
    ..However, Ape1 was able to excise double nucleotide mispairs, apparently through a novel 3'-flap-type endonuclease activity, again activating these substrates for polymerase beta extension...
  59. pmc Uracil residues dependent on the deaminase AID in immunoglobulin gene variable and switch regions
    Robert W Maul
    Laboratory of Molecular Gerontology, National Institute on Aging, National Institutes of Health, Baltimore, Maryland, USA
    Nat Immunol 12:70-6. 2011
    ..Our data provide direct evidence for the model that AID functions by deaminating cytosine residues in DNA...
  60. ncbi request reprint Processing of nonconventional DNA strand break ends
    David M Wilson
    Laboratory of Molecular Gerontology, National Institute on Aging, NIH, Baltimore, MD 21224, USA
    Environ Mol Mutagen 48:772-82. 2007
    ..I review herein the major eukaryotic enzymes (with an emphasis on the human proteins) responsible for the "clean-up" of DNA breaks harboring 3'- or 5'-blocking termini, and the cellular and disease ramifications of unrepaired SSB damage...
  61. pmc Human apurinic/apyrimidinic endonuclease 1
    Mengxia Li
    Intramural Research Program, Laboratory of Molecular Gerontology, National Institute on Aging, National Institutes of Health, Baltimore, Maryland
    Antioxid Redox Signal 20:678-707. 2014
    ..We review herein topics related to this multi-functional DNA repair and stress-response protein...