Michael A Resnick

Summary

Affiliation: National Institutes of Health
Country: USA

Publications

  1. ncbi request reprint Fidelity of DNA polymerase epsilon holoenzyme from budding yeast Saccharomyces cerevisiae
    Kikuo Shimizu
    The Department of Biochemistry and Molecular Biology, Research Institute for Microbial Diseases, Osaka University, 3 1 Yamada oka, Suita, Osaka 565 0871, Japan
    J Biol Chem 277:37422-9. 2002
  2. pmc Transactivation by low and high levels of human p53 reveals new physical rules of engagement and novel super-transactivation sequences
    Daniel Menendez
    Chromosome Stability Section Laboratory of Molecular Genetics National Institute of Environmental Health Sciences NIEHS National Institutes of Health NIH Research Triangle Park, NC USA
    Cell Cycle 11:4287-8. 2012
  3. pmc p53 transactivation and the impact of mutations, cofactors and small molecules using a simplified yeast-based screening system
    Virginia Andreotti
    Unit of Molecular Mutagenesis, National Institute for Cancer Research, IST, Genoa, Italy
    PLoS ONE 6:e20643. 2011
  4. pmc Alkylation base damage is converted into repairable double-strand breaks and complex intermediates in G2 cells lacking AP endonuclease
    Wenjian Ma
    Laboratory of Molecular Genetics, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, North Carolina, United States of America
    PLoS Genet 7:e1002059. 2011
  5. pmc A multistep genomic screen identifies new genes required for repair of DNA double-strand breaks in Saccharomyces cerevisiae
    Jennifer Summers McKinney
    Department of Chemistry and Biochemistry, Texas State University, San Marcos, TX 78666, USA
    BMC Genomics 14:251. 2013
  6. ncbi request reprint Reduced replication: a call to ARMS
    Michael A Resnick
    Laboratory of Molecular Genetics, National Institute of Environmental Health Sciences, NIH, Research Triangle Park, NC 27709, USA
    Cell 120:569-70. 2005
  7. pmc Hidden sources of private industry funding
    David B Resnik
    National Institute of Environmental Health Sciences, National Institutes of Health, Mail Drop NH 06, Box 12233, Research Triangle Park, NC 27709, USA
    Am J Bioeth 8:60-1. 2008
  8. ncbi request reprint Functional diversity in the gene network controlled by the master regulator p53 in humans
    Michael A Resnick
    Laboratory of Molecular Genetics, National Institute of Environmental Health Sciences, NIH, Research Triangle Park, North Carolina, USA
    Cell Cycle 4:1026-9. 2005
  9. pmc Functional mutants of the sequence-specific transcription factor p53 and implications for master genes of diversity
    Michael A Resnick
    Laboratory of Molecular Genetics, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, NC 27709, USA
    Proc Natl Acad Sci U S A 100:9934-9. 2003
  10. ncbi request reprint Potentiating the p53 network
    Daniel Menendez
    Chromosome Stability Group, National Institute of Environmental Health Sciences, NIH, Research Triangle Park, North Carolina 27709, USA
    Discov Med 10:94-100. 2010

Collaborators

Detail Information

Publications81

  1. ncbi request reprint Fidelity of DNA polymerase epsilon holoenzyme from budding yeast Saccharomyces cerevisiae
    Kikuo Shimizu
    The Department of Biochemistry and Molecular Biology, Research Institute for Microbial Diseases, Osaka University, 3 1 Yamada oka, Suita, Osaka 565 0871, Japan
    J Biol Chem 277:37422-9. 2002
    ....
  2. pmc Transactivation by low and high levels of human p53 reveals new physical rules of engagement and novel super-transactivation sequences
    Daniel Menendez
    Chromosome Stability Section Laboratory of Molecular Genetics National Institute of Environmental Health Sciences NIEHS National Institutes of Health NIH Research Triangle Park, NC USA
    Cell Cycle 11:4287-8. 2012
    ..Comment on: Jordan JJ, et al. Proc Natl Acad Sci USA 2012; 109:14387-92...
  3. pmc p53 transactivation and the impact of mutations, cofactors and small molecules using a simplified yeast-based screening system
    Virginia Andreotti
    Unit of Molecular Mutagenesis, National Institute for Cancer Research, IST, Genoa, Italy
    PLoS ONE 6:e20643. 2011
    ..In tumors that retain wild type p53, the pathway can be altered by upstream modulators, particularly the p53 negative regulators MDM2 and MDM4...
  4. pmc Alkylation base damage is converted into repairable double-strand breaks and complex intermediates in G2 cells lacking AP endonuclease
    Wenjian Ma
    Laboratory of Molecular Genetics, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, North Carolina, United States of America
    PLoS Genet 7:e1002059. 2011
    ..Collectively, this study provides new insights into the potential consequences of alkylation base damage in vivo, including creation of novel structures as well as generation and repair of DSBs in nonreplicating cells...
  5. pmc A multistep genomic screen identifies new genes required for repair of DNA double-strand breaks in Saccharomyces cerevisiae
    Jennifer Summers McKinney
    Department of Chemistry and Biochemistry, Texas State University, San Marcos, TX 78666, USA
    BMC Genomics 14:251. 2013
    ..Repair efficiency is also modulated by other processes such as sister chromatid cohesion, nucleosome remodeling and DNA damage checkpoints. The total number of genes influencing DSB repair efficiency is unknown...
  6. ncbi request reprint Reduced replication: a call to ARMS
    Michael A Resnick
    Laboratory of Molecular Genetics, National Institute of Environmental Health Sciences, NIH, Research Triangle Park, NC 27709, USA
    Cell 120:569-70. 2005
    ..The authors identify a hotspot for chromosome aberrations reminiscent of fragile sites in human cells. This hotspot is composed of inverted Ty elements, which lead to a double-strand break under conditions of limited replication...
  7. pmc Hidden sources of private industry funding
    David B Resnik
    National Institute of Environmental Health Sciences, National Institutes of Health, Mail Drop NH 06, Box 12233, Research Triangle Park, NC 27709, USA
    Am J Bioeth 8:60-1. 2008
  8. ncbi request reprint Functional diversity in the gene network controlled by the master regulator p53 in humans
    Michael A Resnick
    Laboratory of Molecular Genetics, National Institute of Environmental Health Sciences, NIH, Research Triangle Park, North Carolina, USA
    Cell Cycle 4:1026-9. 2005
    ..The findings also provide insight into the evolution of complex networks and the role of master regulatory genes, such as p53, in such networks...
  9. pmc Functional mutants of the sequence-specific transcription factor p53 and implications for master genes of diversity
    Michael A Resnick
    Laboratory of Molecular Genetics, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, NC 27709, USA
    Proc Natl Acad Sci U S A 100:9934-9. 2003
    ....
  10. ncbi request reprint Potentiating the p53 network
    Daniel Menendez
    Chromosome Stability Group, National Institute of Environmental Health Sciences, NIH, Research Triangle Park, North Carolina 27709, USA
    Discov Med 10:94-100. 2010
    ..Our findings have important implications for cellular and tissue responses to various stresses...
  11. pmc Noncanonical DNA motifs as transactivation targets by wild type and mutant p53
    Jennifer J Jordan
    Laboratory of Molecular Genetics, National Institute of Environmental Health Sciences, NIH, Research Triangle Park, North Carolina, United States of America
    PLoS Genet 4:e1000104. 2008
    ..Importantly, inclusion of (1/2)- and (3/4)-site REs greatly expands the p53 master regulatory network...
  12. pmc The transition of closely opposed lesions to double-strand breaks during long-patch base excision repair is prevented by the coordinated action of DNA polymerase delta and Rad27/Fen1
    Wenjian Ma
    Laboratory of Molecular Genetics, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, NC 27709, USA
    Mol Cell Biol 29:1212-21. 2009
    ....
  13. pmc Probing the functional impact of sequence variation on p53-DNA interactions using a novel microsphere assay for protein-DNA binding with human cell extracts
    Maher A Noureddine
    Environmental Genomics Group, Laboratory of Molecular Genetics, National Institute of Environmental Health Sciences, NIH, Research Triangle Park, NC, USA
    PLoS Genet 5:e1000462. 2009
    ....
  14. pmc The multiple biological roles of the 3'-->5' exonuclease of Saccharomyces cerevisiae DNA polymerase delta require switching between the polymerase and exonuclease domains
    Yong Hwan Jin
    National Institute of Environmental Health Sciences, D3 01, 101 TW Alexander Dr, P O Box 12233, Research Triangle Park, NC 27709, USA
    Mol Cell Biol 25:461-71. 2005
    ..We conclude that the three biological functions of the 3'-->5' exonuclease addressed in this study are performed intramolecularly within the replicating holoenzyme...
  15. pmc A SNP in the flt-1 promoter integrates the VEGF system into the p53 transcriptional network
    Daniel Menendez
    Chromosome Stability Section, Laboratory of Molecular Genetics, National Institute of Environmental Health Sciences, National Institutes of Health, 111 Alexander Drive, Research Triangle Park, NC 27709, USA
    Proc Natl Acad Sci U S A 103:1406-11. 2006
    ..We suggest that the p53-VEGF-flt-1 interaction is relevant to risks in angiogenesis-associated diseases, including cancer...
  16. pmc RAD50 is required for efficient initiation of resection and recombinational repair at random, gamma-induced double-strand break ends
    Jim Westmoreland
    Chromosome Stability Section, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, North Carolina, United States of America
    PLoS Genet 5:e1000656. 2009
    ..Surprisingly, within 1 hr after irradiation, double-length linear molecules are detected in the WT and rad50, but not in rad52, strains that are likely due to crossovers that are largely resection- and RAD50-independent...
  17. ncbi request reprint The Mre11 complex is required for repair of hairpin-capped double-strand breaks and prevention of chromosome rearrangements
    Kirill S Lobachev
    Laboratory of Molecular Genetics, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, NC 27709, USA
    Cell 108:183-93. 2002
    ..Our results suggest an additional role for the Mre11 complex in maintaining genome stability...
  18. pmc Transcriptional functionality of germ line p53 mutants influences cancer phenotype
    Paola Monti
    Molecular Mutagenesis Unit, Department of Translational Oncology, National Cancer Research Institute, Genoa, Italy
    Clin Cancer Res 13:3789-95. 2007
    ..umd.be:2072/index.html). We have investigated the extent to which the functional features of p53 mutant alleles determine clinical features in patients who have inherited these alleles and have developed cancer...
  19. pmc Differential suppression of DNA repair deficiencies of Yeast rad50, mre11 and xrs2 mutants by EXO1 and TLC1 (the RNA component of telomerase)
    L Kevin Lewis
    Laboratory of Molecular Genetics, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, North Carolina 27709, USA
    Genetics 160:49-62. 2002
    ..Gene-specific suppression by TLC1, which encodes the RNA subunit of the yeast telomerase complex, demonstrates that components of telomerase can also impact on DSB repair pathways...
  20. pmc Low-level p53 expression changes transactivation rules and reveals superactivating sequences
    Jennifer J Jordan
    Chromosome Stability Section, Laboratory of Molecular Genetics, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, NC 27709, USA
    Proc Natl Acad Sci U S A 109:14387-92. 2012
    ....
  21. pmc A single-nucleotide polymorphism in a half-binding site creates p53 and estrogen receptor control of vascular endothelial growth factor receptor 1
    Daniel Menendez
    Laboratory of Molecular Genetics MD3 01, National Institute of Environmental Health Sciences, 111 Alexander Drive, Research Triangle Park, NC 27709, USA
    Mol Cell Biol 27:2590-600. 2007
    ..The mechanism of joint regulation through half-sites is likely relevant to transcriptional control of other targets and expands the number of genes that may be directly controlled in master regulatory networks...
  22. pmc A regulatory loop composed of RAP80-HDM2-p53 provides RAP80-enhanced p53 degradation by HDM2 in response to DNA damage
    Jun Yan
    Cell Biology Section, Laboratory of Respiratory Biology, Chromosome Stability Group, Laboratory of Molecular Genetics, Division of Intramural Research, NIEHS, National Institutes of Health, Research Triangle Park, North Carolina 27709, USA
    J Biol Chem 284:19280-9. 2009
    ..It can function in an autoregulatory loop consisting of RAP80, HDM2, and the p53 master regulatory network, implying an important role for this loop in genome stability and oncogenesis...
  23. pmc Estrogen receptor acting in cis enhances WT and mutant p53 transactivation at canonical and noncanonical p53 target sequences
    Daniel Menendez
    Laboratory of Molecular Genetics, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, NC 27709, USA
    Proc Natl Acad Sci U S A 107:1500-5. 2010
    ..This relationship greatly expands the transcriptional master network regulated by p53 in terms of genes affected and levels of expression and has implications for the appearance and possible treatments of cancer...
  24. pmc Chromosome integrity at a double-strand break requires exonuclease 1 and MRX
    Wataru Nakai
    National Institute of Environmental Health Sciences, NIH, Laboratory of Molecular Genetics, Research Triangle Park, NC 27709, USA
    DNA Repair (Amst) 10:102-10. 2011
    ..In addition, we discovered a thermal sensitive (cold) component to CRB formation in an MRX mutant that has implications for chromosome end mobility and/or end-processing...
  25. pmc Genome-wide model for the normal eukaryotic DNA replication fork
    ANDRES A LARREA
    Laboratory of Molecular Genetics and Laboratory of Structural Biology, Department of Health and Human Services, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, NC 27709, USA
    Proc Natl Acad Sci U S A 107:17674-9. 2010
    ..This strand bias strongly supports the idea that Pol δ is primarily a lagging strand polymerase during replication across the entire nuclear genome...
  26. pmc Cohesin Is limiting for the suppression of DNA damage-induced recombination between homologous chromosomes
    Shay Covo
    Laboratory of Molecular Genetics, National Institute of Environmental Health Sciences NIEHS, National Institutes of Health NIH, Research Triangle Park, North Carolina, United States of America
    PLoS Genet 6:e1001006. 2010
    ..The effects of limited amounts of Mcd1and Smc3 indicate that small changes in cohesin levels may increase the risk of genome instability, which may lead to genetic diseases and cancer...
  27. pmc The choice of nucleotide inserted opposite abasic sites formed within chromosomal DNA reveals the polymerase activities participating in translesion DNA synthesis
    Kin Chan
    Chromosome Stability Section, Laboratory of Molecular Genetics, National Institute of Environmental Health Sciences, National Institutes of Health, 111 T W Alexander Drive, Research Triangle Park, NC 27709, USA Electronic address
    DNA Repair (Amst) 12:878-89. 2013
    ..Our results underscore the utility of this system for studying TLS bypass of many types of lesions within genomic DNA. ..
  28. pmc Hypermutability of damaged single-strand DNA formed at double-strand breaks and uncapped telomeres in yeast Saccharomyces cerevisiae
    Yong Yang
    Department of Health and Human Services, Laboratory of Molecular Genetics, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, North Carolina, United States of America
    PLoS Genet 4:e1000264. 2008
    ..Hypermutability and multiple mutations associated with lesions in transient stretches of long single-strand DNA may be a source of carcinogenesis and provide selective advantage in adaptive evolution...
  29. pmc Coincident resection at both ends of random, γ-induced double-strand breaks requires MRX (MRN), Sae2 (Ctp1), and Mre11-nuclease
    James W Westmoreland
    Chromosome Stability Section, Laboratory of Molecular Genetics, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, North Carolina, United States of America
    PLoS Genet 9:e1003420. 2013
    ..These approaches apply to resection at other DSBs. Given evolutionary conservation, the observations are relevant to DNA repair in human cells...
  30. pmc Functionally distinct polymorphic sequences in the human genome that are targets for p53 transactivation
    Daniel J Tomso
    Laboratory of Molecular Genetics, National Institute of Environmental Health Sciences, National Institutes of Health, Department of Health and Human Services, Research Triangle Park, NC 27709, USA
    Proc Natl Acad Sci U S A 102:6431-6. 2005
    ..Thus, this strategy efficiently identifies SNPs that may differentially affect gene expression responses in the p53 regulatory pathway...
  31. pmc The coordinated p53 and estrogen receptor cis-regulation at an FLT1 promoter SNP is specific to genotoxic stress and estrogenic compound
    Yari Ciribilli
    Unit of Molecular Mutagenesis and DNA Repair, National Institute for Cancer Research, IST, Genoa, Italy
    PLoS ONE 5:e10236. 2010
    ..The transcriptional control required an estrogen receptor (ER) (1/2) site response element (ERE1) 225 nt upstream to the RE-T...
  32. pmc Base damage within single-strand DNA underlies in vivo hypermutability induced by a ubiquitous environmental agent
    Kin Chan
    Chromosome Stability Section, Laboratory of Molecular Genetics, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, North Carolina, United States of America
    PLoS Genet 8:e1003149. 2012
    ..Our results suggest that sulfite-induced lesions in DNA can be particularly deleterious, since cells might not possess the means to repair or bypass such lesions accurately...
  33. pmc Blunt-ended DNA double-strand breaks induced by endonucleases PvuII and EcoRV are poor substrates for repair in Saccharomyces cerevisiae
    James W Westmoreland
    Laboratory of Molecular Genetics, National Institute of Environmental Health Sciences, NIH, Research Triangle Park, NC 27709, USA
    DNA Repair (Amst) 9:617-26. 2010
    ..These results indicate that, unlike DSBs with complementary single-stranded DNA overhangs, blunt-ended DSBs in yeast chromosomes are poor substrates for repair by either NHEJ or recombination...
  34. pmc RNA-templated DNA repair
    Francesca Storici
    Laboratory of Molecular Genetics, National Institute of Environmental Health Sciences NIH, DHHS, Research Triangle Park, North Carolina 27709, USA
    Nature 447:338-41. 2007
    ....
  35. pmc Conservative repair of a chromosomal double-strand break by single-strand DNA through two steps of annealing
    Francesca Storici
    Head Chromosome Stability Section, Laboratory of Molecular Genetics, National Institute of Environmental Health Sciences, NIH, Research Triangle Park, NC 27709, USA
    Mol Cell Biol 26:7645-57. 2006
    ..The repair by single-strand DNA can be conservative and may allow for accurate restoration of chromosomal DNAs with closely spaced DSBs...
  36. pmc Chromosomal site-specific double-strand breaks are efficiently targeted for repair by oligonucleotides in yeast
    Francesca Storici
    Laboratory of Molecular Genetics, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, NC 27709, USA
    Proc Natl Acad Sci U S A 100:14994-9. 2003
    ..These findings expand current models of DSB repair. In addition, we establish a high-throughput system for rapid genome-wide modification with oligonucleotides...
  37. pmc The human TLR innate immune gene family is differentially influenced by DNA stress and p53 status in cancer cells
    Maria Shatz
    Chromosome Stability Group, Laboratory of Molecular Genetics, National Institute of Environmental Health Sciences NIEHS, NIH, Research Triangle Park, North Carolina 27709, USA
    Cancer Res 72:3948-57. 2012
    ..Our findings therefore show that the matrix of p53 status, chromosome stress, and responsiveness of individual TLRs should be considered in TLR-based cancer therapies...
  38. pmc Transactivation specificity is conserved among p53 family proteins and depends on a response element sequence code
    Yari Ciribilli
    Laboratory of Transcriptional Networks, Centre for Integrative Biology CIBIO, University of Trento, TN, 38060 Italy, Molecular Mutagenesis and DNA Repair Unit, IRCSS Azienda Ospedaliera Universitaria San Martino IST Istituto Nazionale per la Ricerca sul Cancro, Genoa 16132, Italy, Department of Chemistry and Biochemistry, University of California San Diego, La Jolla, CA, 92093, USA and Chromosome Stability Group, Laboratory of Molecular Genetics, National Institute of Environmental Health Sciences, NIEHS, NIH, RTP, NC, 27709, USA
    Nucleic Acids Res 41:8637-53. 2013
    ....
  39. pmc Homologous recombination rescues ssDNA gaps generated by nucleotide excision repair and reduced translesion DNA synthesis in yeast G2 cells
    Wenjian Ma
    Chromosome Stability Group, Laboratory of Molecular Genetics, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, NC 27709, USA
    Proc Natl Acad Sci U S A 110:E2895-904. 2013
    ..These findings suggest that ssDNA that might originate during the repair of closely opposed lesions or of ssDNA-containing lesions or from uncoupled replication may drive recombination directly in various species, including humans. ..
  40. pmc Understanding the origins of UV-induced recombination through manipulation of sister chromatid cohesion
    Shay Covo
    Chromosome Stability Section, Laboratory of Molecular Genetics, National Institute of Environmental Health Sciences NIEHS, National Institutes of Health NIH, Research Triangle Park, NC, USA
    Cell Cycle 11:3937-44. 2012
    ..This notion is supported by a direct physical observation of UV-induced DSBs that are dependent on nucleotide excision repair. However, a significant role of nonDSB intermediates in UV-induced recombination cannot be excluded...
  41. pmc RAD53 is limiting in double-strand break repair and in protection against toxicity associated with ribonucleotide reductase inhibition
    Shay Covo
    Chromosome Stability Group, Laboratory of Molecular Genetics, National Institute of Environmental Health Sciences, NIH, Research Triangle Park, NC 27709, USA
    DNA Repair (Amst) 11:317-23. 2012
    ..These results have implications for developing drug enhancers as well as for understanding mechanisms of drug resistance in cells compromised for DNA damage checkpoint...
  42. pmc Apn1 and Apn2 endonucleases prevent accumulation of repair-associated DNA breaks in budding yeast as revealed by direct chromosomal analysis
    Wenjian Ma
    Laboratory of Molecular Genetics, National Institute of Environmental Health Sciences NIH, DHHS, Research Triangle Park, NC 27709, USA
    Nucleic Acids Res 36:1836-46. 2008
    ..This approach provided direct physical evidence that Apn1 and Apn2 not only repair cellular base damage but also prevent break accumulation that can result from AP sites being channeled into other BER pathway(s)...
  43. pmc Altered-function p53 missense mutations identified in breast cancers can have subtle effects on transactivation
    Jennifer J Jordan
    Laboratory of Molecular Genetics, National Institute of Environmental Health Sciences, NIH, Research Triangle Park, North Carolina 27709, USA
    Mol Cancer Res 8:701-16. 2010
    ....
  44. pmc Clustered mutations in yeast and in human cancers can arise from damaged long single-strand DNA regions
    Steven A Roberts
    Laboratory of Molecular Genetics, National Institute of Environmental Health Sciences, NIH, DHHS, Durham, NC 27709, USA
    Mol Cell 46:424-35. 2012
    ..These data indicate that hypermutation via multiple simultaneous changes in randomly formed ssDNA is a general phenomenon that may be an important mechanism producing rapid genetic variation...
  45. pmc Damage-induced localized hypermutability
    Lauranell H Burch
    National Institute of Environmental Health Sciences, Research Triangle Park, NC USA
    Cell Cycle 10:1073-85. 2011
    ..High multiplicity and density of mutations suggest that this novel form of genome instability may play significant roles in generating new alleles for evolutionary selection as well as in the incidence of cancer and genetic disease...
  46. pmc Cadmium is a mutagen that acts by inhibiting mismatch repair
    Yong Hwan Jin
    Laboratory of Molecular Genetics, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, North Carolina 27709, USA
    Nat Genet 34:326-9. 2003
    ..In extracts of human cells, cadmium inhibited at least one step leading to mismatch removal. Together, our data show that a high level of genetic instability can result from environmental impediment of a mutation-avoidance system...
  47. pmc Divergent evolution of human p53 binding sites: cell cycle versus apoptosis
    Monica M Horvath
    Laboratory of Molecular Genetics, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina, United States of America
    PLoS Genet 3:e127. 2007
    ....
  48. pmc The flexible loop of human FEN1 endonuclease is required for flap cleavage during DNA replication and repair
    Francesca Storici
    Laboratory of Molecular Genetics, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, NC 27709, USA
    EMBO J 21:5930-42. 2002
    ..We suggest that the flexible loop is important for efficient cleavage through positioning the 5' flap and the catalytic site...
  49. pmc Diverse stresses dramatically alter genome-wide p53 binding and transactivation landscape in human cancer cells
    Daniel Menendez
    Chromosome Stability Group, Laboratory of Molecular Genetics, National Institute of Environmental Health Sciences NIEHS, National Institutes of Health NIH, Research Triangle Park, NC 27709, USA, Systems Biology Group, Laboratory of Molecular Carcinogenesis, National Institute of Environmental Health Sciences NIEHS, National Institutes of Health NIH, Research Triangle Park, NC 27709, USA, William G Enloe High School, Raleigh, NC 27610, USA and Department of Biology, Brookhaven National Laboratory, Upton, NY 11973, USA
    Nucleic Acids Res 41:7286-301. 2013
    ..We discovered 149 putative new p53 target genes including several that are relevant to tumor suppression, revealing potential new targets for cancer therapy and expanding our understanding of the p53 regulatory network. ..
  50. pmc p53 and NF-κB coregulate proinflammatory gene responses in human macrophages
    Julie M Lowe
    Authors Affiliations Laboratory of Molecular Genetics, Biostatistics Branch, Laboratory of Respiratory Biology, National Institute of Environmental Health Sciences NIEHS, NIH, Research Triangle Park and Epidemiology, Gillings School of Global Public Health, University of North Carolina, Chapel Hill, North Carolina
    Cancer Res 74:2182-92. 2014
    ....
  51. pmc Oxidative stress-induced mutagenesis in single-strand DNA occurs primarily at cytosines and is DNA polymerase zeta-dependent only for adenines and guanines
    Natalya P Degtyareva
    Department of Biochemistry, Winship Cancer Institute, Emory University School of Medicine, 4013 Rollins Research Center, Atlanta, GA 30322, USA, Laboratory of Molecular Genetics, National Institute of Environmental Health Sciences NIH, DHHS, Research Triangle Park, NC 27709, USA and Department of Radiation Oncology, Emory University School of Medicine, 4013 Rollins Research Center, Atlanta, GA 30322, USA
    Nucleic Acids Res 41:8995-9005. 2013
    ..These findings have important implications for understanding mechanisms of oxidative mutagenesis, and could be applied to development of anticancer therapies and cancer prevention. ..
  52. pmc RAP80 is critical in maintaining genomic stability and suppressing tumor development
    Zhengyu Yin
    Laboratory of Respiratory Biology, National Institute of Environmental Sciences, National Institutes of Health, Research Triangle Park, North Carolina 27709, USA
    Cancer Res 72:5080-90. 2012
    ..Our data indicate that RAP80-deficiency promotes genomic instability and causes an increase in cancer risk consistent with the concept that RAP80 exhibits a tumor suppressor function...
  53. pmc Differential effects of poly(ADP-ribose) polymerase inhibition on DNA break repair in human cells are revealed with Epstein-Barr virus
    Wenjian Ma
    Chromosome Stability Section, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, NC 27709, USA
    Proc Natl Acad Sci U S A 109:6590-5. 2012
    ..However, a decrease in PARP1 expression reversed the ability of Iniparib to reduce SSB repair. Because Iniparib disrupts PARP1-DNA binding, the mechanism of inhibition does not appear to involve trapping PARP at SSBs...
  54. pmc The biological impact of the human master regulator p53 can be altered by mutations that change the spectrum and expression of its target genes
    Daniel Menendez
    Chromosome Stability Section, Laboratory of Molecular Genetics, National Institute of Environmental Health Sciences, NIH, Research Triangle Park, North Carolina 27709, USA
    Mol Cell Biol 26:2297-308. 2006
    ....
  55. pmc The novel p53 target TNFAIP8 variant 2 is increased in cancer and offsets p53-dependent tumor suppression
    Julie M Lowe
    Immunity, Inflammation, and Disease Laboratory, National Institute of Environmental Health Sciences, NIH, Research Triangle Park, NC 27709, USA
    Cell Death Differ . 2016
    ..Cell Death and Differentiation advance online publication, 11 November 2016; doi:10.1038/cdd.2016.130...
  56. ncbi request reprint Reduction in frataxin causes progressive accumulation of mitochondrial damage
    Gopalakrishnan Karthikeyan
    Laboratory of Molecular Genetics, National Institute of Environmental Health Sciences, NIH, Research Triangle Park, NC 27709, USA
    Hum Mol Genet 12:3331-42. 2003
    ..We conclude that reduced frataxin levels, which is more representative of the disease state, results in considerable oxidative damage in both mitochondrial and nuclear DNA...
  57. pmc Differential transactivation by the p53 transcription factor is highly dependent on p53 level and promoter target sequence
    Alberto Inga
    Laboratory of Molecular Genetics, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, North Carolina 27709, USA
    Mol Cell Biol 22:8612-25. 2002
    ..In addition, p53 alleles associated with familial breast cancer, previously classified as wild type, showed subtle differences in transactivation capacity towards several REs...
  58. pmc An APOBEC cytidine deaminase mutagenesis pattern is widespread in human cancers
    Steven A Roberts
    Laboratory of Molecular Genetics, National Institute of Environmental Health Sciences, Durham, North Carolina, USA
    Nat Genet 45:970-6. 2013
    ..The APOBEC mutation pattern also extended to cancer-associated genes, implying that ubiquitous APOBEC-mediated mutagenesis is carcinogenic. ..
  59. pmc p53 Integrates host defense and cell fate during bacterial pneumonia
    Jennifer H Madenspacher
    Laboratory of Respiratory Biology, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, NC 27709, USA
    J Exp Med 210:891-904. 2013
    ..p53 thus modulates host defense through regulating microbicidal function and fate of phagocytes, revealing a fundamental link between defense of genome and host during environmental insult...
  60. pmc A single-strand specific lesion drives MMS-induced hyper-mutability at a double-strand break in yeast
    Yong Yang
    Laboratory of Molecular Genetics, National Institute of Environmental Health Sciences, NIH, DHHS, Research Triangle Park, NC 27709, United States
    DNA Repair (Amst) 9:914-21. 2010
    ..These findings with MMS-induced LHM have broad biological implications for unrepaired damage generated in ssDNA and possibly ssRNA...
  61. pmc Characterizing resection at random and unique chromosome double-strand breaks and telomere ends
    Wenjian Ma
    Chromosome Stability Section, National Institute of Environmental Health Sciences NIEHS, NIH, Research Triangle Park, NC 27709, USA
    Methods Mol Biol 745:15-31. 2011
    ..This mobility-shift assay provides a unique opportunity to examine the mechanisms of resection, early events in DSB repair, as well as factors involved in pathway regulation...
  62. ncbi request reprint A novel p53 mutational hotspot in skin tumors from UV-irradiated Xpc mutant mice alters transactivation functions
    Alberto Inga
    Laboratory of Molecular Genetics, National Institute of Environmental Health Sciences, NIH, PO Box 12233, Research Triangle Park, North Carolina, NC 27709, USA
    Oncogene 21:5704-15. 2002
    ..Furthermore, the approach that we have taken also provides for the dissection of functions that may be retained in many p53 tumor alleles...
  63. ncbi request reprint The delitto perfetto approach to in vivo site-directed mutagenesis and chromosome rearrangements with synthetic oligonucleotides in yeast
    Francesca Storici
    Laboratory of Molecular Genetics, Chromosome Stability Section, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, North Carolina, USA
    Methods Enzymol 409:329-45. 2006
    ....
  64. ncbi request reprint The mitochondrial protein frataxin prevents nuclear damage
    Gopalakrishnan Karthikeyan
    Laboratory of Molecular Genetics, National Institute of Enviromental Health Sciences, NIH, PO Box 12233, Research Triangle Park, NC 27709, USA
    Hum Mol Genet 11:1351-62. 2002
    ..Thus, the frataxin protein is concluded to have a protective role for the nucleus as well as the mitochondria...
  65. doi request reprint The expanding universe of p53 targets
    Daniel Menendez
    Laboratory of Molecular Genetics, National Institute of Environmental Health Science, Research Triangle Park, North Carolina 27709, USA
    Nat Rev Cancer 9:724-37. 2009
    ..This Review describes the identification and functionality of REs and highlights the inclusion of non-canonical REs that expand the universe of genes and regulation mechanisms in the p53 tumour suppressor network...
  66. ncbi request reprint Chromosome fragmentation after induction of a double-strand break is an active process prevented by the RMX repair complex
    Kirill Lobachev
    Laboratory of Molecular Genetics, National Institute of Environmental Health Sciences, National Institutes of Health, 101 Alexander Drive, Research Triangle Park, NC 27709 USA
    Curr Biol 14:2107-12. 2004
    ..Thus, the RMX complex holds broken ends together and counteracts mitotic spindle forces that can be destructive to damaged chromosomes...
  67. pmc Mutant TP53 posttranslational modifications: challenges and opportunities
    Thuy Ai Nguyen
    Chromosome Stability Section, Laboratory of Molecular Genetics, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina
    Hum Mutat 35:738-55. 2014
    ..Understanding the signaling pathways that result in TP53 modification and the functions of these modifications in both WT TP53 and its many MUT forms may contribute to more effective cancer therapies. ..
  68. ncbi request reprint Functional dissection of sequence-specific NKX2-5 DNA binding domain mutations associated with human heart septation defects using a yeast-based system
    Alberto Inga
    Chromosome Stability Section, Laboratory of Molecular Genetics, National Institute of Environmental Health Sciences, NIH, Research Triangle Park, NC 27709, USA
    Hum Mol Genet 14:1965-75. 2005
    ..Therefore, mutations of somatic origin in the binding domains of NKX2-5 were associated specifically with AVSD or VSD and resulted in loss of protein function...
  69. ncbi request reprint Delitto perfetto targeted mutagenesis in yeast with oligonucleotides
    Francesca Storici
    Laboratory of Molecular Genetics, National Institute of Environmental Health Sciences, NIH, 111 Alexander Dr, Research Triangle Park, NC 27709, USA
    Genet Eng (N Y) 25:189-207. 2003
  70. pmc The Toll-like receptor gene family is integrated into human DNA damage and p53 networks
    Daniel Menendez
    Chromosome Stability Group, Laboratory of Molecular Genetics, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, North Carolina, United States of America
    PLoS Genet 7:e1001360. 2011
    ....
  71. doi request reprint Interactions between the tumor suppressor p53 and immune responses
    Daniel Menendez
    Laboratory of Molecular Genetics, Chromosome Stability Section, National Institute of Environmental Health Sciences, National Institutes of Health, North Carolina 27709, USA
    Curr Opin Oncol 25:85-92. 2013
    ..Here, we focus on the role of p53 in the immune system. We explore the relationship between p53 and the innate immune response with particular emphasis on the Toll-like receptor (TLR) pathway and implications for cancer therapy...
  72. ncbi request reprint Impact of mitochondria on nuclear genome stability
    Gopalakrishnan Karthikeyan
    Laboratory of Molecular Genetics, National Institute of Environmental Health Sciences, NIH Research Triangle Park, 111 Alexander Drive, North Carolina 27709, USA
    DNA Repair (Amst) 4:141-8. 2005
  73. ncbi request reprint Okazaki fragment maturation in yeast. II. Cooperation between the polymerase and 3'-5'-exonuclease activities of Pol delta in the creation of a ligatable nick
    Yong Hwan Jin
    Laboratory of Molecular Genetics, National Institute for Environmental and Health Sciences, National Institutes of Health, North Carolina 27709, USA
    J Biol Chem 278:1626-33. 2003
    ..Further genetic studies showed that pol3-exo(-) rad27 double mutants were sensitive to alkylation damage consistent with an in vivo defect in gap filling by exonuclease-deficient Pol delta...
  74. ncbi request reprint Tumour p53 mutations exhibit promoter selective dominance over wild type p53
    Paola Monti
    Mutagenesis Laboratory, National Cancer Research Institute IST, Largo R Benzi, 10, 16132 Genova, Italy
    Oncogene 21:1641-8. 2002
    ..The yeast data do not support this explanation, because all BRCA-associated mutants that behaved as wild type in transcription assay were recessive in dominance assays...
  75. pmc Functional evolution of the p53 regulatory network through its target response elements
    Anil G Jegga
    Division of Biomedical Informatics, Cincinnati Children s Hospital Medical Center, Cincinnati, OH 45229 3039, USA
    Proc Natl Acad Sci U S A 105:944-9. 2008
    ..Surprisingly, there was almost no conservation of functional REs for genes involved in DNA metabolism or repair between humans and rodents, suggesting important differences in p53 stress responses and cancer development...
  76. ncbi request reprint Effect of amino acid substitutions in the rad50 ATP binding domain on DNA double strand break repair in yeast
    Ling Chen
    Department of Molecular Medicine, Institute of Biotechnology, The University of Texas Health Science Center at San Antonio, San Antonio, Texas 78245, USA
    J Biol Chem 280:2620-7. 2005
    ..These results provide a molecular explanation for the observed in vivo defects of the rad50 Walker mutant strains and reveal a novel ATP-independent function for Rad50 in DNA end-bridging...
  77. pmc Double-strand breaks associated with repetitive DNA can reshape the genome
    Juan Lucas Argueso
    Department of Molecular Genetics and Microbiology, Duke University Medical Center, Durham, NC 27710, USA
    Proc Natl Acad Sci U S A 105:11845-50. 2008
    ..Because repeat-associated DSBs can efficiently lead to CAs and reshape the genome, they could be a rich source of evolutionary change...
  78. pmc Role of the nuclease activity of Saccharomyces cerevisiae Mre11 in repair of DNA double-strand breaks in mitotic cells
    L Kevin Lewis
    Department of Chemistry and Biochemistry, Texas State University, San Marcos, Texas 78666, USA
    Genetics 166:1701-13. 2004
    ....
  79. pmc Cell cycle progression in G1 and S phases is CCR4 dependent following ionizing radiation or replication stress in Saccharomyces cerevisiae
    Tammy J Westmoreland
    Department of Surgery, Duke University Medical Center, Durham, North Carolina 27710, USA
    Eukaryot Cell 3:430-46. 2004
    ..These results indicate that cell cycle transition through G1 and S phases is CCR4 dependent following radiation or replication stress...
  80. ncbi request reprint Use of a restriction endonuclease cytotoxicity assay to identify inducible GAL1 promoter variants with reduced basal activity
    L Kevin Lewis
    Department of Chemistry and Biochemistry, Texas State University, 601 University Drive, San Marcos, TX 78666, USA
    Gene 363:183-92. 2005
    ..These experiments and additional quantitative luciferase reporter gene assays demonstrate the utility of the approach for identifying promoters that permit more tightly controlled gene expression...
  81. pmc Reduction of nucleosome assembly during new DNA synthesis impairs both major pathways of double-strand break repair
    L Kevin Lewis
    Department of Chemistry and Biochemistry, Texas State University, San Marcos, TX 78666, USA
    Nucleic Acids Res 33:4928-39. 2005
    ..These results demonstrate that defective assembly of nucleosomes during new DNA synthesis compromises each of the known pathways of DSB repair and that the effects can be indirect consequences of changes in silenced chromatin structure...