Richard Kolodner

Summary

Affiliation: University of California
Country: USA

Publications

  1. ncbi request reprint Analysis of gross-chromosomal rearrangements in Saccharomyces cerevisiae
    Kristina H Schmidt
    Ludwig Institute for Cancer Research, University of North Texas, Health Science Center, Fort Worth, USA
    Methods Enzymol 409:462-76. 2006
  2. ncbi request reprint Recombination and the Tel1 and Mec1 checkpoints differentially effect genome rearrangements driven by telomere dysfunction in yeast
    Vincent Pennaneach
    Ludwig Institute for Cancer Research, Cancer Center and Department of Medicine, University of California San Diego School of Medicine CMME 3058, 9500 Gilman Drive, La Jolla, California 92093 0669, USA
    Nat Genet 36:612-7. 2004
  3. pmc An overview of Cdk1-controlled targets and processes
    Jorrit M Enserink
    Department of Molecular Biology, Institute of Medical Microbiology and Centre of Molecular Biology and Neuroscience, Oslo University Hospital, Sognsvannsveien 20, N 0027 Oslo, Norway
    Cell Div 5:11. 2010
  4. ncbi request reprint Germ-line msh6 mutations in colorectal cancer families
    R D Kolodner
    Ludwig Institute for Cancer Research, Department of Medicine and Cancer Center, University of California San Diego Medical School, La Jolla 92093 0660, USA
    Cancer Res 59:5068-74. 1999
  5. pmc Coupling distant sites in DNA during DNA mismatch repair
    Richard D Kolodner
    Ludwig Institute for Cancer Research, Department of Medicine, University of California at San Diego School of Medicine, 9500 Gilman Drive, La Jolla, CA 92093 0669, USA
    Proc Natl Acad Sci U S A 104:12953-4. 2007
  6. ncbi request reprint Maintenance of genome stability in Saccharomyces cerevisiae
    Richard D Kolodner
    Ludwig Institute for Cancer Research, Cancer Center and Department of Medicine, CMME3058, 9500 Gilman Drive, University of California San Diego School of Medicine, La Jolla, CA 92093, USA
    Science 297:552-7. 2002
  7. ncbi request reprint Analysis of the interaction between the Saccharomyces cerevisiae MSH2-MSH6 and MLH1-PMS1 complexes with DNA using a reversible DNA end-blocking system
    Marc L Mendillo
    Ludwig Institute for Cancer Research, Department of Medicine and Cancer Center, School of Medicine, University of California San Diego, 9500 Gilman Drive, La Jolla, CA 92093 0669, USA
    J Biol Chem 280:22245-57. 2005
  8. pmc Saccharomyces cerevisiae as a model system to define the chromosomal instability phenotype
    Christopher D Putnam
    Ludwig Institute for Cancer Research, University of California, San Diego School of Medicine, La Jolla, 92093 0669, USA
    Mol Cell Biol 25:7226-38. 2005
  9. pmc Post-replication repair suppresses duplication-mediated genome instability
    Christopher D Putnam
    Ludwig Institute for Cancer Research, University of California San Diego School of Medicine, La Jolla, California, United States of America
    PLoS Genet 6:e1000933. 2010
  10. ncbi request reprint A biological network in Saccharomyces cerevisiae prevents the deleterious effects of endogenous oxidative DNA damage
    Meng Er Huang
    Ludwig Institute for Cancer Research, CMME 3058, 9500 Gilman Drive, La Jolla, California 92093, USA
    Mol Cell 17:709-20. 2005

Research Grants

  1. ENZYMOLOGY OF MISMATCH REPAIR IN YEAST
    Richard Kolodner; Fiscal Year: 2007
  2. ENZYMOLOGY OF MISMATCH REPAIR IN YEAST
    Richard D Kolodner; Fiscal Year: 2010
  3. ENZYMATIC MECHANISMS OF GENETIC RECOMBINATION
    Richard D Kolodner; Fiscal Year: 2010
  4. ENZYMATIC MECHANISMS OF GENETIC RECOMBINATION
    Richard Kolodner; Fiscal Year: 2007
  5. ENZYMATIC MECHANISMS OF GENETIC RECOMBINATION
    Richard Kolodner; Fiscal Year: 2009
  6. ENZYMOLOGY OF MISMATCH REPAIR IN YEAST
    Richard Kolodner; Fiscal Year: 2009
  7. ENZYMOLOGY OF MISMATCH REPAIR IN YEAST
    Richard Kolodner; Fiscal Year: 2006
  8. ENZYMATIC MECHANISMS OF GENETIC RECOMBINATION
    Richard Kolodner; Fiscal Year: 2005
  9. ENZYMOLOGY OF MISMATCH REPAIR IN YEAST
    Richard Kolodner; Fiscal Year: 1999
  10. ENZYMOLOGY OF MISMATCH REPAIR IN YEAST
    Richard Kolodner; Fiscal Year: 2002

Collaborators

Detail Information

Publications77

  1. ncbi request reprint Analysis of gross-chromosomal rearrangements in Saccharomyces cerevisiae
    Kristina H Schmidt
    Ludwig Institute for Cancer Research, University of North Texas, Health Science Center, Fort Worth, USA
    Methods Enzymol 409:462-76. 2006
    ..This GCR analysis provides an effective tool for the assessment of the contribution by multiple cellular mechanisms to the maintenance of genome integrity...
  2. ncbi request reprint Recombination and the Tel1 and Mec1 checkpoints differentially effect genome rearrangements driven by telomere dysfunction in yeast
    Vincent Pennaneach
    Ludwig Institute for Cancer Research, Cancer Center and Department of Medicine, University of California San Diego School of Medicine CMME 3058, 9500 Gilman Drive, La Jolla, California 92093 0669, USA
    Nat Genet 36:612-7. 2004
    ..In contrast, inactivation of Mec1 resulted in more inversion translocations such as the isochromosomes seen in human tumors. These inversion translocations seemed to be formed by recombination after replication of broken chromosomes...
  3. pmc An overview of Cdk1-controlled targets and processes
    Jorrit M Enserink
    Department of Molecular Biology, Institute of Medical Microbiology and Centre of Molecular Biology and Neuroscience, Oslo University Hospital, Sognsvannsveien 20, N 0027 Oslo, Norway
    Cell Div 5:11. 2010
    ..In this review we discuss currently known targets of Cdk1 in the budding yeast S. cerevisiae and highlight the role of Cdk1 in several crucial processes including maintenance of genome stability...
  4. ncbi request reprint Germ-line msh6 mutations in colorectal cancer families
    R D Kolodner
    Ludwig Institute for Cancer Research, Department of Medicine and Cancer Center, University of California San Diego Medical School, La Jolla 92093 0660, USA
    Cancer Res 59:5068-74. 1999
    ..Our data suggest that germ-line msh6 mutations predispose individuals to primarily late-onset, familial colorectal carcinomas that do not fulfill classic criteria for HNPCC...
  5. pmc Coupling distant sites in DNA during DNA mismatch repair
    Richard D Kolodner
    Ludwig Institute for Cancer Research, Department of Medicine, University of California at San Diego School of Medicine, 9500 Gilman Drive, La Jolla, CA 92093 0669, USA
    Proc Natl Acad Sci U S A 104:12953-4. 2007
  6. ncbi request reprint Maintenance of genome stability in Saccharomyces cerevisiae
    Richard D Kolodner
    Ludwig Institute for Cancer Research, Cancer Center and Department of Medicine, CMME3058, 9500 Gilman Drive, University of California San Diego School of Medicine, La Jolla, CA 92093, USA
    Science 297:552-7. 2002
    ..Human homologs of several of these genes have well-established roles as tumor suppressors, consistent with the hypothesis that the mechanisms preserving genome stability in yeast are the same mechanisms that go awry in cancer...
  7. ncbi request reprint Analysis of the interaction between the Saccharomyces cerevisiae MSH2-MSH6 and MLH1-PMS1 complexes with DNA using a reversible DNA end-blocking system
    Marc L Mendillo
    Ludwig Institute for Cancer Research, Department of Medicine and Cancer Center, School of Medicine, University of California San Diego, 9500 Gilman Drive, La Jolla, CA 92093 0669, USA
    J Biol Chem 280:22245-57. 2005
    ..The mispair-dependent ternary complexes were formed in the highest yield on DNA molecules with blocked ends, required ATP and magnesium for formation, and showed both dissociation via the DNA ends and direct dissociation from the DNA...
  8. pmc Saccharomyces cerevisiae as a model system to define the chromosomal instability phenotype
    Christopher D Putnam
    Ludwig Institute for Cancer Research, University of California, San Diego School of Medicine, La Jolla, 92093 0669, USA
    Mol Cell Biol 25:7226-38. 2005
    ..An analysis of human cancer-associated rearrangements revealed parallels to the effects that strain genotypes have on classes of rearrangement in S. cerevisiae...
  9. pmc Post-replication repair suppresses duplication-mediated genome instability
    Christopher D Putnam
    Ludwig Institute for Cancer Research, University of California San Diego School of Medicine, La Jolla, California, United States of America
    PLoS Genet 6:e1000933. 2010
    ..Our analysis is consistent with models in which PRR prevents replication damage from becoming double strand breaks (DSBs) and/or regulates the activity of HR on DSBs...
  10. ncbi request reprint A biological network in Saccharomyces cerevisiae prevents the deleterious effects of endogenous oxidative DNA damage
    Meng Er Huang
    Ludwig Institute for Cancer Research, CMME 3058, 9500 Gilman Drive, La Jolla, California 92093, USA
    Mol Cell 17:709-20. 2005
    ..These findings may provide insight in understanding the consequences of various pathophysiological processes in regard to genomic instability...
  11. pmc The Saccharomyces cerevisiae Rad6 postreplication repair and Siz1/Srs2 homologous recombination-inhibiting pathways process DNA damage that arises in asf1 mutants
    Ellen S Kats
    Ludwig Institute for Cancer Research, Departments of Medicine and Cellular and Molecular Medicine, and Biomedical Sciences Graduate Program, UC San Diego School of Medicine, 9500 Gilman Drive, La Jolla, CA 92093 0669, USA
    Mol Cell Biol 29:5226-37. 2009
    ..Our results show that ASF1 probably contributes to the maintenance of genome stability through multiple mechanisms, some of which involve the PRR and HRS pathways...
  12. pmc Requirement of Rrm3 helicase for repair of spontaneous DNA lesions in cells lacking Srs2 or Sgs1 helicase
    Kristina H Schmidt
    Ludwig Institute for Cancer Research, University of California San Diego School of Medicine, La Jolla, California 92093, USA
    Mol Cell Biol 24:3213-26. 2004
    ..These observations identify Rrm3 as a new member of a network of pathways, involving Sgs1 and Srs2 helicases and Mus81 endonuclease, suggested to act during repair of stalled replication forks...
  13. pmc Suppression of genome instability by redundant S-phase checkpoint pathways in Saccharomyces cerevisiae
    Kyungjae Myung
    Ludwig Institute for Cancer Research, Cancer Center, and Department of Medicine, University of California at San Diego School of Medicine, La Jolla, CA 92093, USA
    Proc Natl Acad Sci U S A 99:4500-7. 2002
    ..These data support the view that spontaneous genome rearrangements result from DNA replication errors and indicate that there is a high degree of redundancy among the checkpoints that act in S phase to suppress such genome instability...
  14. pmc Specific pathways prevent duplication-mediated genome rearrangements
    Christopher D Putnam
    Ludwig Institute for Cancer Research, Department of Medicine, University of California School of Medicine, San Diego, 9500 Gilman Drive, La Jolla, California 92093 0669, USA
    Nature 460:984-9. 2009
    ..This explains how extensive genome instability is prevented in eukaryotic cells whose genomes contain numerous divergent repeated sequences...
  15. pmc Comprehensive molecular analysis of mismatch repair gene defects in suspected Lynch syndrome (hereditary nonpolyposis colorectal cancer) cases
    James Mueller
    Ludwig Institute for Cancer Research, Department of Medicine, Biomedical Sciences Graduate Program, University of California at San Diego School of Medicine, La Jolla, California 92093 0669, USA
    Cancer Res 69:7053-61. 2009
    ....
  16. pmc Suppression of spontaneous genome rearrangements in yeast DNA helicase mutants
    Kristina H Schmidt
    Ludwig Institute for Cancer Research, University of California at San Diego, La Jolla, CA 92093, USA
    Proc Natl Acad Sci U S A 103:18196-201. 2006
    ..These findings demonstrate that different nonreplicative helicases function at the interface between replication and repair to maintain genome integrity...
  17. ncbi request reprint Inhibition of Msh6 ATPase activity by mispaired DNA induces a Msh2(ATP)-Msh6(ATP) state capable of hydrolysis-independent movement along DNA
    Dan J Mazur
    Ludwig Institute for Cancer Research, CMME 3058, 9500 Gilman Drive, La Jolla, California 92093, USA
    Mol Cell 22:39-49. 2006
    ..Our results support a model in which mispair binding encourages a dual-occupancy state with ATP bound to Msh6 and Msh2; this state supports hydrolysis-independent sliding along DNA...
  18. pmc Checkpoint functions are required for normal S-phase progression in Saccharomyces cerevisiae RCAF- and CAF-I-defective mutants
    Ellen S Kats
    Ludwig Institute for Cancer Research, Department of Medicine, University of California at San Diego School of Medicine, 9500 Gilman Drive, La Jolla, CA 92093 0669, USA
    Proc Natl Acad Sci U S A 103:3710-5. 2006
    ..Our data suggest that RCAF defects lead to unstable replication forks that are then stabilized by replication checkpoint proteins, whereas CAF-I defects likely cause different types of DNA damage...
  19. pmc Interaction of mismatch repair protein PMS2 and the p53-related transcription factor p73 in apoptosis response to cisplatin
    Hideki Shimodaira
    Ludwig Institute for Cancer Research, University of California at San Diego, Bonner Hall 3326, 9500 Gilman Drive, La Jolla, CA 92093, USA
    Proc Natl Acad Sci U S A 100:2420-5. 2003
    ..Moreover, stimulation of the p73 proapoptotic function by cisplatin requires PMS2. These results suggest that PMS2 contributes to genome integrity not only through DNA repair but also by enhancing DNA damage-induced apoptosis...
  20. pmc Interaction between the Msh2 and Msh6 nucleotide-binding sites in the Saccharomyces cerevisiae Msh2-Msh6 complex
    Victoria V Hargreaves
    Department of Medicine and Cellular, Cancer Center, Ludwig Institute for Cancer Research, University of California San Diego School of Medicine, La Jolla, California 92093 0669, USA
    J Biol Chem 285:9301-10. 2010
    ....
  21. pmc Rewiring of genetic networks in response to DNA damage
    Sourav Bandyopadhyay
    Department of Medicine, University of California, San Diego, La Jolla, CA 92093, USA
    Science 330:1385-9. 2010
    ..Differential networks chart a new type of genetic landscape that is invaluable for mapping cellular responses to stimuli...
  22. pmc Isolation and characterization of new proliferating cell nuclear antigen (POL30) mutator mutants that are defective in DNA mismatch repair
    Patrick J Lau
    Ludwig Institute for Cancer Research, Cancer Center, La Jolla, California 92093 0660, USA
    Mol Cell Biol 22:6669-80. 2002
    ..These results indicate that the interaction between PCNA and MMR proteins is more complex than was previously appreciated...
  23. pmc Apoptotic function of human PMS2 compromised by the nonsynonymous single-nucleotide polymorphic variant R20Q
    Ivana Marinovic-Terzic
    Moores Cancer Center, University of California, San Diego, School of Medicine, 3855 Health Sciences Drive, La Jolla, CA 92093, USA
    Proc Natl Acad Sci U S A 105:13993-8. 2008
    ..Because PMS2(R20Q) lacks proapoptotic activity, this polymorphic allele may modulate tumor responses to cisplatin among cancer patients...
  24. pmc Saccharomyces cerevisiae Msh2-Msh3 acts in repair of base-base mispairs
    Jill M Harrington
    Ludwig Institute for Cancer Research, University of California, San Diego School of Medicine, 9500 Gilman Drive, La Jolla, CA 92093 0669, USA
    Mol Cell Biol 27:6546-54. 2007
    ....
  25. ncbi request reprint Dominant Saccharomyces cerevisiae msh6 mutations cause increased mispair binding and decreased dissociation from mispairs by Msh2-Msh6 in the presence of ATP
    Martin T Hess
    Ludwig Institute for Cancer Research, Cancer Center, and Department of Medicine, University of California San Diego School of Medicine, La Jolla 92093 0660, USA
    J Biol Chem 277:25545-53. 2002
    ..These results indicate that the dominant msh6 mutations cause more stable binding to mispairs and suggest that there may be differences in how base base and insertion mispairs are recognized...
  26. pmc Saccharomyces cerevisiae chromatin-assembly factors that act during DNA replication function in the maintenance of genome stability
    Kyungjae Myung
    Ludwig Institute for Cancer Research, Cancer Center and Department of Medicine, University of California at San Diego School of Medicine, La Jolla 92093, USA
    Proc Natl Acad Sci U S A 100:6640-5. 2003
    ..These results indicate that coupling of chromatin assembly to DNA replication and DNA repair is critical to maintaining genome stability...
  27. ncbi request reprint Transfer of the MSH2.MSH6 complex from proliferating cell nuclear antigen to mispaired bases in DNA
    Patrick J Lau
    Ludwig Institute for Cancer Research, Cancer Center and Department of Medicine, University of California San Diego School of Medicine, La Jolla, California 92093 0660, USA
    J Biol Chem 278:14-7. 2003
    ..MSH6 binding to the heteroduplex (G/T) DNA. These results support a model in which MSH2.MSH6 binds to PCNA loaded on newly replicated DNA and is transferred from PCNA to mispaired bases in DNA...
  28. ncbi request reprint Chromosome healing by de novo telomere addition in Saccharomyces cerevisiae
    Vincent Pennaneach
    Ludwig Institute for Cancer Research, Department of Medicine, University of California, San Diego School of Medicine, 9500 Gilman Drive, La Jolla, 92093 0669, USA
    Mol Microbiol 59:1357-68. 2006
    ..cerevisiae...
  29. pmc Recruiting research participants at community education sites
    Georgia Robins Sadler
    Rebecca and John Moores Cancer Center, La Jolla, CA, USA
    J Cancer Educ 20:235-9. 2005
    ..In this study, we explored whether community-based cancer education sites and educators serving the African American community could be used to recruit minority participants to research...
  30. pmc Perspectives on the DNA damage and replication checkpoint responses in Saccharomyces cerevisiae
    Christopher D Putnam
    Ludwig Institute for Cancer Research, Department of Medicine and Cancer Center, University of California School of Medicine, San Diego, 9500 Gilman Drive, La Jolla, CA 92093 0669, United States
    DNA Repair (Amst) 8:974-82. 2009
    ....
  31. pmc Biochemical basis for dominant mutations in the Saccharomyces cerevisiae MSH6 gene
    Martin T Hess
    Department of Medicine, Cancer Center, Ludwig Institute for Cancer Research, University of California, San Diego School of Medicine, 9500 Gilman Drive, La Jolla, CA 92093 0669, USA
    Proc Natl Acad Sci U S A 103:558-63. 2006
    ....
  32. ncbi request reprint A hereditary nonpolyposis colorectal carcinoma case associated with hypermethylation of the MLH1 gene in normal tissue and loss of heterozygosity of the unmethylated allele in the resulting microsatellite instability-high tumor
    Isabella Gazzoli
    Ludwig Institute of Cancer Research, University of California San Diego School of Medicine, La Jolla, California 92093, USA
    Cancer Res 62:3925-8. 2002
    ..This biallelic inactivation resulted in loss of expression of MLH1 in the tumor as confirmed by immunohistochemistry. These results suggest a novel mode of germ-line inactivation of a cancer susceptibility gene...
  33. pmc Chimeric Saccharomyces cerevisiae Msh6 protein with an Msh3 mispair-binding domain combines properties of both proteins
    Scarlet S Shell
    Ludwig Institute for Cancer Research, Departments of Medicine and Cellular and Molecular Medicine, and Cancer Center, University of California at San Diego, 9500 Gilman Drive, La Jolla, CA 92093 0669, USA
    Proc Natl Acad Sci U S A 104:10956-61. 2007
    ....
  34. pmc Functional studies and homology modeling of Msh2-Msh3 predict that mispair recognition involves DNA bending and strand separation
    Jill M Dowen
    Ludwig Institute for Cancer Research, University of California, San Diego, School of Medicine, 9500 Gilman Drive, La Jolla, CA 92093 0669, USA
    Mol Cell Biol 30:3321-8. 2010
    ..Mapping of the two classes of mutations onto the Msh3 MBD model appears to distinguish mispair recognition regions from DNA stabilization regions...
  35. ncbi request reprint The mismatch repair complex hMutS alpha recognizes 5-fluorouracil-modified DNA: implications for chemosensitivity and resistance
    Akihiro Tajima
    Department of Medicine, University of California, La Jolla, California, USA
    Gastroenterology 127:1678-84. 2004
    ..We examined whether the component of the DNA mismatch repair (MMR) system that normally recognizes single base pair mismatches could specifically recognize 5-FU incorporated into DNA as a potential mechanism for chemosensitivity...
  36. pmc Functional analysis of human mismatch repair gene mutations identifies weak alleles and polymorphisms capable of polygenic interactions
    Sandra L Martinez
    Department of Medicine, Ludwig Institute for Cancer Research, UC San Diego School of Medicine, La Jolla, CA 92093 0669, USA
    Proc Natl Acad Sci U S A 107:5070-5. 2010
    ..These results indicate that weak MMR gene alleles capable of polygenic interactions with other MMR gene alleles may be relatively common...
  37. pmc Determination of gross chromosomal rearrangement rates
    Christopher D Putnam
    Ludwig Institute for Cancer Research, La Jolla, CA 92093 2385, USA
    Cold Spring Harb Protoc 2010:pdb.prot5492. 2010
    ..The GCR assay allows for detailed analysis of the contributions of individual genes and different pathways in the suppression of genomic instability...
  38. pmc Regulation of the human MSH6 gene by the Sp1 transcription factor and alteration of promoter activity and expression by polymorphisms
    Isabella Gazzoli
    Ludwig Institute for Cancer Research University of California San Diego School of Medicine, CMME 3058, 9500 Gilman Drive, La Jolla, CA 92093, USA
    Mol Cell Biol 23:7992-8007. 2003
    ..An additional 2% of Caucasians contained another polymorphism, -210 C-->T, which inactivated a single Sp1 site that also contributes to promoter activity...
  39. pmc The N terminus of Saccharomyces cerevisiae Msh6 is an unstructured tether to PCNA
    Scarlet S Shell
    Ludwig Institute for Cancer Research, University of California, San Diego, School of Medicine, 9500 Gilman Drive, La Jolla, CA 92093 0669, USA
    Mol Cell 26:565-78. 2007
    ..cerevisiae proteome indicated that flexible linkers are a common theme for PCNA-interacting proteins that may serve to localize these binding partners without tightly restraining them to the immediate vicinity of PCNA...
  40. ncbi request reprint Saccharomyces cerevisiae Mer3 helicase stimulates 3'-5' heteroduplex extension by Rad51; implications for crossover control in meiotic recombination
    Olga M Mazina
    Ludwig Institute for Cancer Research, Cancer Center and Department of Medicine, University of California San Diego School of Medicine, La Jolla, CA 92093, USA
    Cell 117:47-56. 2004
    ....
  41. ncbi request reprint Fine structure mapping of CIAS1: identification of an ancestral haplotype and a common FCAS mutation, L353P
    Hal M Hoffman
    Division of Rheumatology, Allergy, and Immunology, University of California at San Diego, 9500 Gilman Drive, La Jolla, California 92093 0635, USA
    Hum Genet 112:209-16. 2003
    ..We also report a comprehensive list of intragenic single nucleotide polymorphisms. The data provided here will assist others researching the 1q44 region and will aid clinicians in the diagnosis of FCAS...
  42. pmc Identification of EpCAM as the gene for congenital tufting enteropathy
    Mamata Sivagnanam
    Division of Gastroenterology, Hepatology, and Nutrition, Department of Pediatrics, University of California San Diego, La Jolla, California, USA
    Gastroenterology 135:429-37. 2008
    ..The pathogenesis and genetics of this disorder are not well understood. The objective of this study was to identify the gene responsible for CTE...
  43. ncbi request reprint Saccharomyces cerevisiae RRM3, a 5' to 3' DNA helicase, physically interacts with proliferating cell nuclear antigen
    Kristina H Schmidt
    Ludwig Institute for Cancer Research, Cancer Center, and Department of Medicine, University of California San Diego School of Medicine, La Jolla, California 92093 0660, USA
    J Biol Chem 277:45331-7. 2002
    ..The results presented here suggest that the RRM3 helicase functions at the replication fork...
  44. pmc Cdc28/Cdk1 positively and negatively affects genome stability in S. cerevisiae
    Jorrit M Enserink
    Department of Medicine, Cancer Center, Ludwig Institute for Cancer Research, University of California, San Diego School of Medicine, La Jolla, CA 92093, USA
    J Cell Biol 185:423-37. 2009
    ..Thus, we conclude that Cdc28 functions in a genetic network that supports cell viability during DNA damage while promoting the formation of GCRs...
  45. pmc An FHA domain-mediated protein interaction network of Rad53 reveals its role in polarized cell growth
    Marcus B Smolka
    Ludwig Institute for Cancer Research, Department of Cellular and Molecular Medicine, University of California, San Diego, La Jolla, CA 92093, USA
    J Cell Biol 175:743-53. 2006
    ..Collectively, the results suggest a novel function of Rad53 in the regulation of polarized cell growth in response to DNA replication stress...
  46. pmc Probing DNA- and ATP-mediated conformational changes in the MutS family of mispair recognition proteins using deuterium exchange mass spectrometry
    Marc L Mendillo
    Department of Medicine, University of California, San Diego School of Medicine, La Jolla, California 92093 0669, USA
    J Biol Chem 285:13170-82. 2010
    ....
  47. ncbi request reprint The MER3 DNA helicase catalyzes the unwinding of holliday junctions
    Takuro Nakagawa
    Ludwig Institute for Cancer Research, Cancer Center and Department of Medicine, University of California San Diego School of Medicine, La Jolla, California 92093 0660, USA
    J Biol Chem 277:28019-24. 2002
    ..Possible roles for Holliday junction unwinding in meiotic crossover are discussed...
  48. pmc Saccharomyces cerevisiae Mer3 is a DNA helicase involved in meiotic crossing over
    Takuro Nakagawa
    Ludwig Institute for Cancer Research, Cancer Center and Department of Medicine, University of California San Diego School of Medicine, La Jolla, California 92093 0660, USA
    Mol Cell Biol 22:3281-91. 2002
    ..The mer3KA mutation eliminated the ATPase activity of the wild-type protein. These results demonstrate that Mer3 is a DNA helicase that functions in meiotic crossing over...
  49. pmc Dynamic changes in protein-protein interaction and protein phosphorylation probed with amine-reactive isotope tag
    Marcus B Smolka
    Ludwig Institute for Cancer Research, Department of Cellular and Molecular Medicine, University of California San Diego, La Jolla, California 92093, USA
    Mol Cell Proteomics 4:1358-69. 2005
    ....
  50. ncbi request reprint Induction of genome instability by DNA damage in Saccharomyces cerevisiae
    Kyungjae Myung
    Department of Medicine, School of Medicine, University of California at San Diego, CMME3058, 9500 Gilman Drive, La Jolla, CA 92093 0669, USA
    DNA Repair (Amst) 2:243-58. 2003
    ..Genetic analysis indicated that HO DSB-induced GCRs were suppressed by a number of pathways including the DNA damage checkpoints, DSB repair pathways and NHEJ...
  51. pmc Chromosome healing through terminal deletions generated by de novo telomere additions in Saccharomyces cerevisiae
    Christopher D Putnam
    Ludwig Institute for Cancer Research, Department of Medicine, Cancer Center, University of California at San Diego School of Medicine, 9500 Gilman Drive, La Jolla, CA 92093 0669, USA
    Proc Natl Acad Sci U S A 101:13262-7. 2004
    ....
  52. pmc A genomewide screen in Saccharomyces cerevisiae for genes that suppress the accumulation of mutations
    Meng Er Huang
    Ludwig Institute for Cancer Research, Department of Medicine and Cancer Center, University of California at San Diego, School of Medicine, La Jolla, CA 92093, USA
    Proc Natl Acad Sci U S A 100:11529-34. 2003
    ..Study of such genes should provide useful clues in identification of human genes potentially involved in cancer predisposition and in understanding their mechanisms of action...
  53. ncbi request reprint Escherichia coli MutS tetramerization domain structure reveals that stable dimers but not tetramers are essential for DNA mismatch repair in vivo
    Marc L Mendillo
    Ludwig Institute for Cancer Research, Department of Medicine, University of California, San Diego School of Medicine, La Jolla, California 92093 0669, USA
    J Biol Chem 282:16345-54. 2007
    ..These results demonstrate that dimerization but not tetramerization of the MutS C terminus is essential for mismatch repair...
  54. pmc Stabilization of dicentric translocations through secondary rearrangements mediated by multiple mechanisms in S. cerevisiae
    Vincent Pennaneach
    Ludwig Institute for Cancer Research, Department of Medicine, and Moores UCSD Cancer Center, University of California San Diego School of Medicine, La Jolla, California, United States of America
    PLoS ONE 4:e6389. 2009
    ..These GCRs resemble the genome rearrangements found as mutations underlying inherited diseases as well as in the karyotypes of many cancers exhibiting ongoing genome instability..
  55. pmc Checkpoint proteins control morphogenetic events during DNA replication stress in Saccharomyces cerevisiae
    Jorrit M Enserink
    Ludwig Institute for Cancer Research, University of California, San Diego School of Medicine, La Jolla, CA 92093, USA
    J Cell Biol 175:729-41. 2006
    ..Thus, checkpoint proteins play an important role in coordinating morphogenetic events with DNA replication during replication stress...
  56. pmc A conserved MutS homolog connector domain interface interacts with MutL homologs
    Marc L Mendillo
    Ludwig Institute for Cancer Research, University of California, San Diego School of Medicine, La Jolla, CA 92093 0669, USA
    Proc Natl Acad Sci U S A 106:22223-8. 2009
    ....
  57. pmc Haploinsufficiency of Flap endonuclease (Fen1) leads to rapid tumor progression
    Melanie Kucherlapati
    Department of Medicine and Harvard Partners Center for Genetics and Genomics, Harvard Medical School, Boston, MA 02115, USA
    Proc Natl Acad Sci U S A 99:9924-9. 2002
    ..The tumors from these mice show microsatellite instability. Because one copy of the Fen1 gene remained intact in tumors, Fen1 haploinsufficiency appears to lead to rapid progression of cancer...
  58. ncbi request reprint Clinical presentation correlates with the type of mismatch repair gene involved in hereditary nonpolyposis colon cancer
    Prathap Bandipalliam
    Gastroenterology 126:936-7. 2004
  59. ncbi request reprint Evaluation of microsatellite instability and immunohistochemistry for the prediction of germ-line MSH2 and MLH1 mutations in hereditary nonpolyposis colon cancer families
    Siobhan S Wahlberg
    Dana Farber Cancer Institute, Harvard Medical School, Boston, Massachusetts 02115, USA
    Cancer Res 62:3485-92. 2002
    ..A combination of the Bethesda criteria for HNPCC and an MSI-H phenotype defined the smallest number of cases having all of the germ-line MSH2 and MLH1 mutations that could be detected by DNA sequencing...
  60. pmc Approaching a complete repository of sequence-verified protein-encoding clones for Saccharomyces cerevisiae
    Yanhui Hu
    Harvard Institute of Proteomics, Harvard Medical School, Cambridge, MA 02141, USA
    Genome Res 17:536-43. 2007
    ..Availability of this collection makes possible a wide variety of studies from purified proteins to mutation suppression analysis, which should contribute to a global understanding of yeast protein function...
  61. ncbi request reprint Mutation in Rpa1 results in defective DNA double-strand break repair, chromosomal instability and cancer in mice
    Yuxun Wang
    Department of Cell Biology, Albert Einstein College of Medicine, Bronx, New York 10461, USA
    Nat Genet 37:750-5. 2005
    ..These results indicate that Rpa1 functions in DNA metabolism are essential for the maintenance of chromosomal stability and tumor suppression...
  62. ncbi request reprint Suppression of gross chromosomal rearrangements by the multiple functions of the Mre11-Rad50-Xrs2 complex in Saccharomyces cerevisiae
    Stephanie Smith
    Genome Instability Section, Genetics and Molecular Biology Branch, National Human Genome Research Institute, National Institutes of Health, 49 Convent Drive, Bethesda, MD 20892, USA
    DNA Repair (Amst) 4:606-17. 2005
    ..However, the non-homologous end joining function of MRX complex does not appear to participate in the suppression of GCRs...
  63. ncbi request reprint Dominant effects of an Msh6 missense mutation on DNA repair and cancer susceptibility
    Guohze Yang
    Department of Cell Biology, Albert Einstein College of Medicine, Bronx, NY 10461, USA
    Cancer Cell 6:139-50. 2004
    ..Our results demonstrate that MSH6 missense mutations can effectively separate the two functions, and that increased mutation rates associated with the loss of DNA repair are sufficient to drive tumorigenesis in MMR-defective tumors...
  64. ncbi request reprint The recombination-deficient mutant RPA (rfa1-t11) is displaced slowly from single-stranded DNA by Rad51 protein
    Noriko Kantake
    Sections of Microbiology and of Molecular and Cellular Biology, Center for Genetics and Development, University of California, Davis, California 95616, USA
    J Biol Chem 278:23410-7. 2003
    ..These in vitro results suggest that, in vivo, RPA is bound to ssDNA prior to Rad51 protein and that RPA displacement by Rad51 protein is a critical step in homologous recombination, which is impaired in the rfa1-t11 mutation...
  65. pmc Inactivation of Exonuclease 1 in mice results in DNA mismatch repair defects, increased cancer susceptibility, and male and female sterility
    Kaichun Wei
    Department of Cell Biology, Albert Einstein College of Medicine, Bronx, New York 10461, USA
    Genes Dev 17:603-14. 2003
    ..Our results show that mammalian Exo1 functions in mutation avoidance and is essential for male and female meiosis...
  66. ncbi request reprint Lynch syndrome (hereditary nonpolyposis colorectal cancer) diagnostics
    Kristina Lagerstedt Robinson
    Department of Clinical Genetics, Karolinska University Hospital, S 17176 Stockholm, Sweden
    J Natl Cancer Inst 99:291-9. 2007
    ..The syndrome is explained by germline mutations in DNA mismatch repair (MMR) genes, and there is a need for diagnostic tools to preselect patients for genetic testing to diagnose those with HNPCC...
  67. pmc Mitotic checkpoint function in the formation of gross chromosomal rearrangements in Saccharomyces cerevisiae
    Kyungjae Myung
    National Human Genome Research Institute, National Institutes of Health, Bethesda, MD 20892, USA
    Proc Natl Acad Sci U S A 101:15980-5. 2004
    ..These data suggest that functional mitotic checkpoints can play a role in the formation of genome rearrangements...
  68. ncbi request reprint The clinical continuum of cryopyrinopathies: novel CIAS1 mutations in North American patients and a new cryopyrin model
    Ivona Aksentijevich
    Genetics and Genomics Branch, National Institute of Arthritis and Musculoskeletal and Skin Diseases, National Institutes of Health, Bethesda, Maryland 20892 1820, USA
    Arthritis Rheum 56:1273-85. 2007
    ..This study was undertaken to investigate the structural effect of disease-causing mutations on cryopyrin, in order to gain better understanding of the impact of disease-associated mutations on protein function...
  69. ncbi request reprint Functional analysis of human MLH1 variants using yeast and in vitro mismatch repair assays
    Masanobu Takahashi
    Department of Clinical Oncology, Institute of Development, Aging and Cancer, Tohoku University Hospital, Tohoku University, Sendai, Japan
    Cancer Res 67:4595-604. 2007
    ..Integrated functional evaluations contribute to a better prediction of the cancer risk in individuals or families carrying MLH1 variants and provide insights into the function-structure relationships in MLH1...
  70. pmc Oxygen metabolism and reactive oxygen species cause chromosomal rearrangements and cell death
    Sandrine Ragu
    Centre National de la Recherche Scientifique, Unité Mixte de Recherche 2027, Institut Curie, Batiment 110, Centre Universitaire, 91405 Orsay, France
    Proc Natl Acad Sci U S A 104:9747-52. 2007
    ..H(2)O(2) treatment also induced the GCRs. Our results provide in vivo evidence that oxygen metabolism and reactive oxygen species are important sources of DNA damages that can lead to GCRs and lethal effects in S. cerevisiae...
  71. pmc Control of translocations between highly diverged genes by Sgs1, the Saccharomyces cerevisiae homolog of the Bloom's syndrome protein
    Kristina H Schmidt
    Department of Biology, University of South Florida, 4202 E Fowler Avenue, SCA110, Tampa, FL 33620, USA
    Mol Cell Biol 26:5406-20. 2006
    ..The translocation structures observed suggest involvement of a dicentric intermediate and break-induced replication with multiple cycles of DNA template switching...
  72. pmc Hallmarks of homology recognition by RecA-like recombinases are exhibited by the unrelated Escherichia coli RecT protein
    Philippe Noirot
    Laboratoire de Genetique Microbienne, INRA, 78352 Jouy en Josas Cedex, France
    EMBO J 22:324-34. 2003
    ..Taken together, our results show that RecT shares fundamental homology-recognition properties with the RecA homologs, and provide new insights on an underlying universal mechanism of homologous recognition...
  73. ncbi request reprint EXO1 variants occur commonly in normal population: evidence against a role in hereditary nonpolyposis colorectal cancer
    Shantie Jagmohan-Changur
    Center for Human and Clinical Genetics, Leiden University Medical Center, Leiden, The Netherlands 2333
    Cancer Res 63:154-8. 2003
    ..Thus, little evidence was obtained to support a major causative role of EXO1 in HNPCC, although we cannot exclude a role for EXO1 as a low penetrance cancer susceptibility or modifying gene...
  74. pmc The C-terminal domain of yeast PCNA is required for physical and functional interactions with Cdc9 DNA ligase
    Sangeetha Vijayakumar
    Radiation Oncology Research Laboratory, Department of Radiation Oncology and The Marlene and Stewart Greenebaum Cancer Center, University of Maryland School of Medicine, Baltimore, MD 21201 1509, USA
    Nucleic Acids Res 35:1624-37. 2007
    ....
  75. pmc Human peroxiredoxin PrxI is an orthologue of yeast Tsa1, capable of suppressing genome instability in Saccharomyces cerevisiae
    Ismail Iraqui
    UMR2027 Centre National de la Recherche Scientifique, Institut Curie, Centre Universitaire, Orsay, France
    Cancer Res 68:1055-63. 2008
    ..The S. cerevisiae system described here could provide a sensitive tool to uncover the mechanisms that underlie the function of human Prxs...
  76. pmc Alpha-synuclein blocks ER-Golgi traffic and Rab1 rescues neuron loss in Parkinson's models
    Antony A Cooper
    School of Biological Sciences, University of Missouri Kansas City, Kansas City, MO 64110, USA
    Science 313:324-8. 2006
    ..Thus, synucleinopathies may result from disruptions in basic cellular functions that interface with the unique biology of particular neurons to make them especially vulnerable...
  77. ncbi request reprint Effect of 8-oxoguanine on transcription elongation by T7 RNA polymerase and mammalian RNA polymerase II
    Silvia Tornaletti
    Department of Biological Sciences, Stanford University, Stanford, CA 94305 5020, USA
    DNA Repair (Amst) 3:483-94. 2004
    ..These results are discussed in the context of possible models for TCR...

Research Grants25

  1. ENZYMOLOGY OF MISMATCH REPAIR IN YEAST
    Richard Kolodner; Fiscal Year: 2007
    ..cerevisiae. As a consequence, it is anticipated that these studies will provide genetic and biochemical insights that can be applied to the study of the genetics of human cancer susceptibility. ..
  2. ENZYMOLOGY OF MISMATCH REPAIR IN YEAST
    Richard D Kolodner; Fiscal Year: 2010
    ..cerevisiae. As a consequence, it is anticipated that these studies will provide genetic and biochemical insights that can be applied to the study of the genetics of human cancer susceptibility. ..
  3. ENZYMATIC MECHANISMS OF GENETIC RECOMBINATION
    Richard D Kolodner; Fiscal Year: 2010
    ....
  4. ENZYMATIC MECHANISMS OF GENETIC RECOMBINATION
    Richard Kolodner; Fiscal Year: 2007
    ..The ultimate goal of these studies will be to provide a comprehensive picture of the pathways and mechanisms that suppress genome instability. ..
  5. ENZYMATIC MECHANISMS OF GENETIC RECOMBINATION
    Richard Kolodner; Fiscal Year: 2009
    ..The ultimate goal of these studies will be to provide a comprehensive picture of the pathways and mechanisms that suppress genome instability. ..
  6. ENZYMOLOGY OF MISMATCH REPAIR IN YEAST
    Richard Kolodner; Fiscal Year: 2009
    ..cerevisiae. As a consequence, it is anticipated that these studies will provide genetic and biochemical insights that can be applied to the study of the genetics of human cancer susceptibility. ..
  7. ENZYMOLOGY OF MISMATCH REPAIR IN YEAST
    Richard Kolodner; Fiscal Year: 2006
    ..It is also anticipated that these studies will provide genetic and biochemical insights that can be applied to the study of the genetics of human cancer susceptibility. ..
  8. ENZYMATIC MECHANISMS OF GENETIC RECOMBINATION
    Richard Kolodner; Fiscal Year: 2005
    ..The ultimate goal of these studies will be to provide a comprehensive picture of the pathways and mechanisms that suppress genome instability. ..
  9. ENZYMOLOGY OF MISMATCH REPAIR IN YEAST
    Richard Kolodner; Fiscal Year: 1999
    ..It is also anticipated that these studies will provide tools for identifying additional MMR genes in higher eukaryotes for use in studying MMR and the genetics of human cancer susceptibility. ..
  10. ENZYMOLOGY OF MISMATCH REPAIR IN YEAST
    Richard Kolodner; Fiscal Year: 2002
    ..In addition, it is anticipated that these studies will provide tools for use in the analysis of mismatch repair in higher eukaryotes. ..
  11. ENZYMOLOGY OF MISMATCH REPAIR IN YEAST
    Richard Kolodner; Fiscal Year: 2003
    ..It is also anticipated that these studies will provide genetic and biochemical insights that can be applied to the study of the genetics of human cancer susceptibility. ..
  12. ENZYMOLOGY OF MISMATCH REPAIR IN YEAST
    Richard D Kolodner; Fiscal Year: 2011
    ..These insights will lead to new tools for cancer diagnostics as well as insights for use in improving the efficacy of known chemotherapeutic agents as well as for use in the development of new therapeutic approaches. ..