Research Topics
| Richard KolodnerSummaryAffiliation: University of California Country: USA Publications
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Publications
Analysis of gross-chromosomal rearrangements in Saccharomyces cerevisiaeKristina 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...- Recombination and the Tel1 and Mec1 checkpoints differentially effect genome rearrangements driven by telomere dysfunction in yeastVincent 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... 
An overview of Cdk1-controlled targets and processesJorrit 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...- Germ-line msh6 mutations in colorectal cancer familiesR 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... - Coupling distant sites in DNA during DNA mismatch repairRichard 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 - Maintenance of genome stability in Saccharomyces cerevisiaeRichard 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... - Analysis of the interaction between the Saccharomyces cerevisiae MSH2-MSH6 and MLH1-PMS1 complexes with DNA using a reversible DNA end-blocking systemMarc 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... - Saccharomyces cerevisiae as a model system to define the chromosomal instability phenotypeChristopher 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... - Post-replication repair suppresses duplication-mediated genome instabilityChristopher 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... - A biological network in Saccharomyces cerevisiae prevents the deleterious effects of endogenous oxidative DNA damageMeng 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... - The Saccharomyces cerevisiae Rad6 postreplication repair and Siz1/Srs2 homologous recombination-inhibiting pathways process DNA damage that arises in asf1 mutantsEllen 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... - Requirement of Rrm3 helicase for repair of spontaneous DNA lesions in cells lacking Srs2 or Sgs1 helicaseKristina 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... - Suppression of genome instability by redundant S-phase checkpoint pathways in Saccharomyces cerevisiaeKyungjae 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... - Specific pathways prevent duplication-mediated genome rearrangementsChristopher 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... - Comprehensive molecular analysis of mismatch repair gene defects in suspected Lynch syndrome (hereditary nonpolyposis colorectal cancer) casesJames 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.... - Suppression of spontaneous genome rearrangements in yeast DNA helicase mutantsKristina 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... - Inhibition of Msh6 ATPase activity by mispaired DNA induces a Msh2(ATP)-Msh6(ATP) state capable of hydrolysis-independent movement along DNADan 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... - Checkpoint functions are required for normal S-phase progression in Saccharomyces cerevisiae RCAF- and CAF-I-defective mutantsEllen 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... - Interaction of mismatch repair protein PMS2 and the p53-related transcription factor p73 in apoptosis response to cisplatinHideki 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... - Interaction between the Msh2 and Msh6 nucleotide-binding sites in the Saccharomyces cerevisiae Msh2-Msh6 complexVictoria 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.... - Rewiring of genetic networks in response to DNA damageSourav 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... - Isolation and characterization of new proliferating cell nuclear antigen (POL30) mutator mutants that are defective in DNA mismatch repairPatrick 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... - Apoptotic function of human PMS2 compromised by the nonsynonymous single-nucleotide polymorphic variant R20QIvana 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... - Saccharomyces cerevisiae Msh2-Msh3 acts in repair of base-base mispairsJill 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.... - Dominant Saccharomyces cerevisiae msh6 mutations cause increased mispair binding and decreased dissociation from mispairs by Msh2-Msh6 in the presence of ATPMartin 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... - Saccharomyces cerevisiae chromatin-assembly factors that act during DNA replication function in the maintenance of genome stabilityKyungjae 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... - Transfer of the MSH2.MSH6 complex from proliferating cell nuclear antigen to mispaired bases in DNAPatrick 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... - Chromosome healing by de novo telomere addition in Saccharomyces cerevisiaeVincent 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... - Recruiting research participants at community education sitesGeorgia 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... - Perspectives on the DNA damage and replication checkpoint responses in Saccharomyces cerevisiaeChristopher 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.... - Biochemical basis for dominant mutations in the Saccharomyces cerevisiae MSH6 geneMartin 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.... - 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 tumorIsabella 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... - Chimeric Saccharomyces cerevisiae Msh6 protein with an Msh3 mispair-binding domain combines properties of both proteinsScarlet 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.... - Functional studies and homology modeling of Msh2-Msh3 predict that mispair recognition involves DNA bending and strand separationJill 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... - The mismatch repair complex hMutS alpha recognizes 5-fluorouracil-modified DNA: implications for chemosensitivity and resistanceAkihiro Tajima
Department of Medicine, University of California, La Jolla, California, USA
Gastroenterology 127:1678-84. 2004.... - Functional analysis of human mismatch repair gene mutations identifies weak alleles and polymorphisms capable of polygenic interactionsSandra 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... - Determination of gross chromosomal rearrangement ratesChristopher 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... - Regulation of the human MSH6 gene by the Sp1 transcription factor and alteration of promoter activity and expression by polymorphismsIsabella 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... - The N terminus of Saccharomyces cerevisiae Msh6 is an unstructured tether to PCNAScarlet 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... - Saccharomyces cerevisiae Mer3 helicase stimulates 3'-5' heteroduplex extension by Rad51; implications for crossover control in meiotic recombinationOlga 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.... - Fine structure mapping of CIAS1: identification of an ancestral haplotype and a common FCAS mutation, L353PHal 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... - Identification of EpCAM as the gene for congenital tufting enteropathyMamata 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... - Saccharomyces cerevisiae RRM3, a 5' to 3' DNA helicase, physically interacts with proliferating cell nuclear antigenKristina 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... - Cdc28/Cdk1 positively and negatively affects genome stability in S. cerevisiaeJorrit 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... - An FHA domain-mediated protein interaction network of Rad53 reveals its role in polarized cell growthMarcus 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... - Probing DNA- and ATP-mediated conformational changes in the MutS family of mispair recognition proteins using deuterium exchange mass spectrometryMarc 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.... - The MER3 DNA helicase catalyzes the unwinding of holliday junctionsTakuro 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... - Saccharomyces cerevisiae Mer3 is a DNA helicase involved in meiotic crossing overTakuro 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... - Dynamic changes in protein-protein interaction and protein phosphorylation probed with amine-reactive isotope tagMarcus 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.... - Induction of genome instability by DNA damage in Saccharomyces cerevisiaeKyungjae 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... - Chromosome healing through terminal deletions generated by de novo telomere additions in Saccharomyces cerevisiaeChristopher 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.... - A genomewide screen in Saccharomyces cerevisiae for genes that suppress the accumulation of mutationsMeng-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... - Escherichia coli MutS tetramerization domain structure reveals that stable dimers but not tetramers are essential for DNA mismatch repair in vivoMarc 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... - Stabilization of dicentric translocations through secondary rearrangements mediated by multiple mechanisms in S. cerevisiaeVincent 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.. - Checkpoint proteins control morphogenetic events during DNA replication stress in Saccharomyces cerevisiaeJorrit 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... - A conserved MutS homolog connector domain interface interacts with MutL homologsMarc 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.... - Haploinsufficiency of Flap endonuclease (Fen1) leads to rapid tumor progressionMelanie 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... - Clinical presentation correlates with the type of mismatch repair gene involved in hereditary nonpolyposis colon cancerPrathap Bandipalliam
Gastroenterology 126:936-7. 2004 - Evaluation of microsatellite instability and immunohistochemistry for the prediction of germ-line MSH2 and MLH1 mutations in hereditary nonpolyposis colon cancer familiesSiobhan 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... - Approaching a complete repository of sequence-verified protein-encoding clones for Saccharomyces cerevisiaeYanhui 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... - Mutation in Rpa1 results in defective DNA double-strand break repair, chromosomal instability and cancer in miceYuxun 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... - Suppression of gross chromosomal rearrangements by the multiple functions of the Mre11-Rad50-Xrs2 complex in Saccharomyces cerevisiaeStephanie 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... - Dominant effects of an Msh6 missense mutation on DNA repair and cancer susceptibilityGuohze 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... - The recombination-deficient mutant RPA (rfa1-t11) is displaced slowly from single-stranded DNA by Rad51 proteinNoriko 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... - Inactivation of Exonuclease 1 in mice results in DNA mismatch repair defects, increased cancer susceptibility, and male and female sterilityKaichun 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... - Lynch syndrome (hereditary nonpolyposis colorectal cancer) diagnosticsKristina 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... - Mitotic checkpoint function in the formation of gross chromosomal rearrangements in Saccharomyces cerevisiaeKyungjae 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... - The clinical continuum of cryopyrinopathies: novel CIAS1 mutations in North American patients and a new cryopyrin modelIvona 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... - Functional analysis of human MLH1 variants using yeast and in vitro mismatch repair assaysMasanobu 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... - Oxygen metabolism and reactive oxygen species cause chromosomal rearrangements and cell deathSandrine 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... - Control of translocations between highly diverged genes by Sgs1, the Saccharomyces cerevisiae homolog of the Bloom's syndrome proteinKristina 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... - Hallmarks of homology recognition by RecA-like recombinases are exhibited by the unrelated Escherichia coli RecT proteinPhilippe 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... - EXO1 variants occur commonly in normal population: evidence against a role in hereditary nonpolyposis colorectal cancerShantie 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... - The C-terminal domain of yeast PCNA is required for physical and functional interactions with Cdc9 DNA ligaseSangeetha 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.... - Human peroxiredoxin PrxI is an orthologue of yeast Tsa1, capable of suppressing genome instability in Saccharomyces cerevisiaeIsmail 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... - Alpha-synuclein blocks ER-Golgi traffic and Rab1 rescues neuron loss in Parkinson's modelsAntony 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... - Effect of 8-oxoguanine on transcription elongation by T7 RNA polymerase and mammalian RNA polymerase IISilvia 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 Grants
- ENZYMOLOGY OF MISMATCH REPAIR IN YEASTRichard 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. ..
- ENZYMOLOGY OF MISMATCH REPAIR IN YEASTRichard 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. ..
- ENZYMATIC MECHANISMS OF GENETIC RECOMBINATIONRichard D Kolodner; Fiscal Year: 2010....
- ENZYMATIC MECHANISMS OF GENETIC RECOMBINATIONRichard 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. ..
- ENZYMATIC MECHANISMS OF GENETIC RECOMBINATIONRichard 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. ..
- ENZYMOLOGY OF MISMATCH REPAIR IN YEASTRichard 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. ..
- ENZYMOLOGY OF MISMATCH REPAIR IN YEASTRichard 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. ..
- ENZYMATIC MECHANISMS OF GENETIC RECOMBINATIONRichard 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. ..
- ENZYMOLOGY OF MISMATCH REPAIR IN YEASTRichard 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. ..
- ENZYMOLOGY OF MISMATCH REPAIR IN YEASTRichard 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. ..
- ENZYMOLOGY OF MISMATCH REPAIR IN YEASTRichard 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. ..
- ENZYMOLOGY OF MISMATCH REPAIR IN YEASTRichard 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. ..