W Edelmann

Summary

Affiliation: Albert Einstein College of Medicine
Country: USA

Publications

  1. ncbi request reprint An Msh2 point mutation uncouples DNA mismatch repair and apoptosis
    Diana P Lin
    Department of Cell Biology, Albert Einstein College of Medicine, Bronx, New York, USA
    Cancer Res 64:517-22. 2004
  2. ncbi request reprint Mammalian MutS homologue 5 is required for chromosome pairing in meiosis
    W Edelmann
    Department of Cell Biology, Albert Einstein College of Medicine, Bronx, New York 10461, USA
    Nat Genet 21:123-7. 1999
  3. pmc MutS homolog 4 localization to meiotic chromosomes is required for chromosome pairing during meiosis in male and female mice
    B Kneitz
    Department of Cell Biology, Albert Einstein College of Medicine, The Bronx, New York 10461 USA
    Genes Dev 14:1085-97. 2000
  4. ncbi request reprint Tumorigenesis in Mlh1 and Mlh1/Apc1638N mutant mice
    W Edelmann
    Department of Molecular Genetics, Albert Einstein College of Medicine, Bronx, New York 10461, USA
    Cancer Res 59:1301-7. 1999
  5. ncbi request reprint The DNA mismatch repair genes Msh3 and Msh6 cooperate in intestinal tumor suppression
    W Edelmann
    Department of Cell Biology, Albert Einstein College of Medicine, Bronx, New York 10461, USA
    Cancer Res 60:803-7. 2000
  6. ncbi request reprint Mutation in the mismatch repair gene Msh6 causes cancer susceptibility
    W Edelmann
    Department of Cell Biology, Albert Einstein College of Medicine, Bronx, New York 10461, USA
    Cell 91:467-77. 1997
  7. ncbi request reprint Rescue of embryonic lethality in reduced folate carrier-deficient mice by maternal folic acid supplementation reveals early neonatal failure of hematopoietic organs
    R Zhao
    Departments of Medicine and Molecular Pharmacology, Albert Einstein College of Medicine, Bronx, New York 10461, USA
    J Biol Chem 276:10224-8. 2001
  8. ncbi request reprint Short-chain fatty acid metabolism, apoptosis, and Apc-initiated tumorigenesis in the mouse gastrointestinal mucosa
    L H Augenlicht
    Department of Oncology, Albert Einstein Cancer Center, Montefiore Hospital, Bronx, New York 10467, USA
    Cancer Res 59:6005-9. 1999
  9. pmc Postgastrulation Smad2-deficient embryos show defects in embryo turning and anterior morphogenesis
    J Heyer
    Departments of Molecular Genetics, Albert Einstein College of Medicine, Bronx, NY 10461, USA
    Proc Natl Acad Sci U S A 96:12595-600. 1999
  10. ncbi request reprint p21(WAF1/cip1) is an important determinant of intestinal cell response to sulindac in vitro and in vivo
    W Yang
    Department of Oncology, Albert Einstein Cancer Center, Bronx, New York 10467, USA
    Cancer Res 61:6297-302. 2001

Research Grants

  1. Exonuclease 1 in DNA Meiosis, Mismatch Repair and Canc
    Winfried Edelmann; Fiscal Year: 2006
  2. DNA MISMATCH REPAIR AND CANCER IN MURINE MODELS
    Winfried Edelmann; Fiscal Year: 2006
  3. The Role of Late MMR Proteins in DNA Repair and Cancer
    Winfried Edelmann; Fiscal Year: 2007
  4. DNA MISMATCH REPAIR AND CANCER IN MURINE MODELS
    Winfried Edelmann; Fiscal Year: 2007
  5. DNA MISMATCH REPAIR AND CANCER IN MURINE MODELS
    Winfried Edelmann; Fiscal Year: 2002
  6. DNA MISMATCH REPAIR AND CANCER IN MURINE MODELS
    Winfried Edelmann; Fiscal Year: 2003

Collaborators

Detail Information

Publications71

  1. ncbi request reprint An Msh2 point mutation uncouples DNA mismatch repair and apoptosis
    Diana P Lin
    Department of Cell Biology, Albert Einstein College of Medicine, Bronx, New York, USA
    Cancer Res 64:517-22. 2004
    ....
  2. ncbi request reprint Mammalian MutS homologue 5 is required for chromosome pairing in meiosis
    W Edelmann
    Department of Cell Biology, Albert Einstein College of Medicine, Bronx, New York 10461, USA
    Nat Genet 21:123-7. 1999
    ..We found that this meiotic failure leads to a diminution in testicular size and a complete loss of ovarian structures. Our results show that normal Msh5 function is essential for meiotic progression and, in females, gonadal maintenance...
  3. pmc MutS homolog 4 localization to meiotic chromosomes is required for chromosome pairing during meiosis in male and female mice
    B Kneitz
    Department of Cell Biology, Albert Einstein College of Medicine, The Bronx, New York 10461 USA
    Genes Dev 14:1085-97. 2000
    ..Our results show that MSH4 localization on chromosomes during the early stages of meiosis is essential for normal chromosome synapsis in prophase I and that it acts in the same pathway as MSH5...
  4. ncbi request reprint Tumorigenesis in Mlh1 and Mlh1/Apc1638N mutant mice
    W Edelmann
    Department of Molecular Genetics, Albert Einstein College of Medicine, Bronx, New York 10461, USA
    Cancer Res 59:1301-7. 1999
    ....
  5. ncbi request reprint The DNA mismatch repair genes Msh3 and Msh6 cooperate in intestinal tumor suppression
    W Edelmann
    Department of Cell Biology, Albert Einstein College of Medicine, Bronx, New York 10461, USA
    Cancer Res 60:803-7. 2000
    ..When the Msh3-/- and Msh6-/- mutations are combined, the tumor predisposition phenotype is indistinguishable from Msh2-/- or Mlh1-/- mice. These results suggest that MSH3 cooperates with MSH6 in tumor suppression...
  6. ncbi request reprint Mutation in the mismatch repair gene Msh6 causes cancer susceptibility
    W Edelmann
    Department of Cell Biology, Albert Einstein College of Medicine, Bronx, New York 10461, USA
    Cell 91:467-77. 1997
    ....
  7. ncbi request reprint Rescue of embryonic lethality in reduced folate carrier-deficient mice by maternal folic acid supplementation reveals early neonatal failure of hematopoietic organs
    R Zhao
    Departments of Medicine and Molecular Pharmacology, Albert Einstein College of Medicine, Bronx, New York 10461, USA
    J Biol Chem 276:10224-8. 2001
    ..In addition, there was some impairment of renal and seminiferous tubule development. These data indicate that in the absence of RFC1 function, neonatal animals die due to failure of hematopoietic organs...
  8. ncbi request reprint Short-chain fatty acid metabolism, apoptosis, and Apc-initiated tumorigenesis in the mouse gastrointestinal mucosa
    L H Augenlicht
    Department of Oncology, Albert Einstein Cancer Center, Montefiore Hospital, Bronx, New York 10467, USA
    Cancer Res 59:6005-9. 1999
    ....
  9. pmc Postgastrulation Smad2-deficient embryos show defects in embryo turning and anterior morphogenesis
    J Heyer
    Departments of Molecular Genetics, Albert Einstein College of Medicine, Bronx, NY 10461, USA
    Proc Natl Acad Sci U S A 96:12595-600. 1999
    ..The rescued postgastrulation embryos showed malformation of head structures, abnormal embryo turning, and cyclopia. Our results show that Smad2 expression is required at several stages during embryogenesis...
  10. ncbi request reprint p21(WAF1/cip1) is an important determinant of intestinal cell response to sulindac in vitro and in vivo
    W Yang
    Department of Oncology, Albert Einstein Cancer Center, Bronx, New York 10467, USA
    Cancer Res 61:6297-302. 2001
    ..Thus, p21 is essential for tumor inhibition by this drug. The array data can be accessed on the Internet at http://sequence.aecom.yu.edu/genome/...
  11. ncbi request reprint Targeted inactivation of the p21(WAF1/cip1) gene enhances Apc-initiated tumor formation and the tumor-promoting activity of a Western-style high-risk diet by altering cell maturation in the intestinal mucosal
    W C Yang
    Albert Einstein Cancer Center, Bronx, New York 10467, USA
    Cancer Res 61:565-9. 2001
    ..Decreased expression of p21 is also a marker of poor prognosis in patients, and the data presented suggest that dietary alterations in patients undergoing treatment for colon cancer might be highly effective in improving outcome...
  12. ncbi request reprint Caveolin-1 null mice are viable but show evidence of hyperproliferative and vascular abnormalities
    B Razani
    Department of Molecular Pharmacology and The Albert Einstein Cancer Center, The Albert Einstein College of Medicine, Bronx, New York 10461, USA
    J Biol Chem 276:38121-38. 2001
    ....
  13. ncbi request reprint Meiotic pachytene arrest in MLH1-deficient mice
    W Edelmann
    Department of Molecular Genetics, Albert Einstein College of Medicine, Bronx, New York, USA
    Cell 85:1125-34. 1996
    ..The phenotypes of the mlh1 mutant mice are distinct from those deficient in msh2 and pms2. The different phenotypes of the three types of mutant mice suggest that these three genes may have independent functions in mammalian meiosis...
  14. pmc Experimental autoimmune encephalomyelitis in mice lacking glial fibrillary acidic protein is characterized by a more severe clinical course and an infiltrative central nervous system lesion
    W Liedtke
    Department of Pathology, Albert Einstein College of Medicine, Bronx, New York, USA
    Am J Pathol 152:251-9. 1998
    ....
  15. ncbi request reprint Mouse keratin 4 is necessary for internal epithelial integrity
    S L Ness
    Department of Molecular Genetics, Albert Einstein College of Medicine, Bronx, New York 10461, USA
    J Biol Chem 273:23904-11. 1998
    ..As mutations in K4 in humans lead to a disorder called white sponge nevus, the K4-deficient mice may serve as models for white sponge nevus and for understanding the role of K4 in cellular proliferation and differentiation...
  16. ncbi request reprint A new mouse model for evaluating the immunotherapy of human colorectal cancer
    H Horig
    Department of Surgery, Albert Einstein College of Medicine, Bronx, New York 10461, USA
    Cancer Res 61:8520-6. 2001
    ..This model provides a powerful system for evaluating antigen-specific tumor immunity against spontaneous tumors arising in an orthotopic location and permits evaluation of therapeutic vaccine strategies for human colorectal cancer...
  17. ncbi request reprint Cardiac defects and renal failure in mice with targeted mutations in Pkd2
    G Wu
    Department of Medicine, Albert Einstein College of Medicine, Bronx, New York, USA
    Nat Genet 24:75-8. 2000
    ..Our studies advance our understanding of the function of polycystin-2 in development and our mouse models recapitulate the complex human ADPKD phenotype...
  18. ncbi request reprint Functional consequences of DNA mismatch repair missense mutations in murine models and their impact on cancer predisposition
    S J Scherer
    Department of Cell Biology, Albert Einstein College of Medicine, 1300 Morris Park Avenue, Bronx, NY 10461, USA
    Biochem Soc Trans 33:689-93. 2005
    ..These studies in mice indicate that, although the increased mutation rates caused by MMR defects are sufficient to drive tumorigenesis, both functions co-operate in tumour suppression...
  19. pmc Somatic hypermutation in MutS homologue (MSH)3-, MSH6-, and MSH3/MSH6-deficient mice reveals a role for the MSH2-MSH6 heterodimer in modulating the base substitution pattern
    M Wiesendanger
    Department of Cell Biology, Albert Einstein College of Medicine, Bronx, New York 10461, USA
    J Exp Med 191:579-84. 2000
    ..In contrast, Msh3(-)/- mice show no differences from their littermate controls. These findings indicate that the MSH2-MSH6 heterodimer, but not the MSH2-MSH3 complex, is responsible for modulating Ig hypermutation...
  20. ncbi request reprint GFAP is necessary for the integrity of CNS white matter architecture and long-term maintenance of myelination
    W Liedtke
    Department of Pathology Division of Neuropathology, Albert Einstein College of Medicine, Bronx, New York 10016, USA
    Neuron 17:607-15. 1996
    ..Thus, GFAP expression is essential for normal white matter architecture and blood-brain barrier integrity, and its absence leads to late-onset CNS dysmyelination...
  21. ncbi request reprint Caveolin-3 null mice show a loss of caveolae, changes in the microdomain distribution of the dystrophin-glycoprotein complex, and t-tubule abnormalities
    F Galbiati
    Department of Molecular Pharmacology, Albert Einstein Comprehensive Cancer Center, Albert Einstein College of Medicine, Bronx, New York 10461, USA
    J Biol Chem 276:21425-33. 2001
    ..These results have clear mechanistic implications for understanding the pathogenesis of LGMD-1C at a molecular level...
  22. ncbi request reprint Mouse models for colorectal cancer
    J Heyer
    Department of Molecular Genetics, Albert Einstein College of Medicine, 1300 Morris Park Avenue, Bronx, NY 10461, USA
    Oncogene 18:5325-33. 1999
    ..Mice with mutations in Mlh1, Pms2 and Msh5 have defects in meiosis suggesting unique roles for these genes in gametogenesis...
  23. ncbi request reprint Somatic inactivation of Pkd2 results in polycystic kidney disease
    G Wu
    Department of Medicine, Albert Einstein College of Medicine, Bronx, New York 10461, USA
    Cell 93:177-88. 1998
    ..Somatic loss of Pkd2 expression is both necessary and sufficient for renal cyst formation in ADPKD, suggesting that PKD2 occurs by a cellular recessive mechanism...
  24. ncbi request reprint Mouse models for human familial adenomatous polyposis
    R Kucherlapati
    Department of Molecular Genetics, Albert Einstein College of Medicine, 1300 Morris Park Avenue, Bronx, NY 10461, USA
    Semin Cancer Biol 11:219-25. 2001
    ..We will provide a brief overview of these mouse models for CRC and what they have contributed to our understanding of the events involved in the initiation and progression of this cancer...
  25. pmc Neuronal abnormalities in microtubule-associated protein 1B mutant mice
    W Edelmann
    Department of Molecular Genetics, Albert Einstein College of Medicine, Bronx, NY 10461, USA
    Proc Natl Acad Sci U S A 93:1270-5. 1996
    ..Similar histological and immunochemical changes were observed in the olfactory bulb, hippocampus, and retina, providing a basis for the observed phenotypes...
  26. ncbi request reprint The mismatch repair protein Msh6 influences the in vivo AID targeting to the Ig locus
    Ziqiang Li
    Department of Cell Biology, Albert Einstein College of Medicine, 1300 Morris Park Avenue, Bronx, New York 10461, USA
    Immunity 24:393-403. 2006
    ..Our data suggest that Msh6 plays a scaffolding role in the first phase of SHM, in addition to its enzymatic role in the second phase of SHM...
  27. pmc Examination of Msh6- and Msh3-deficient mice in class switching reveals overlapping and distinct roles of MutS homologues in antibody diversification
    Ziqiang Li
    Department of Cell Biology, Albert Einstein College of Medicine, 1300 Morris Park Ave, Chanin 403, Bronx, NY 10461, USA
    J Exp Med 200:47-59. 2004
    ..Together, our data suggest that MutS homologues Msh2, Msh3, and Msh6 play overlapping and distinct roles during antibody diversification processes...
  28. pmc Growth and muscle defects in mice lacking adult myosin heavy chain genes
    L J Acakpo-Satchivi
    Department of Molecular Genetics, Albert Einstein College of Medicine, New York 10461, USA
    J Cell Biol 139:1219-29. 1997
    ..Many of the phenotypes demonstrated by these mice are typical in human muscle disease and should provide insight into their etiology...
  29. pmc Localization of MMR proteins on meiotic chromosomes in mice indicates distinct functions during prophase I
    Nadine K Kolas
    Department of Molecular Genetics, Albert Einstein College of Medicine, Bronx, NY 10461, USA
    J Cell Biol 171:447-58. 2005
    ....
  30. ncbi request reprint Normal development of mice lacking metablastin (P19), a phosphoprotein implicated in cell cycle regulation
    U K Schubart
    Department of Medicine, Albert Einstein College of Medicine, Bronx, New York 10461, USA
    J Biol Chem 271:14062-6. 1996
    ..Although the data suggest that metablastin is not essential for mammalian development, the knockout mice should prove valuable in exploring the role of this protein in cell cycle regulation...
  31. pmc The murine N-ras gene is not essential for growth and development
    H Umanoff
    Department of Molecular Genetics, Albert Einstein College of Medicine, Bronx, NY 10461
    Proc Natl Acad Sci U S A 92:1709-13. 1995
    ..Our results show that N-ras gene function is dispensable for normal mouse development, growth, and fertility...
  32. 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...
  33. 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...
  34. ncbi request reprint Altered somatic hypermutation and reduced class-switch recombination in exonuclease 1-mutant mice
    Philip D Bardwell
    Department of Cell Biology, Albert Einstein College of Medicine, 1300 Morris Park Avenue, Bronx, NY 10461, USA
    Nat Immunol 5:224-9. 2004
    ..The phenotype of Exo1(-/-) mice and the finding that Exo1 and Mlh1 are physically associated with mutating variable regions support the idea that Exo1 and MMR participate directly in SHM and CSR...
  35. pmc PMS2 endonuclease activity has distinct biological functions and is essential for genome maintenance
    Johanna M M van Oers
    Department of Cell Biology, and Cancer Center, Albert Einstein College of Medicine, Bronx, NY 10461, USA
    Proc Natl Acad Sci U S A 107:13384-9. 2010
    ..Therefore, the PMS2 endonuclease activity has distinct biological functions and is essential for genome maintenance and tumor suppression...
  36. pmc Ubiquitylated PCNA plays a role in somatic hypermutation and class-switch recombination and is required for meiotic progression
    Sergio Roa
    Departments of Cell Biology and Systems and Computational Biology, Albert Einstein College of Medicine, Bronx, NY 10461, USA
    Proc Natl Acad Sci U S A 105:16248-53. 2008
    ....
  37. ncbi request reprint Mouse models for human DNA mismatch-repair gene defects
    Kaichun Wei
    Dept of Cell Biology, Albert Einstein College of Medicine, 1300 Morris Park Avenue, Bronx, NY 10461, USA
    Trends Mol Med 8:346-53. 2002
    ..These analyses were critical for our understanding of the function of these genes at the organismal level and also revealed an essential role for some of the DNA mismatch-repair genes in mammalian meiosis...
  38. ncbi request reprint Cutting edge: the G-U mismatch glycosylase methyl-CpG binding domain 4 is dispensable for somatic hypermutation and class switch recombination
    Philip D Bardwell
    Department of Cell Biology, Albert Einstein College of Medicine, 1300 Morris Park Avenue, Chanin 403, Bronx, NY 10461, USA
    J Immunol 170:1620-4. 2003
    ..These data indicate that the Mbd4 glycosylase does not significantly contribute to mechanisms of Ab diversification...
  39. pmc Mice develop normally without the H1(0) linker histone
    A M Sirotkin
    Department of Cell Biology, Albert Einstein College of Medicine, Bronx, NY 10461, USA
    Proc Natl Acad Sci U S A 92:6434-8. 1995
    ..Our results indicate that despite the unique properties and expression pattern of H1(0), its function is dispensable for normal mouse development...
  40. ncbi request reprint Inactivation of Tbx1 in the pharyngeal endoderm results in 22q11DS malformations
    Jelena S Arnold
    Department of Molecular Genetics, Albert Einstein College of Medicine, 1300 Morris Park Avenue, Bronx, NY 10461, USA
    Development 133:977-87. 2006
    ..These results show that Tbx1 in the PE is required for the patterning and development of the pharyngeal apparatus, thereby disrupting the formation of its derivative structures...
  41. ncbi request reprint Mouse models of colon cancer
    Makoto Mark Taketo
    Department of Cell Biology, Albert Einstein College of Medicine, Bronx, New York, USA
    Gastroenterology 136:780-98. 2009
    ..This review discusses what models have been developed most recently and what they have taught us about colon cancer formation, progression, and possible treatment strategies...
  42. pmc Cis lethal genetic interactions attenuate and alter p53 tumorigenesis
    Yuxun Wang
    Department of Cell Biology, Albert Einstein College of Medicine, Bronx, NY 10461, USA
    Proc Natl Acad Sci U S A 107:5511-5. 2010
    ..These studies indicate that polymorphic genetic variants in cell essential genes can genetically affect closely linked tumor suppressor loci via allelic phasing, which can result in profound phenotypic variations in tumorigenesis...
  43. pmc MSH2/MSH6 complex promotes error-free repair of AID-induced dU:G mispairs as well as error-prone hypermutation of A:T sites
    Sergio Roa
    Department of Cell Biology, Albert Einstein College of Medicine, New York, New York, USA
    PLoS ONE 5:e11182. 2010
    ..We propose a model for the role of MutSalpha at the immunoglobulin locus where the local balance of error-free and error-prone repair has an impact in the spectrum of mutations introduced during Phase 2 of SHM...
  44. ncbi request reprint A panel of repeat markers for detection of microsatellite instability in murine tumors
    Omar Kabbarah
    Division of Biology and Biomedical Sciences and Department of Surgery, Washington University in St Louis, St Louis, Missouri 63110, USA
    Mol Carcinog 38:155-9. 2003
    ....
  45. 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...
  46. pmc Differing patterns of genetic instability in mice deficient in the mismatch repair genes Pms2, Mlh1, Msh2, Msh3 and Msh6
    Denise Campisi Hegan
    Department of Therapeutic Radiology, Yale University School of Medicine, PO Box 208040, New Haven, CT 06520 8040, USA
    Carcinogenesis 27:2402-8. 2006
    ..Taken together, our results further characterize the functions of the MMR factors in mutation avoidance and provide in vivo correlation to biochemical models of the MMR pathway...
  47. pmc MUS81 generates a subset of MLH1-MLH3-independent crossovers in mammalian meiosis
    J Kim Holloway
    Department of Biomedical Sciences, Cornell University, Ithaca, New York, United States of America
    PLoS Genet 4:e1000186. 2008
    ..This study is the first in-depth analysis of meiotic progression in Mus81-nullizygous mice, and our results implicate the MUS81 pathway as a regulator of crossover frequency and placement in mammals...
  48. ncbi request reprint Elevated mutant frequencies and predominance of G:C to A:T transition mutations in Msh6(-/-) small intestinal epithelium
    Sean C Mark
    Department of Biochemistry and Molecular Biology, University of Calgary, Calgary, Alberta, Canada T2N 4N1
    Oncogene 21:7126-30. 2002
    ..Furthermore, the lacI gene mutation spectrum was dominated by G:C to A:T transitions, highlighting the critical importance of the MutS(alpha) complex in suppressing this frequently observed type of spontaneous mutation...
  49. pmc DNA mismatch repair deficiency accelerates endometrial tumorigenesis in Pten heterozygous mice
    Hong Wang
    Department of Pathology, Weill Medical Collegeof Cornell University, New York
    Am J Pathol 160:1481-6. 2002
    ....
  50. 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...
  51. ncbi request reprint (CAG)(n)-hairpin DNA binds to Msh2-Msh3 and changes properties of mismatch recognition
    Barbara A L Owen
    Department of Molecular Pharmacology and Experimental Therapeutics, Mayo Clinic Rochester, Rochester, Minnesota 55905, USA
    Nat Struct Mol Biol 12:663-70. 2005
    ..A mispaired bases in the stem of the hairpin and on the hairpin DNA structure per se. These studies identify critical functional defects in the Msh2-Msh3-CAG hairpin complex that could misdirect the DNA repair process...
  52. pmc Msh2 ATPase activity is essential for somatic hypermutation at a-T basepairs and for efficient class switch recombination
    Alberto Martin
    Department of Immunology, University of Toronto, Medical Sciences Bldg, Toronto, Canada, M5S 1A8
    J Exp Med 198:1171-8. 2003
    ..These results indicate that Msh2 adenosine triphosphatase activity is required for A-T mutations, and suggest that Msh2 has more than one role in CSR...
  53. pmc Mbd4 inactivation increases Cright-arrowT transition mutations and promotes gastrointestinal tumor formation
    Edmund Wong
    Department of Cell Biology, Biostatistics Core, Albert Einstein Cancer Center, Albert Einstein College of Medicine, 1300 Morris Park Avenue, Bronx, NY 10461, USA
    Proc Natl Acad Sci U S A 99:14937-42. 2002
    ..These studies indicate that, although inactivation of Mbd4 does not by itself cause cancer predisposition in mice, it can alter the mutation spectrum in cancer cells and modify the cancer predisposition phenotype...
  54. ncbi request reprint DNA mismatch repair protein Msh6 is required for optimal levels of ultraviolet-B-induced apoptosis in primary mouse fibroblasts
    Leah C Young
    Department of Medical Genetics, University of Alberta, Edmonton, Alberta, Canada
    J Invest Dermatol 121:876-80. 2003
    ..These data support a role for Msh6 in protective cellular responses of primary cells to ultraviolet-B-induced mutagenesis and, hence, the prevention of skin cancer...
  55. ncbi request reprint Loss of DNA mismatch repair function and cancer predisposition in the mouse: animal models for human hereditary nonpolyposis colorectal cancer
    Lisa Edelmann
    Human Genetics, Mt Sinai School of Medicine, New York, NY, USA
    Am J Med Genet C Semin Med Genet 129:91-9. 2004
    ....
  56. pmc Distinct DNA-damage-dependent and -independent responses drive the loss of oocytes in recombination-defective mouse mutants
    Monica Di Giacomo
    Molecular Biology Program, Memorial Sloan Kettering Cancer Center and Weill Graduate School of Medical Sciences of Cornell University, 1275 York Avenue, New York, NY 10021, USA
    Proc Natl Acad Sci U S A 102:737-42. 2005
    ..The absence of ATM caused defects in folliculogenesis that were similar to those in Dmc1 mutants and that could be suppressed by Spo11 mutation, implying that oocyte death in Atm-deficient animals is a response to defective DSB repair...
  57. pmc Distinct effects of the recurrent Mlh1G67R mutation on MMR functions, cancer, and meiosis
    Elena Avdievich
    Department of Cell Biology and Cancer Center, Albert Einstein College of Medicine, Bronx, NY 10461, USA
    Proc Natl Acad Sci U S A 105:4247-52. 2008
    ....
  58. 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...
  59. ncbi request reprint DNA damage invokes mismatch repair-dependent cyclin D1 attenuation and retinoblastoma signaling pathways to inhibit CDK2
    Zhengdao Lan
    Department of Cell Biology, University of Cincinnati, Cincinnati, Ohio 45267, USA
    J Biol Chem 277:8372-81. 2002
    ..Together, these studies couple the activity of the retinoblastoma and mismatch repair tumor suppressor pathways through the degradation of cyclin D1 and dual attenuation of CDK2 activity...
  60. pmc Caveolin-2-deficient mice show evidence of severe pulmonary dysfunction without disruption of caveolae
    Babak Razani
    Department of Molecular Pharmacology, Institute for Smooth Muscle Biology, The Albert Einstein Cancer Center, Albert Einstein College of Medicine, Bronx, New York 10461, USA
    Mol Cell Biol 22:2329-44. 2002
    ..Taken together, our data show for the first time a specific role for caveolin-2 in mammalian physiology independent of caveolin-1...
  61. pmc Novel roles for MLH3 deficiency and TLE6-like amplification in DNA mismatch repair-deficient gastrointestinal tumorigenesis and progression
    Peng Chieh Chen
    Department of Biological Chemistry, University of California Irvine, Irvine, California, USA
    PLoS Genet 4:e1000092. 2008
    ....
  62. ncbi request reprint Piroxicam increases colon tumorigenesis and promotes apoptosis in Mlh1 +/- /Apc1638(N/+) mice
    Emanuela Palmerini
    Department of Musculoskeletal Oncology, Istituti Ortopedici Rizzoli, Bologna, Italy
    Anticancer Res 27:3807-12. 2007
    ..The present study examines the effect of piroxicam, a non-steroidal anti-inflammatory drug, on tumor development in Mlh1+/- /Apc1638(N/+) mice, in a preclinical model of human colon cancer...
  63. ncbi request reprint Comparative analysis of meiotic progression in female mice bearing mutations in genes of the DNA mismatch repair pathway
    Rui Kan
    Department of Biomedical Sciences, Cornell University College of Veterinary Medicine, Ithaca, NY 14850, USA
    Biol Reprod 78:462-71. 2008
    ....
  64. pmc Exonuclease-1 deletion impairs DNA damage signaling and prolongs lifespan of telomere-dysfunctional mice
    Sonja Schaetzlein
    Department of Gastroenterology, Hepatology and Endocrinology, Medical School Hannover, 30625 Hanover, Germany
    Cell 130:863-77. 2007
    ..Together, these studies provide evidence that EXO1 contributes to DNA damage signal induction in mammalian cells, and deletion of Exo1 can prolong survival in the context of telomere dysfunction...
  65. ncbi request reprint Mismatch repair proteins as sensors of alkylation DNA damage
    Jean Y J Wang
    Division of Hematology Oncology, Department of Medicine and Moores Cancer Center, University of California, San Diego, School of Medicine, 3855 Health Sciences Drive, La Jolla, California 92093, USA
    Cancer Cell 9:417-8. 2006
    ....
  66. ncbi request reprint Trans-heterozygous Pkd1 and Pkd2 mutations modify expression of polycystic kidney disease
    Guanqing Wu
    Department of Internal Medicine, Yale University School of Medicine, New Haven, CT, USA
    Hum Mol Genet 11:1845-54. 2002
    ..The data suggest a modifier role for the 'trans' polycystin gene in cystic kidney disease, and support a contribution from threshold effects to cyst formation and growth...
  67. pmc APC-dependent suppression of colon carcinogenesis by PPARgamma
    Geoffrey D Girnun
    Dana Farber Cancer Institute and Department of Cell Biology, Harvard Medical School, One Jimmy Fund Way, Boston, MA 02115, USA
    Proc Natl Acad Sci U S A 99:13771-6. 2002
    ..This finding suggests a potentially important use for PPARgamma ligands as chemopreventative agents in colon cancer...
  68. ncbi request reprint Impaired hippocampal long-term potentiation in microtubule-associated protein 1B-deficient mice
    Mark Zervas
    Skirball Institute, New York University School of Medicine, New York, USA
    J Neurosci Res 82:83-92. 2005
    ....
  69. ncbi request reprint Peroxisome proliferator-activated receptor gamma agonist troglitazone induces colon tumors in normal C57BL/6J mice and enhances colonic carcinogenesis in Apc1638 N/+ Mlh1+/- double mutant mice
    Kan Yang
    Strang Cancer Research Laboratory at The Rockefeller University, New York, NY, USA
    Int J Cancer 116:495-9. 2005
    ..This observation indicates that preexisting mutational events are not necessary for induction of colonic tumors by activated PPAR-gamma in vivo...
  70. pmc Spontaneous aberrant crypt foci in Apc1638N mice with a mutant Apc allele
    Theresa P Pretlow
    Institute of Pathology, Case Western Reserve University Medical Center, 2085 Adelbert Road, Cleveland, OH 44106, USA
    Am J Pathol 163:1757-63. 2003
    ....
  71. pmc Lack of MSH2 involvement differentiates V(D)J recombination from other non-homologous end joining events
    Mani Larijani
    Department of Immunology, University of Toronto, Medical Sciences Building 5265, Toronto, Canada, M5S 1A8
    Nucleic Acids Res 33:6733-42. 2005
    ..This highlights a distinction between the repair of V(D)J recombination and other NHEJ reactions...

Research Grants23

  1. Exonuclease 1 in DNA Meiosis, Mismatch Repair and Canc
    Winfried Edelmann; Fiscal Year: 2006
    ..abstract_text> ..
  2. DNA MISMATCH REPAIR AND CANCER IN MURINE MODELS
    Winfried Edelmann; Fiscal Year: 2006
    ..abstract_text> ..
  3. The Role of Late MMR Proteins in DNA Repair and Cancer
    Winfried Edelmann; Fiscal Year: 2007
    ..We also propose to establish an in vivo system for the analysis of MMR complex formation and the identification of novel MMR associated proteins in mouse tissue. ..
  4. DNA MISMATCH REPAIR AND CANCER IN MURINE MODELS
    Winfried Edelmann; Fiscal Year: 2007
    ..abstract_text> ..
  5. DNA MISMATCH REPAIR AND CANCER IN MURINE MODELS
    Winfried Edelmann; Fiscal Year: 2002
    ....
  6. DNA MISMATCH REPAIR AND CANCER IN MURINE MODELS
    Winfried Edelmann; Fiscal Year: 2003
    ..abstract_text> ..