Research Topics
Genomes and Genes
| W EdelmannSummaryAffiliation: Albert Einstein College of Medicine Country: USA Publications
Research Grants
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Detail Information
Publications
An Msh2 point mutation uncouples DNA mismatch repair and apoptosisDiana P Lin
Department of Cell Biology, Albert Einstein College of Medicine, Bronx, New York, USA
Cancer Res 64:517-22. 2004....- Mammalian MutS homologue 5 is required for chromosome pairing in meiosisW 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... 
MutS homolog 4 localization to meiotic chromosomes is required for chromosome pairing during meiosis in male and female miceB 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...- Tumorigenesis in Mlh1 and Mlh1/Apc1638N mutant miceW Edelmann
Department of Molecular Genetics, Albert Einstein College of Medicine, Bronx, New York 10461, USA
Cancer Res 59:1301-7. 1999.... - The DNA mismatch repair genes Msh3 and Msh6 cooperate in intestinal tumor suppressionW 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... - Mutation in the mismatch repair gene Msh6 causes cancer susceptibilityW Edelmann
Department of Cell Biology, Albert Einstein College of Medicine, Bronx, New York 10461, USA
Cell 91:467-77. 1997.... - Rescue of embryonic lethality in reduced folate carrier-deficient mice by maternal folic acid supplementation reveals early neonatal failure of hematopoietic organsR 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... - Short-chain fatty acid metabolism, apoptosis, and Apc-initiated tumorigenesis in the mouse gastrointestinal mucosaL H Augenlicht
Department of Oncology, Albert Einstein Cancer Center, Montefiore Hospital, Bronx, New York 10467, USA
Cancer Res 59:6005-9. 1999.... - Postgastrulation Smad2-deficient embryos show defects in embryo turning and anterior morphogenesisJ 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... - p21(WAF1/cip1) is an important determinant of intestinal cell response to sulindac in vitro and in vivoW 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/... - 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 mucosalW 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... - Caveolin-1 null mice are viable but show evidence of hyperproliferative and vascular abnormalitiesB 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.... - Meiotic pachytene arrest in MLH1-deficient miceW 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... - Experimental autoimmune encephalomyelitis in mice lacking glial fibrillary acidic protein is characterized by a more severe clinical course and an infiltrative central nervous system lesionW Liedtke
Department of Pathology, Albert Einstein College of Medicine, Bronx, New York, USA
Am J Pathol 152:251-9. 1998.... - Mouse keratin 4 is necessary for internal epithelial integrityS 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... - A new mouse model for evaluating the immunotherapy of human colorectal cancerH 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... - Cardiac defects and renal failure in mice with targeted mutations in Pkd2G 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... - Functional consequences of DNA mismatch repair missense mutations in murine models and their impact on cancer predispositionS 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... 
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 patternM 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...- GFAP is necessary for the integrity of CNS white matter architecture and long-term maintenance of myelinationW 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... - Caveolin-3 null mice show a loss of caveolae, changes in the microdomain distribution of the dystrophin-glycoprotein complex, and t-tubule abnormalitiesF 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... - Mouse models for colorectal cancerJ 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... - Somatic inactivation of Pkd2 results in polycystic kidney diseaseG 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... - Mouse models for human familial adenomatous polyposisR 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... - Neuronal abnormalities in microtubule-associated protein 1B mutant miceW 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... - The mismatch repair protein Msh6 influences the in vivo AID targeting to the Ig locusZiqiang 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... - Examination of Msh6- and Msh3-deficient mice in class switching reveals overlapping and distinct roles of MutS homologues in antibody diversificationZiqiang 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... - Growth and muscle defects in mice lacking adult myosin heavy chain genesL 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... - Localization of MMR proteins on meiotic chromosomes in mice indicates distinct functions during prophase INadine K Kolas
Department of Molecular Genetics, Albert Einstein College of Medicine, Bronx, NY 10461, USA
J Cell Biol 171:447-58. 2005.... - Normal development of mice lacking metablastin (P19), a phosphoprotein implicated in cell cycle regulationU 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... - The murine N-ras gene is not essential for growth and developmentH 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... - 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... - 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... - Altered somatic hypermutation and reduced class-switch recombination in exonuclease 1-mutant micePhilip 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... - PMS2 endonuclease activity has distinct biological functions and is essential for genome maintenanceJohanna 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... - Ubiquitylated PCNA plays a role in somatic hypermutation and class-switch recombination and is required for meiotic progressionSergio 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.... - Mouse models for human DNA mismatch-repair gene defectsKaichun 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... - Cutting edge: the G-U mismatch glycosylase methyl-CpG binding domain 4 is dispensable for somatic hypermutation and class switch recombinationPhilip 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... - Mice develop normally without the H1(0) linker histoneA 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... - Inactivation of Tbx1 in the pharyngeal endoderm results in 22q11DS malformationsJelena 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... - Mouse models of colon cancerMakoto 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... - Cis lethal genetic interactions attenuate and alter p53 tumorigenesisYuxun 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... - MSH2/MSH6 complex promotes error-free repair of AID-induced dU:G mispairs as well as error-prone hypermutation of A:T sitesSergio 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... - A panel of repeat markers for detection of microsatellite instability in murine tumorsOmar 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.... - 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... - Differing patterns of genetic instability in mice deficient in the mismatch repair genes Pms2, Mlh1, Msh2, Msh3 and Msh6Denise 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... - MUS81 generates a subset of MLH1-MLH3-independent crossovers in mammalian meiosisJ 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... - Elevated mutant frequencies and predominance of G:C to A:T transition mutations in Msh6(-/-) small intestinal epitheliumSean 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... - DNA mismatch repair deficiency accelerates endometrial tumorigenesis in Pten heterozygous miceHong Wang
Department of Pathology, Weill Medical Collegeof Cornell University, New York
Am J Pathol 160:1481-6. 2002.... - 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... - (CAG)(n)-hairpin DNA binds to Msh2-Msh3 and changes properties of mismatch recognitionBarbara 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... - Msh2 ATPase activity is essential for somatic hypermutation at a-T basepairs and for efficient class switch recombinationAlberto 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... - Mbd4 inactivation increases Cright-arrowT transition mutations and promotes gastrointestinal tumor formationEdmund 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... - DNA mismatch repair protein Msh6 is required for optimal levels of ultraviolet-B-induced apoptosis in primary mouse fibroblastsLeah 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... - Loss of DNA mismatch repair function and cancer predisposition in the mouse: animal models for human hereditary nonpolyposis colorectal cancerLisa Edelmann
Human Genetics, Mt. Sinai School of Medicine, New York, NY, USA
Am J Med Genet C Semin Med Genet 129:91-9. 2004.... - Distinct DNA-damage-dependent and -independent responses drive the loss of oocytes in recombination-defective mouse mutantsMonica 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... - Distinct effects of the recurrent Mlh1G67R mutation on MMR functions, cancer, and meiosisElena 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.... - 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... - DNA damage invokes mismatch repair-dependent cyclin D1 attenuation and retinoblastoma signaling pathways to inhibit CDK2Zhengdao 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... - Caveolin-2-deficient mice show evidence of severe pulmonary dysfunction without disruption of caveolaeBabak 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... - Novel roles for MLH3 deficiency and TLE6-like amplification in DNA mismatch repair-deficient gastrointestinal tumorigenesis and progressionPeng Chieh Chen
Department of Biological Chemistry, University of California Irvine, Irvine, California, USA
PLoS Genet 4:e1000092. 2008.... - Piroxicam increases colon tumorigenesis and promotes apoptosis in Mlh1 +/- /Apc1638(N/+) miceEmanuela 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... - Comparative analysis of meiotic progression in female mice bearing mutations in genes of the DNA mismatch repair pathwayRui Kan
Department of Biomedical Sciences, Cornell University College of Veterinary Medicine, Ithaca, NY 14850, USA
Biol Reprod 78:462-71. 2008.... - Exonuclease-1 deletion impairs DNA damage signaling and prolongs lifespan of telomere-dysfunctional miceSonja 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... - Mismatch repair proteins as sensors of alkylation DNA damageJean 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.... - Trans-heterozygous Pkd1 and Pkd2 mutations modify expression of polycystic kidney diseaseGuanqing 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... - APC-dependent suppression of colon carcinogenesis by PPARgammaGeoffrey 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... - Impaired hippocampal long-term potentiation in microtubule-associated protein 1B-deficient miceMark Zervas
Skirball Institute, New York University School of Medicine, New York, USA
J Neurosci Res 82:83-92. 2005.... - 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 miceKan 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... - Spontaneous aberrant crypt foci in Apc1638N mice with a mutant Apc alleleTheresa 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.... - Lack of MSH2 involvement differentiates V(D)J recombination from other non-homologous end joining eventsMani 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 Grants
- Exonuclease 1 in DNA Meiosis, Mismatch Repair and CancWinfried Edelmann; Fiscal Year: 2006..abstract_text> ..
- DNA MISMATCH REPAIR AND CANCER IN MURINE MODELSWinfried Edelmann; Fiscal Year: 2006..abstract_text> ..
- The Role of Late MMR Proteins in DNA Repair and CancerWinfried 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. ..
- DNA MISMATCH REPAIR AND CANCER IN MURINE MODELSWinfried Edelmann; Fiscal Year: 2007..abstract_text> ..
- DNA MISMATCH REPAIR AND CANCER IN MURINE MODELSWinfried Edelmann; Fiscal Year: 2002....
- DNA MISMATCH REPAIR AND CANCER IN MURINE MODELSWinfried Edelmann; Fiscal Year: 2003..abstract_text> ..