archive-org.com » ORG » I » IMGS.ORG

Total: 854

Choose link from "Titles, links and description words view":

Or switch to "Titles and links view".
  • 17th International Mouse Genome Conference (2003)
    Flaswinkel H Institute of Molecular Animal Breeding Gene Center Feodor Lynen Str 25 82377 München Germany Co Authors 1 Rathkolb B 2 Reindl W 1 Howaldt M 3 Jakob T 3 Köllisch G 1 Sandholzer N 4 Soewarto D 1 Krebs O 5 Kremmer E 4 Hrabe de Angelis M 6 Balling R 7 Pfeffer K 1 Wolf E Institutions 1 Institute of Molecular Animal Breeding Gene Center Feodor Lynen Str 25 82377 München Germany 2 Institute for Medical Microbiology Technische Universität München Troger Str 4a 81675 München Germany 3 Division Environmental Dermatology and Allergology GSF TUM Ingolstädter Landstr 1 85764 Neuherberg Germany 4 Institute of Experimental Genetics GSF Research Center for Environment and Health Neuherberg Germany 5 Institute of Molecular Immunology GSF Research Center for Environment and Health Marchionistr 25 81377 München Germany 6 Gesellschaft für Biotechnologische Forschung mbH Mascheroder Weg 1 38124 Braunschweig Germany 7 Institute for Med Microbiology Heinrich Heine Universität Düsseldorf Universitätsstr 1 40225 Düsseldorf Analysis of gene function in vivo is mostly performed by transgenic insertion gene inactivation by homologous recombination in embryonic stem cells and gene trapping We have complemented this approach by a genome wide chemical mutagenesis in mice using ethyl nitrosourea ENU followed by subsequent phenotype specific screening We used ELISA to identify mutants with elevated levels of rheumatoid factor and anti DNA antibodies ELISA was also used to identify deviations in the basal level of single or multiple immunoglobulin isotypes Employing flow cytometry we screened for mouse mutants in which the percentage of defined cell types or the expression level of relevant cell surface proteins is altered Until to date we have recovered and genetically confirmed more than 70 mutant mouse lines with phenotypes ranging from modest increase of single immunoglobulin isotypes to the complete loss of B and T cells

    Original URL path: http://www.imgs.org/Archive/abstracts/2003abstracts/file28.shtml (2016-02-17)
    Open archived version from archive

  • 17th International Mouse Genome Conference (2003)
    Research Center for Biotechnology Department of Experimental Dermatology Co Authors 1 Roers A 1 Siewe L 1 Strittmatter E 2 Deckert M 3 Schlüter D 2 Stenzel W 4 Gruber AD 1 Krieg T 5 Rajewsky K Institutions 1 University of Cologne Department of Dermatology 2 University of Cologne Department of Neuropathology 3 University of Heidelberg University Hospital Mannheim 4 University of Hannover School of Veterinary Medicine Department of Pathology 5 Harvard Medical School Center for Blood Research Interleukin 10 IL 10 is a regulator of inflammatory responses and is secreted by a variety of different cell types including T cells T regulatory cells have been shown to suppress immune responses by IL 10 dependent but also IL 10 independent mechanisms Herein we address the role of T cell derived IL 10 using T cell specific Cre loxP mediated targeting of the IL 10 gene Splenocytes from mice with an inactivation of the IL 10 gene restricted to T cells secrete increased amounts of proinflammatory cytokines after activation in vitro compared to cells from control animals The T cell specific IL 10 mutants spontaneously develop chronic intestinal inflammation show enhanced contact hypersensitivity reactions and succumb to severe immunopathology upon infection

    Original URL path: http://www.imgs.org/Archive/abstracts/2003abstracts/file29.shtml (2016-02-17)
    Open archived version from archive

  • 17th International Mouse Genome Conference (2003)
    45 HRS FROM THE MIN MOUSE MODEL TO STUDIES OF THE INTESTINAL EPITHELIUM AND ITS NEOPLASMS IN THE MOUSE AND THE HUMAN Dove W F University of Wisconsin Madison Co Authors Chen X Clipson L Ehrhardt W Haigis K Halberg R Hoff P Kwong L Newton M Meyerand E Pasch C Shedlovsky A Thliveris A Weichert J White A Institutions University of Wisconsin Madison One major pathway to colon cancer in mammals involves loss of function of the gatekeeper gene APC Apc Adenomatous polyposis coli The Min nonsense allele of the murine Apc gene was induced by germline ENU mutagenesis identified by its neoplastic phenotype and cloned by a combination of low resolution mapping and candidate testing A single basepair change from the wildtype C57BL 6 Apc allele was detected illustrating the power of the coisogenic strategy for positional cloning Our laboratory and others are studying a number of issues in the biology of intestinal neoplasia in the mouse employing this Min model Multiple intestinal neoplasia The different somatic genetic and epigenetic processes whereby the wildtype Apc function is lost in the early adenomas of Apc Min miceThe regional distribution of these distinct processes over the intestinal tractThe clonality of

    Original URL path: http://www.imgs.org/Archive/abstracts/2003abstracts/file30.shtml (2016-02-17)
    Open archived version from archive

  • 17th International Mouse Genome Conference (2003)
    V 1 Haynes A E 1 Hugill A 1 Paul C L 1 Bentley E 2 Horner E J 1 3 Anstee Q M 1 Cox R D Institutions 1 Diabetes QTL and Modifier Loci Group MRC Harwell Oxfordshire 2 Etiologics Ltd Harwell Oxfordshire 3 Department of Medicine Imperial College London Type II diabetes is a complex genetic disease with some rare monogenic subtypes In order to identify new diabetes genes and develop new mouse models for basic research and for therapeutics development we have initiated a sensitised ENU mutagenesis screen Mice heterozygous for either the Insulin Receptor IR or the Insulin Receptor Substrate 1 IRS 1 are treated with ENU and offspring assayed for diabetic phenotypes 1292 F1 mice have been generated and assayed for glucose tolerance utilising an IPGTT To date 20 F1 mice have entered inheritance testing 4 have additionally entered genotyping lines IGT 4 and IGT 10 being localised to chromosomes 13 and 14 respectively Fine mapping and candidate gene analysis is currently underway for these two lines Additionally histological analysis of various tissues from these four lines is currently underway IGT 3 and IGT 6 show marked hyperinsulinaemia and a compensatory increase in islet cell

    Original URL path: http://www.imgs.org/Archive/abstracts/2003abstracts/file31.shtml (2016-02-17)
    Open archived version from archive

  • 17th International Mouse Genome Conference (2003)
    J C Rajendra R Departments of Pathology and Developmental Biology Howard Hughes Medical Institute Stanford University Medical School Co Authors Wu J I Artzt K Institutions Departments of Pathology and Developmental Biology Howard Hughes Medical Institute Stanford University Medical School The Notch Delta signaling pathway controls many conserved cell determination events While the Notch end is fairly well understood the Delta end has been the dark side Recent evidence indicates that Delta signaling is as complex as the Notch side Delta Dll1 is cleaved at least twice with an intracellular fragment transported to the nucleus presumably to affect downstream transcription factors Delta can be ubiquitinated and endocytosed by neuralized Neur However Neur is non essential in mammals as the knockout is not lethal Another RING finger E3 ligase responsible for ubiquitination of Delta is mindbomb mib When mutated in zebrafish dramatic over production of early neurons is evident Itoh et al 2003 A second target of mib was determined biochemically to be death associated protein kinase DAPK Jin et al 2002 We have analyzed the knockout of Mib1 in mouse Mib1 embryos die at E10 5 and have the entire Notch Delta pathway rendered non functional The consequences are abnormal

    Original URL path: http://www.imgs.org/Archive/abstracts/2003abstracts/file32.shtml (2016-02-17)
    Open archived version from archive

  • 17th International Mouse Genome Conference (2003)
    FENS1 IN MICE LEADS TO INABILITY OF SPERM TO FERTILIZE Bishop C Baylor College of Medicine Co Authors Rohozinski j Ty M Matzuk M El Din N Lamb D Institutions Baylor College of Medicine Using meiotic mapping we have placed the mouse homologue of the gene coding for the human FENS1 protein FYVE domain containing protein localised to endosomes within the 1 5Mb Jsd juvenile spermatogonial depletion critical interval on mouse chromosome 1 In situ RNA hybridization to mouse testes sections showed that Fens1 expression was restricted to the germline being strongest during stage IV of spermatogenesis suggesting a possible role in germ cell development and fertility Analysis of Fens1 function by gene targeting indicated that Fens1 and Fens1 females were fully fertile as were heterozygous Fens1 males In contrast Fens1 males were totally sterile Complementation assays involving Fens1 and jsd compound male hereozygotes showed that Fens1 was not allelic to jsd excluding this gene as a candidate for the jsd mutation Evaluation of Fens1 testes showed that they were of normal size with normal numbers of motile sperm in the epididymus Histologically the tubules were abnormal in that greater than 90 contained fully mature sperm They also contained approximately

    Original URL path: http://www.imgs.org/Archive/abstracts/2003abstracts/file33.shtml (2016-02-17)
    Open archived version from archive

  • 17th International Mouse Genome Conference (2003)
    Women s Hospital Harvard Medical School Boston MA Co Authors 1 Rao C 1 Foernzler D 2 Loftus S 1 Liu S 3 McPherson J 4 Jungers K 5 Apte S 2 Pavan W Institutions 1 Genetics Division Brigham and Women s Hospital Harvard Medical School Boston MA 2 National Human Genome Research Institute National Institutes of Health Bethesda MD 3 Department of Genetics Washington University St Louis MO 4 Dept of Biomedical Engineering Cleveland Clinic Foundation Cleveland OH Several features of the pigment defect in belted bt mutant mice suggest that it occurs as a result of a defect in melanocyte development that is unique from those described for other classical white spotting mutations Using a positional cloning strategy we have determined that bt is due to a defect in a novel ADAMTS A Disintegrin like And Metalloprotease reprolysin type with ThromboSpondin type I motif protein which is a member of a large family of secreted metelloproteases that are presumed to interact with the extracellular matrix ECM A homologous and highly similar protease Gon 1 has been shown to play a crucial role in cell migration in C elegans Our results suggest this function has been conserved in mammalian

    Original URL path: http://www.imgs.org/Archive/abstracts/2003abstracts/file34.shtml (2016-02-17)
    Open archived version from archive

  • 17th International Mouse Genome Conference (2003)
    Infectious Disease Verne Chapman Memorial Lecture Table of Contents Sponsor Exhibitor List Awards Photographs ORAL PRESENTATION TUESDAY 11 NOVEMBER 14 30 14 45 HRS NOVEL COMPONENTS OF DELTA NOTCH SIGNAL TRANSDUCTION Pfister S GSF National Research Center for Environment and Health Co Authors Przemeck G K Gerber J K Beckers J Adamski J Hrabe de Angelis M Institutions GSF National Research Center for Environment and Health The evolutionary conserved Notch signal transduction pathway regulates cell fate and cellular differentiation in various tissues and has essential functions in embryonic patterning and tumorigenesis Cell cell signaling by the Notch pathway is mediated by the interaction of the transmembrane receptor Notch with its ligands Delta and Jagged presented on adjacent cells Whereas signal transduction to Notch expressing cells has been described it is yet unclear whether Delta dependent signaling may also exist within the Delta expressing cell Here we report on the identification of proteins interacting with the intracellular domain of Delta1 Dll1 In situ expression analyses in mouse embryos reveal distinct expression patterns partly overlapping with Dll1 for example in the central nervous system and the vibrissae buds In addition we find that expression of at least one of the proteins is

    Original URL path: http://www.imgs.org/Archive/abstracts/2003abstracts/file35.shtml (2016-02-17)
    Open archived version from archive



  •