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  • The 16th International Mouse Genome Conference (2002)
    2 Furukawa H 1 Medicinal Safety Research Laboratories 2 Biomedical Research Laboratories Sankyo Co Ltd Angiopoietin 1 and Angiopoietin 2 bind a tyrosine kinase receptor Tie 2 and regulate vascular formation Angiopoietins contain a signal peptide fibrinogen like domain and coiled coil domain Recently novel subfamilies of Angiopoietin which contain the characteristic domains were discovered We reported that an insertional mutation in the Angiopoietin like 3 Angptl3 gene caused hypolipidemia

    Original URL path: http://www.imgs.org/Archive/abstracts/2002abstracts/file147.shtml (2016-02-17)
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  • The 16th International Mouse Genome Conference (2002)
    Table of Contents Photographs Awards POSTER 148 ANALYSIS OF THE HOMEOBOX GENE HEX AS AN ONCOGENE IN MURINE T CELL DERIVED LYMPHOMAS A George Baylor College of Medicine Justice MJ Baylor College of Medicine Proviral insertions at the novel viral insertion site Lvis1 occur frequently in B and T cell leukemias and lymphomas in AKXD mice and appear to activate two genes the divergent homeobox gene Hex and the kinesin related spindle protein gene mEg5 located near the Lvis1 locus To determine whether Hex plays a role in the induction of lymphomas we have generated transgenic mice ectopically expressing Hex in hematopoietic cells We have also carried out transplants of bone marrow transduced with a Hex cDNA carrying retrovirus into recipient mice to determine if transplanted cells undergo altered differentiation or transformation in vivo Both transgenic and bone marrow transplant recipient mice develop hematologic neoplasias that have clonal rearrangements of the TCR locus and are Thy1 and CD4 CD8 or CD4 CD8 indicating tumor origin from a precursor T cell population Proviral insertions in tumours in transplant mice are clonal and are transcriptionally active indicating a causal role for Hex proviral insertions in the onset of neoplasia Preliminary data also

    Original URL path: http://www.imgs.org/Archive/abstracts/2002abstracts/file148.shtml (2016-02-17)
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  • The 16th International Mouse Genome Conference (2002)
    Witherden AS 2 Bowen S 3 Ball S 3 Peters J 2 Martin JE 1 Fisher EMC 1 Institute of Neurology University College London 2 Department of Histopathology Queen Mary College London 3 MRC Mammalian Genetics Unit The Loa mouse was identified in the progeny of a male mouse treated with ENU These mice exhibit progressive motor function deficit in their hind limbs which has an autosomal dominant pattern of inheritance Heterozygous Loa mice have a normal life span and can be identified by a characteristic clasping of hind limbs when suspended by the tail They perform progressively more poorly in the rotarod test and balance of coordination when compared with their wild type littermates Histopathological analysis has revealed a significant decrease in the number of anterior horn cells in aged heterozygous animals but no muscle denervation has been observed indicating that Loa is a neuropathy Homozygotes however die within 24 hours after birth with apoptosis throughout the CNS although the gross anatomy of the progeny is apparently normal indicating normal development We have mapped the Loa to the distal portion of Mmu12 and in our effort to identify this gene we have generated genetic physical radiation hybrid and transcription

    Original URL path: http://www.imgs.org/Archive/abstracts/2002abstracts/file149.shtml (2016-02-17)
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  • The 16th International Mouse Genome Conference (2002)
    APPROACH OF HUMAN CHROMOSOME 5q31 q33 M Hernandez Valladares International Livestock Research Institute ILRI and Institute of Molecular and Cell Biology Africa IMCB A 1 ole MoiYoi OK 2 Iraqi F 1 Institute of Molecular and Cell Biology Africa IMCB A Kenya 2 International Livestock Research Institute ILRI Human malaria remains a major cause of mortality in many tropical countries mainly those in sub Saharan Africa A recent review has concluded that about 1 million deaths occur yearly more than 75 of them in children Human genetic responses to malaria infection are not well understood but need to be better studied if successful strategies for control of malaria are to be realized These complex traits can be more easily dissected in genetically well defined inbred mouse strains Among the murine malaria models Plasmodium chabaudi provides a valuable experimental model of the human disease with many similarities to Plasmodium falciparum infection In the last few years several studies in backcross and F2 populations as well as in recombinant congenic strains infected with Plasmodium chabaudi have located a number of susceptibility loci on chromosomes 3 8 9 and 17 Recently we have developed a F11 advanced intercross line AIL population of C57Bl

    Original URL path: http://www.imgs.org/Archive/abstracts/2002abstracts/file150.shtml (2016-02-17)
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  • The 16th International Mouse Genome Conference (2002)
    J 2 Spurr N 2 Rastan S 3 Martin J 4 Fisher E 2 Hunter AJ 3 Brown SDM 1 MRC 2 GlaxoSmithKline 3 Queen Mary School of Medicine and Dentistry 4 Institute of Neurology The Harwell ENU mutagenesis programme aims to generate novel mouse mutants and investigate the mutations responsible for their specific phenotypes One focus of the programme was a blood biochemistry screen Around the ages of 8 14 weeks a blood sample was collected from the F1 offspring of mutagenised BALB c male mice crossed to C3H females 125ml of plasma was used to perform a profile of 17 standard biochemical tests on an Olympus analyser In total 1 961 F1 s were screened Outliers were identified using running means and standard deviations Of 70 mice showing consistent abnormalities in plasma biochemistry 43 were entered into inheritance testing Of these 15 phenotypes were confirmed as inherited 21 found not to be inherited and 7 are still being tested Two of the lines for which inheritance has been confirmed GENA 328 and GENA 381 respectively display significantly lowered and elevated levels of plasma alkaline phosphatase ALP GENA 328 low ALP is of particular interest for the study of

    Original URL path: http://www.imgs.org/Archive/abstracts/2002abstracts/file151.shtml (2016-02-17)
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  • The 16th International Mouse Genome Conference (2002)
    3 Shigeyama Y 1 Kobayashi K 1 Wakana S 1 Gondo Y 1 Minowa O 1 Shiroishi T 1 Noda T 1 RIKEN GSC 2 University of Tokyo 3 Kobe University To generate mouse models of human diabetes we utilized clinical biochemistry test in the course of ENU mutagenesis procedure as the first step of mutant screening At 11 weeks of age 200 ul of blood was collected from G1 animals offspring of ENU mutagenized male mice and 75 ul of its serum was analyzed by automatic analyser JCA BM2250 JEOL About 8 500 G1 animals were screened where 22 animals showed high blood glucose and 18 were entered into inheritance testing Of these 18 7 lines were confirmed as inherited 6 were found not to be inherited and 5 are still being tested To detect more detailed phenotypes of each mutant line oral glucose tolerance tests OGTT and insulin tolerance tests ITT were performed for the mutant founders offspring Before the OGTT mice were fasted for 16 18 hrs and then given 1 5 mg of glucose g of body weight Blood glucose and or plasma insulin levels were measured at 0 30 60 and 120 min after glucose

    Original URL path: http://www.imgs.org/Archive/abstracts/2002abstracts/file152.shtml (2016-02-17)
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  • The 16th International Mouse Genome Conference (2002)
    E 2 Bradley A 1 Luo G 1 Case Western Reserve University 2 The Sanger Centre The RecQ DNA helicase genes encode a class of conserved proteins in diverged organisms from bacteria and yeast to humans Loss of function mutations in three of the five known human RecQ helicase genes BLM WRN and RECQL4 cause three autosomal recessive human syndromes Bloom BS Werner WS and Rothmund Thompson RTS respectively Each of these syndromes manifests a multitude of clinical phenotypes many of which are unique to a specific disorder Yet despite this they also share the common themes of premature aging genomic instability and cancer predisposition The presentation of both common and distinctive features in these three syndromes suggests that in mammals the individual RecQ helicase proteins have acquired non redundant functions while maintaining conserved biochemical properties We are using the mouse as a model system to address the function of mammalian RecQ DNA helicases Previously we have reported a Blm mouse model which recapitulates many key phenotypes of BS We are expanding upon our studies of the RecQ DNA helicase gene family to include functional studies of Recql4 To this end we have created Recql4 mutant mice that harbor a

    Original URL path: http://www.imgs.org/Archive/abstracts/2002abstracts/file153.shtml (2016-02-17)
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  • The 16th International Mouse Genome Conference (2002)
    N 1 Jenkins N 1 National Cancer Institute 2 SAIC Frederick Human autoimmune diseases are complex and the identification of a single gene mouse model may provide unique insights into the etiology of diseases such as SLE IBD and Crohn s disease and potentially uncover novel targets for anti inflammatory drugs Mice homozygous for the itchy itch mutation develop an autoimmune like disease characterized by generalized systemic inflammation and die of hypoxia caused by chronic pulmonary inflammation with alveolar proteinosis at 6 8 months of age IgG deposits can be detected in the glomeruli and anti nuclear antibodies in the sera as early as 10 weeks of age This autoimmune like disease results from a loss of function mutation in a HECT E3 ubiquitin protein ligase Phylogentic analysis suggests that Itch is the mouse ortholog of Drosophila suppressor of deltex Su dx Su dx functions in Notch signaling as loss of function Su dx mutations enhance gain of function mutations in Notch Further in vitro studies show that Itch is capable of attenuating Notch signaling by ubiquitinating mouse Notch1 In order to assess the role of Itch in Notch signaling in vivo we bred itch mice with mice carrying an

    Original URL path: http://www.imgs.org/Archive/abstracts/2002abstracts/file154.shtml (2016-02-17)
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