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  • 1
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    A genetic linkage map of the mouse: current applications and future prospects (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-10-01
    Description: Technological advances have made possible the development of high-resolution genetic linkage maps for the mouse. These maps in turn offer exciting prospects for understanding mammalian genome evolution through comparative mapping, for developing mouse models of human disease, and for identifying the function of all genes in the organism.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Copeland, N G -- Jenkins, N A -- Gilbert, D J -- Eppig, J T -- Maltais, L J -- Miller, J C -- Dietrich, W F -- Weaver, A -- Lincoln, S E -- Steen, R G -- HG00198/HG/NHGRI NIH HHS/ -- N01-CO-74101/CO/NCI NIH HHS/ -- New York, N.Y. -- Science. 1993 Oct 1;262(5130):57-66.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉ABL-Basic Research Program, National Cancer Institute-Frederick Cancer Research and Development Center, MD 21702.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8211130" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Biological Evolution ; *Chromosome Mapping ; Cloning, Molecular ; Crosses, Genetic ; Female ; Genetic Markers ; *Genome ; Human Genome Project ; Humans ; Male ; Mice/*genetics ; Multigene Family ; Muridae/*genetics ; Mutation ; Neoplasms/genetics
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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  • 2
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    Reversal of left-right asymmetry: a situs inversus mutation (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-04-30
    Description: A recessive mutation was identified in a family of transgenic mice that resulted in a reversal of left-right polarity (situs inversus) in 100 percent of the homozygous transgenic mice tested. Sequences that flanked the transgenic integration site were cloned and mapped to mouse chromosome 4, between the Tsha and Hxb loci. During early embryonic development, the direction of postimplantation turning, one of the earliest manifestations of left-right asymmetry, was reversed in homozygous transgenic embryos. This insertional mutation identifies a gene that controls embryonic turning and visceral left-right polarity.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Yokoyama, T -- Copeland, N G -- Jenkins, N A -- Montgomery, C A -- Elder, F F -- Overbeek, P A -- HD25340/HD/NICHD NIH HHS/ -- N01-CO-74101/CO/NCI NIH HHS/ -- New York, N.Y. -- Science. 1993 Apr 30;260(5108):679-82.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cell Biology, Baylor College of Medicine, Houston, TX 77030.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8480178" target="_blank"〉PubMed〈/a〉
    Keywords: Alleles ; Animals ; Chromosome Mapping ; Cloning, Molecular ; Embryonic and Fetal Development/*genetics ; Female ; *Genes, Recessive ; Homozygote ; Male ; Mice ; Mice, Transgenic ; Mutagenesis, Insertional ; Situs Inversus/*genetics
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 3
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    CD40 ligand gene defects responsible for X-linked hyper-IgM syndrome (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-02-12
    Description: The ligand for CD40 (CD40L) is a membrane glycoprotein on activated T cells that induces B cell proliferation and immunoglobulin secretion. Abnormalities in the CD40L gene were associated with an X-linked immunodeficiency in humans [hyper-IgM (immunoglobulin M) syndrome]. This disease is characterized by elevated concentrations of serum IgM and decreased amounts of all other isotypes. CD40L complementary DNAs from three of four patients with this syndrome contained distinct point mutations. Recombinant expression of two of the mutant CD40L complementary DNAs resulted in proteins incapable of binding to CD40 and unable to induce proliferation or IgE secretion from normal B cells. Activated T cells from the four affected patients failed to express wild-type CD40L, although their B cells responded normally to wild-type CD40L. Thus, these CD40L defects lead to a T cell abnormality that results in the failure of patient B cells to undergo immunoglobulin class switching.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Allen, R C -- Armitage, R J -- Conley, M E -- Rosenblatt, H -- Jenkins, N A -- Copeland, N G -- Bedell, M A -- Edelhoff, S -- Disteche, C M -- Simoneaux, D K -- A125129/PHS HHS/ -- N01-CO-74101/CO/NCI NIH HHS/ -- New York, N.Y. -- Science. 1993 Feb 12;259(5097):990-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Baylor College of Medicine, Houston, TX 77030.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7679801" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, CD/*metabolism ; Antigens, CD40 ; Antigens, Differentiation, B-Lymphocyte/*metabolism ; Base Sequence ; CD40 Ligand ; DNA/chemistry/genetics ; Humans ; Immunoglobulin M/*blood ; Immunologic Deficiency Syndromes/*genetics/immunology ; Ligands ; Male ; Membrane Glycoproteins/*genetics ; Mice ; Molecular Sequence Data ; *Point Mutation ; Polymerase Chain Reaction ; T-Lymphocytes/*immunology ; Transfection ; *X Chromosome
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 4
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    Mutation of unique region of Bruton's tyrosine kinase in immunodeficient XID mice (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-07-16
    Description: The cytoplasmic tyrosine kinase, Bruton's tyrosine kinase (Btk, formerly bpk or atk), is crucial for B cell development. Loss of kinase activity results in the human immunodeficiency, X-linked agammaglobulinemia, characterized by a failure to produce B cells. In the murine X-linked immunodeficiency (XID), B cells are present but respond abnormally to activating signals. The Btk gene, btk, was mapped to the xid region of the mouse X chromosome by interspecific backcross analysis. A single conserved residue within the amino terminal unique region of Btk was mutated in XID mice. This change in xid probably interferes with normal B cell signaling mediated by Btk protein interactions.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rawlings, D J -- Saffran, D C -- Tsukada, S -- Largaespada, D A -- Grimaldi, J C -- Cohen, L -- Mohr, R N -- Bazan, J F -- Howard, M -- Copeland, N G -- AR36834/AR/NIAMS NIH HHS/ -- N01-CO-74101/CO/NCI NIH HHS/ -- New York, N.Y. -- Science. 1993 Jul 16;261(5119):358-61.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Microbiology and Molecular Genetics, University of California, Los Angeles 90024.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8332901" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; B-Lymphocytes/*enzymology/immunology ; Base Sequence ; Cell Line ; Chromosome Mapping ; Crosses, Genetic ; Exons ; Female ; Genetic Linkage ; Immunologic Deficiency Syndromes/enzymology/*genetics/immunology ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Inbred CBA ; Mice, Inbred DBA ; Mice, Mutant Strains ; Molecular Sequence Data ; Protein-Tyrosine Kinases/chemistry/*genetics/metabolism ; *X Chromosome
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 5
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    Onset and progression in inherited ALS determined by motor neurons and microglia (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-06-03
    Description: Dominant mutations in superoxide dismutase cause amyotrophic lateral sclerosis (ALS), a progressive paralytic disease characterized by loss of motor neurons. With the use of mice carrying a deletable mutant gene, expression within motor neurons was shown to be a primary determinant of disease onset and of an early phase of disease progression. Diminishing the mutant levels in microglia had little effect on the early disease phase but sharply slowed later disease progression. Onset and progression thus represent distinct disease phases defined by mutant action within different cell types to generate non-cell-autonomous killing of motor neurons; these findings validate therapies, including cell replacement, targeted to the non-neuronal cells.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Boillee, Severine -- Yamanaka, Koji -- Lobsiger, Christian S -- Copeland, Neal G -- Jenkins, Nancy A -- Kassiotis, George -- Kollias, George -- Cleveland, Don W -- MC_U117581330/Medical Research Council/United Kingdom -- NS 27036/NS/NINDS NIH HHS/ -- R37 NS027036/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 2006 Jun 2;312(5778):1389-92.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Ludwig Institute for Cancer Research and Departments of Medicine and Neuroscience, University of California at San Diego, 9500 Gilman Drive, La Jolla, CA 92093, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16741123" target="_blank"〉PubMed〈/a〉
    Keywords: Amyotrophic Lateral Sclerosis/*enzymology/genetics/pathology/physiopathology ; Animals ; Antigens, CD11b/genetics ; Disease Progression ; Female ; Humans ; Integrases/genetics ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Transgenic ; Microglia/*metabolism ; Motor Neurons/*metabolism ; Mutation ; Superoxide Dismutase/genetics/*metabolism
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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  • 6
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    Reprogramming of T cells to natural killer-like cells upon Bcl11b deletion (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-06-12
    Description: T cells develop in the thymus and are critical for adaptive immunity. Natural killer (NK) lymphocytes constitute an essential component of the innate immune system in tumor surveillance, reproduction, and defense against microbes and viruses. Here, we show that the transcription factor Bcl11b was expressed in all T cell compartments and was indispensable for T lineage development. When Bcl11b was deleted, T cells from all developmental stages acquired NK cell properties and concomitantly lost or decreased T cell-associated gene expression. These induced T-to-natural killer (ITNK) cells, which were morphologically and genetically similar to conventional NK cells, killed tumor cells in vitro, and effectively prevented tumor metastasis in vivo. Therefore, ITNKs may represent a new cell source for cell-based therapies.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3628452/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3628452/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Li, Peng -- Burke, Shannon -- Wang, Juexuan -- Chen, Xiongfeng -- Ortiz, Mariaestela -- Lee, Song-Choon -- Lu, Dong -- Campos, Lia -- Goulding, David -- Ng, Bee Ling -- Dougan, Gordon -- Huntly, Brian -- Gottgens, Bertie -- Jenkins, Nancy A -- Copeland, Neal G -- Colucci, Francesco -- Liu, Pentao -- 076962/Wellcome Trust/United Kingdom -- 077186/Wellcome Trust/United Kingdom -- G0501150/Medical Research Council/United Kingdom -- G0800784/Medical Research Council/United Kingdom -- G116/187/Medical Research Council/United Kingdom -- Biotechnology and Biological Sciences Research Council/United Kingdom -- Wellcome Trust/United Kingdom -- Medical Research Council/United Kingdom -- New York, N.Y. -- Science. 2010 Jul 2;329(5987):85-9. doi: 10.1126/science.1188063. Epub 2010 Jun 10.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Wellcome Trust Sanger Institute, Hinxton, Cambridge CB10 1HH, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20538915" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Line, Tumor ; *Cell Lineage ; Cells, Cultured ; Coculture Techniques ; Cytotoxicity, Immunologic ; Gene Deletion ; Gene Expression Profiling ; Gene Expression Regulation, Developmental ; Gene Knock-In Techniques ; Genes, T-Cell Receptor beta ; Killer Cells, Natural/cytology/immunology/*physiology ; *Lymphopoiesis/genetics ; Melanoma, Experimental/immunology/therapy ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Oligonucleotide Array Sequence Analysis ; Precursor Cells, T-Lymphoid/cytology/physiology ; Receptors, Antigen, T-Cell, alpha-beta/metabolism ; Repressor Proteins/*genetics/*metabolism ; Signal Transduction ; Stromal Cells/cytology/physiology ; T-Lymphocytes/cytology/immunology/*physiology/transplantation ; Tamoxifen/analogs & derivatives/pharmacology ; Tumor Suppressor Proteins/*genetics/*metabolism
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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