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  • Mice  (181)
  • 2020-2022
  • 2000-2004  (181)
  • 1945-1949
  • 2000  (181)
  • 1
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    Functional requirement for class I MHC in CNS development and plasticity (2000)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2000-12-16
    Description: Class I major histocompatibility complex (class I MHC) molecules, known to be important for immune responses to antigen, are expressed also by neurons that undergo activity-dependent, long-term structural and synaptic modifications. Here, we show that in mice genetically deficient for cell surface class I MHC or for a class I MHC receptor component, CD3zeta, refinement of connections between retina and central targets during development is incomplete. In the hippocampus of adult mutants, N-methyl-D-aspartate receptor-dependent long-term potentiation (LTP) is enhanced, and long-term depression (LTD) is absent. Specific class I MHC messenger RNAs are expressed by distinct mosaics of neurons, reflecting a potential for diverse neuronal functions. These results demonstrate an important role for these molecules in the activity-dependent remodeling and plasticity of connections in the developing and mature mammalian central nervous system (CNS).〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2175035/" 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/PMC2175035/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Huh, G S -- Boulanger, L M -- Du, H -- Riquelme, P A -- Brotz, T M -- Shatz, C J -- 1F32EY07016/EY/NEI NIH HHS/ -- EY06912/EY/NEI NIH HHS/ -- F32 EY007016/EY/NEI NIH HHS/ -- F32 EY007016-02/EY/NEI NIH HHS/ -- F32 EY007016-03/EY/NEI NIH HHS/ -- MH48108/MH/NIMH NIH HHS/ -- New York, N.Y. -- Science. 2000 Dec 15;290(5499):2155-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurobiology, Harvard Medical School, 220 Longwood Avenue, Boston, MA 02115, USA. gshuh@alum.mit.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11118151" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, CD3/genetics/*physiology ; Brain/growth & development/*physiology ; Excitatory Postsynaptic Potentials ; Gene Expression Profiling ; Genes, MHC Class I ; Geniculate Bodies/physiology ; Hippocampus/growth & development/physiology ; Histocompatibility Antigens Class I/genetics/*physiology ; In Situ Hybridization ; Long-Term Potentiation ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Mice, Mutant Strains ; Neural Pathways ; *Neuronal Plasticity ; Neurons/*physiology ; Receptors, GABA-A/metabolism ; Receptors, N-Methyl-D-Aspartate/metabolism ; Retina/growth & development/physiology ; Retinal Ganglion Cells/physiology ; Signal Transduction ; Synapses/*physiology ; Synaptic Transmission ; Visual Pathways
    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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  • 2
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    Development of CD8alpha-positive dendritic cells from a common myeloid progenitor (2000)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2000-12-16
    Description: Dendritic cells (DCs) are critical in both initiating adaptive immune responses and maintaining tolerance to self antigens. These apparently contradictory roles have been suggested to depend on different subsets of DCs that arise from either myeloid or lymphoid hematopoietic origins, respectively. Although DC expression of CD8alpha is attributed to a lymphoid origin, here we show that both CD8alpha+ and CD8alpha- DCs can arise from clonogenic common myeloid progenitors in both thymus and spleen. Thus, expression of CD8alpha is not indicative of a lymphoid origin, and phenotypic and functional differences among DC subsets are likely to reflect maturation status rather than ontogeny.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Traver, D -- Akashi, K -- Manz, M -- Merad, M -- Miyamoto, T -- Engleman, E G -- Weissman, I L -- 5T32 AI-07290/AI/NIAID NIH HHS/ -- CA42551/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 2000 Dec 15;290(5499):2152-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology, Stanford University, Stanford, CA 94305, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11118150" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, CD/analysis ; Antigens, CD8/*analysis ; B-Lymphocytes/cytology/immunology ; Cell Lineage ; Dendritic Cells/*cytology/*immunology ; Hematopoietic Stem Cell Transplantation ; Hematopoietic Stem Cells/cytology ; Immunophenotyping ; Mice ; Mice, Inbred C57BL ; Myeloid Progenitor Cells/*cytology/transplantation ; Spleen/*cytology/immunology ; T-Lymphocytes/cytology/immunology ; Thymus Gland/*cytology/immunology
    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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    Docosahexaenoic acid, a ligand for the retinoid X receptor in mouse brain (2000)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2000-12-16
    Description: The retinoid X receptor (RXR) is a nuclear receptor that functions as a ligand-activated transcription factor. Little is known about the ligands that activate RXR in vivo. Here, we identified a factor in brain tissue from adult mice that activates RXR in cell-based assays. Purification and analysis of the factor by mass spectrometry revealed that it is docosahexaenoic acid (DHA), a long-chain polyunsaturated fatty acid that is highly enriched in the adult mammalian brain. Previous work has shown that DHA is essential for brain maturation, and deficiency of DHA in both rodents and humans leads to impaired spatial learning and other abnormalities. These data suggest that DHA may influence neural function through activation of an RXR signaling pathway.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉de Urquiza, A M -- Liu, S -- Sjoberg, M -- Zetterstrom, R H -- Griffiths, W -- Sjovall, J -- Perlmann, T -- New York, N.Y. -- Science. 2000 Dec 15;290(5499):2140-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Ludwig Institute for Cancer Research, Stockholm Branch, Box 240, S-171 77 Stockholm, Sweden.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11118147" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Biological Assay ; Brain/growth & development/metabolism ; *Brain Chemistry ; Cell Line ; Chromatography, High Pressure Liquid ; Culture Media, Conditioned ; Dimerization ; Docosahexaenoic Acids/*isolation & purification/*metabolism/pharmacology ; Fatty Acids, Unsaturated/pharmacology ; Histone Acetyltransferases ; Humans ; Ligands ; Male ; Mice ; Nuclear Receptor Coactivator 1 ; Receptors, Retinoic Acid/genetics/*metabolism ; Recombinant Fusion Proteins/metabolism ; Retinoid X Receptors ; Signal Transduction ; Spectrometry, Mass, Electrospray Ionization ; Transcription Factors/genetics/*metabolism ; Transfection ; Tumor Cells, Cultured
    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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    Response to RAG-mediated VDJ cleavage by NBS1 and gamma-H2AX (2000)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2000-12-09
    Description: Genetic disorders affecting cellular responses to DNA damage are characterized by high rates of translocations involving antigen receptor loci and increased susceptibility to lymphoid malignancies. We report that the Nijmegen breakage syndrome protein (NBS1) and histone gamma-H2AX, which associate with irradiation-induced DNA double-strand breaks (DSBs), are also found at sites of VDJ (variable, diversity, joining) recombination-induced DSBs. In developing thymocytes, NBS1 and gamma-H2AX form nuclear foci that colocalize with the T cell receptor alpha locus in response to recombination activating gene (RAG) protein-mediated VDJ cleavage. Our results suggest that surveillance of T cell receptor recombination intermediates by NBS1 and gamma-H2AX may be important for preventing oncogenic translocations.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4721589/" 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/PMC4721589/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chen, H T -- Bhandoola, A -- Difilippantonio, M J -- Zhu, J -- Brown, M J -- Tai, X -- Rogakou, E P -- Brotz, T M -- Bonner, W M -- Ried, T -- Nussenzweig, A -- Z99 CA999999/Intramural NIH HHS/ -- New York, N.Y. -- Science. 2000 Dec 8;290(5498):1962-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Experimental Immunology Branch, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11110662" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Cell Nucleus/metabolism ; DNA Damage ; DNA-Binding Proteins/metabolism ; Fluorescent Antibody Technique ; *Gene Rearrangement, alpha-Chain T-Cell Antigen Receptor ; *Genes, T-Cell Receptor alpha ; Histones/*metabolism ; Homeodomain Proteins/metabolism ; Mice ; Mice, Transgenic ; Microscopy, Confocal ; Molecular Sequence Data ; Nuclear Proteins/*metabolism ; Phosphorylation ; *Recombination, Genetic ; T-Lymphocytes/*metabolism
    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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    Glucose-dependent insulin release from genetically engineered K cells (2000)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2000-12-09
    Description: Genetic engineering of non-beta cells to release insulin upon feeding could be a therapeutic modality for patients with diabetes. A tumor-derived K-cell line was induced to produce human insulin by providing the cells with the human insulin gene linked to the 5'-regulatory region of the gene encoding glucose-dependent insulinotropic polypeptide (GIP). Mice expressing this transgene produced human insulin specifically in gut K cells. This insulin protected the mice from developing diabetes and maintained glucose tolerance after destruction of the native insulin-producing beta cells.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cheung, A T -- Dayanandan, B -- Lewis, J T -- Korbutt, G S -- Rajotte, R V -- Bryer-Ash, M -- Boylan, M O -- Wolfe, M M -- Kieffer, T J -- New York, N.Y. -- Science. 2000 Dec 8;290(5498):1959-62.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine, University of Alberta, Edmonton, AB T6G 2S2, Canada.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11110661" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Blood Glucose/metabolism ; Cell Line ; Cloning, Molecular ; Diabetes Mellitus, Experimental/metabolism/*therapy ; Enteroendocrine Cells/*cytology/*metabolism ; Gastric Inhibitory Polypeptide/biosynthesis/genetics ; Gene Expression ; Genetic Engineering ; *Genetic Therapy ; Glucose/administration & dosage/*metabolism ; Glucose Tolerance Test ; Humans ; Insulin/biosynthesis/genetics/*metabolism ; Mice ; Mice, Transgenic ; Proinsulin/genetics ; Promoter Regions, Genetic ; Protein Precursors/genetics ; Stem Cells/cytology/metabolism ; Streptozocin ; Transfection ; Transgenes ; Tumor Cells, Cultured
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 6
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    From marrow to brain: expression of neuronal phenotypes in adult mice (2000)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2000-12-02
    Description: After intravascular delivery of genetically marked adult mouse bone marrow into lethally irradiated normal adult hosts, donor-derived cells expressing neuronal proteins (neuronal phenotypes) developed in the central nervous system. Flow cytometry revealed a population of donor-derived cells in the brain with characteristics distinct from bone marrow. Confocal microscopy of individual cells showed that hundreds of marrow-derived cells in brain sections expressed gene products typical of neurons (NeuN, 200-kilodalton neurofilament, and class III beta-tubulin) and were able to activate the transcription factor cAMP response element-binding protein (CREB). The generation of neuronal phenotypes in the adult brain 1 to 6 months after an adult bone marrow transplant demonstrates a remarkable plasticity of adult tissues with potential clinical applications.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Brazelton, T R -- Rossi, F M -- Keshet, G I -- Blau, H M -- AG09521/AG/NIA NIH HHS/ -- CA59717/CA/NCI NIH HHS/ -- HD18179/HD/NICHD NIH HHS/ -- New York, N.Y. -- Science. 2000 Dec 1;290(5497):1775-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Pharmacology, CCSR 4215, 269 Campus Drive, Stanford University, Stanford, CA 94305-5175, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11099418" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Biomarkers/analysis ; Bone Marrow Cells/*cytology ; *Bone Marrow Transplantation ; Brain/*cytology ; Cell Differentiation ; Cell Size ; Cyclic AMP Response Element-Binding Protein/metabolism ; Flow Cytometry ; Gene Expression ; Green Fluorescent Proteins ; Luminescent Proteins/analysis ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Transgenic ; Microscopy, Confocal ; Nerve Tissue Proteins/analysis/genetics ; Neurons/chemistry/*cytology/metabolism ; Olfactory Bulb/cytology ; Phenotype ; Phosphorylation
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 7
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    Turning blood into brain: cells bearing neuronal antigens generated in vivo from bone marrow (2000)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2000-12-02
    Description: Bone marrow stem cells give rise to a variety of hematopoietic lineages and repopulate the blood throughout adult life. We show that, in a strain of mice incapable of developing cells of the myeloid and lymphoid lineages, transplanted adult bone marrow cells migrated into the brain and differentiated into cells that expressed neuron-specific antigens. These findings raise the possibility that bone marrow-derived cells may provide an alternative source of neurons in patients with neurodegenerative diseases or central nervous system injury.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Mezey, E -- Chandross, K J -- Harta, G -- Maki, R A -- McKercher, S R -- AI30656/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 2000 Dec 1;290(5497):1779-82.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Basic Neuroscience Program, Laboratory of Developmental Neurogenetics, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD 20892, USA. mezey@codon.nih.gov〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11099419" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens/analysis ; Biomarkers/analysis ; Bone Marrow Cells/*cytology/physiology ; *Bone Marrow Transplantation ; Brain/*cytology ; Cell Differentiation ; Cell Movement ; Female ; Immunoenzyme Techniques ; Intermediate Filament Proteins/analysis ; Male ; Mice ; Mice, Knockout ; Microscopy, Confocal ; Nerve Tissue Proteins/analysis/immunology ; Nestin ; Neurons/chemistry/*cytology/immunology ; Phosphopyruvate Hydratase/analysis ; *Stem Cell Transplantation ; Stem Cells/chemistry/*cytology ; Y 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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  • 8
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    Posttranslational N-myristoylation of BID as a molecular switch for targeting mitochondria and apoptosis (2000)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2000-12-02
    Description: Many apoptotic molecules relocate subcellularly in cells undergoing apoptosis. The pro-apoptotic protein BID underwent posttranslational (rather than classic cotranslational) N-myristoylation when cleavage by caspase 8 caused exposure of a glycine residue. N-myristoylation enabled the targeting of a complex of p7 and myristoylated p15 fragments of BID to artificial membranes bearing the lipid composition of mitochondria, as well as to intact mitochondria. This post-proteolytic N-myristoylation serves as an activating switch, enhancing BID-induced release of cytochrome c and cell death.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zha, J -- Weiler, S -- Oh, K J -- Wei, M C -- Korsmeyer, S J -- CA50239-13/CA/NCI NIH HHS/ -- K01 CA82231/CA/NCI NIH HHS/ -- T32 CA72320-01A1/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 2000 Dec 1;290(5497):1761-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Dana-Farber Cancer Institute, Departments of Pathology and Medicine, Harvard Medical School, Boston, MA 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11099414" target="_blank"〉PubMed〈/a〉
    Keywords: Acyltransferases/genetics/metabolism ; Animals ; *Apoptosis ; BH3 Interacting Domain Death Agonist Protein ; Carrier Proteins/chemistry/*metabolism ; Caspase 8 ; Caspase 9 ; Caspases/metabolism ; Cytochrome c Group/metabolism ; Humans ; Intracellular Membranes/*metabolism ; Jurkat Cells ; Liposomes/metabolism ; Mice ; Mitochondria/*metabolism ; Myristic Acid/*metabolism ; Peptide Fragments/metabolism ; Protein Conformation ; Protein Processing, Post-Translational ; Protein Structure, Tertiary ; Protein Transport ; Recombinant Fusion Proteins/metabolism
    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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  • 9
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    Down-regulation of the macrophage lineage through interaction with OX2 (CD200) (2000)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2000-12-02
    Description: OX2 (CD200) is a broadly expressed membrane glycoprotein, shown here to be important for regulation of the macrophage lineage. In mice lacking CD200, macrophage lineage cells, including brain microglia, exhibited an activated phenotype and were more numerous. Upon facial nerve transection, damaged CD200-deficient neurons elicited an accelerated microglial response. Lack of CD200 resulted in a more rapid onset of experimental autoimmune encephalomyelitis (EAE). Outside the brain, disruption of CD200-CD200 receptor interaction precipitated susceptibility to collagen-induced arthritis (CIA) in mice normally resistant to this disease. Thus, in diverse tissues OX2 delivers an inhibitory signal for the macrophage lineage.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hoek, R M -- Ruuls, S R -- Murphy, C A -- Wright, G J -- Goddard, R -- Zurawski, S M -- Blom, B -- Homola, M E -- Streit, W J -- Brown, M H -- Barclay, A N -- Sedgwick, J D -- New York, N.Y. -- Science. 2000 Dec 1;290(5497):1768-71.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉DNAX Research Institute of Molecular and Cellular Biology, 901 California Avenue, Palo Alto, CA 94304, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11099416" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, CD ; Antigens, Surface/*metabolism ; Arthritis, Experimental/immunology/pathology ; Cell Lineage ; Central Nervous System/immunology/pathology ; Denervation ; *Down-Regulation ; Encephalomyelitis, Autoimmune, Experimental/immunology/pathology ; Facial Nerve ; Gene Targeting ; Joints/immunology/pathology ; Lymph Nodes/cytology ; Macrophage Activation ; Macrophages/cytology/metabolism/*physiology ; Mice ; Mice, Inbred C57BL ; Microglia/physiology ; Neurons/physiology ; Rats ; Receptors, Immunologic/metabolism ; Spleen/cytology
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 10
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    Requirement of the RNA editing deaminase ADAR1 gene for embryonic erythropoiesis (2000)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2000-12-02
    Description: The members of the ADAR (adenosine deaminase acting on RNA) gene family are involved in site-selective RNA editing that changes adenosine residues of target substrate RNAs to inosine. Analysis of staged chimeric mouse embryos with a high contribution from embryonic stem cells with a functional null allele for ADAR1 revealed a heterozygous embryonic-lethal phenotype. Most ADAR1+/- chimeric embryos died before embryonic day 14 with defects in the hematopoietic system. Our results suggest the importance of regulated levels of ADAR1 expression, which is critical for embryonic erythropoiesis in the liver.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wang, Q -- Khillan, J -- Gadue, P -- Nishikura, K -- New York, N.Y. -- Science. 2000 Dec 1;290(5497):1765-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Wistar Institute, Philadelphia, PA 19104, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11099415" target="_blank"〉PubMed〈/a〉
    Keywords: Adenosine Deaminase/*genetics/metabolism ; Alleles ; Animals ; Chimera ; Embryonic and Fetal Development ; Erythroblasts/cytology ; *Erythropoiesis ; Female ; Hematopoietic Stem Cells/*cytology/enzymology ; Hepatocytes/cytology ; Immunoenzyme Techniques ; Liver/cytology/*embryology/enzymology ; Mice ; Mice, Inbred BALB C ; Mice, SCID ; Phenotype ; *RNA Editing ; RNA-Binding Proteins ; Stem Cells/cytology/enzymology ; Teratoma/genetics/pathology
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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