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  • 1
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    Liver organogenesis promoted by endothelial cells prior to vascular function (2001)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2001-09-29
    Description: The embryonic role of endothelial cells and nascent vessels in promoting organogenesis, prior to vascular function, is unclear. We find that early endothelial cells in mouse embryos surround newly specified hepatic endoderm and delimit the mesenchymal domain into which the liver bud grows. In flk-1 mutant embryos, which lack endothelial cells, hepatic specification occurs, but liver morphogenesis fails prior to mesenchyme invasion. We developed an embryo tissue explant system that permits liver bud vasculogenesis and show that in the absence of endothelial cells, or when the latter are inhibited, there is a selective defect in hepatic outgrowth. We conclude that vasculogenic endothelial cells and nascent vessels are critical for the earliest stages of organogenesis, prior to blood vessel function.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Matsumoto, K -- Yoshitomi, H -- Rossant, J -- Zaret, K S -- CA06297/CA/NCI NIH HHS/ -- GM36477/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2001 Oct 19;294(5542):559-63. Epub 2001 Sep 27.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Cell and Developmental Biology Program, Fox Chase Cancer Center, 7701 Burholme Avenue, Philadelphia, PA 19111, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11577199" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Blood Vessels/cytology/embryology/physiology ; Culture Techniques ; *Embryonic Induction ; Endoderm/*physiology ; Endothelium, Vascular/cytology/embryology/*physiology ; Female ; Hepatocyte Growth Factor/antagonists & inhibitors/metabolism/pharmacology ; Hepatocytes/physiology ; Liver/blood supply/cytology/drug effects/*embryology ; Male ; Mesoderm/physiology ; Mice ; Mice, Inbred C3H ; *Mitogens ; Morphogenesis ; Mutation ; Neovascularization, Physiologic ; Receptor Protein-Tyrosine Kinases/genetics/physiology ; Receptors, Growth Factor/genetics/physiology ; Receptors, Vascular Endothelial Growth Factor ; Signal Transduction/drug effects
    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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    Sequence interpretation. Functional annotation of mouse genome sequences (2001)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2001-03-10
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Nadeau, J H -- Balling, R -- Barsh, G -- Beier, D -- Brown, S D -- Bucan, M -- Camper, S -- Carlson, G -- Copeland, N -- Eppig, J -- Fletcher, C -- Frankel, W N -- Ganten, D -- Goldowitz, D -- Goodnow, C -- Guenet, J L -- Hicks, G -- Hrabe de Angelis, M -- Jackson, I -- Jacob, H J -- Jenkins, N -- Johnson, D -- Justice, M -- Kay, S -- Kingsley, D -- Lehrach, H -- Magnuson, T -- Meisler, M -- Poustka, A -- Rinchik, E M -- Rossant, J -- Russell, L B -- Schimenti, J -- Shiroishi, T -- Skarnes, W C -- Soriano, P -- Stanford, W -- Takahashi, J S -- Wurst, W -- Zimmer, A -- International Mouse Mutagenesis Consortium -- New York, N.Y. -- Science. 2001 Feb 16;291(5507):1251-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Genetics, BRB 624, Case Western Reserve University School of Medicine, 10900 Euclid Avenue, Cleveland, OH 44106, USA. jhn4@po.cwru.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11233449" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Chromosome Mapping ; *Computational Biology ; Costs and Cost Analysis ; Genes/physiology ; Genetic Techniques ; *Genome ; *Genomics ; International Cooperation ; Mice/*genetics ; Mutagenesis ; Mutation ; Phenotype ; Private Sector ; Public Sector ; Research Support as Topic ; *Sequence Analysis, DNA
    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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    Subtle cerebellar phenotype in mice homozygous for a targeted deletion of the En-2 homeobox (1991)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1991-03-08
    Description: The two mouse genes, En-1 and En-2, that are homologs of the Drosophila segmentation gene engrailed, show overlapping spatially restricted patterns of expression in the neural tube during embryogenesis, suggestive of a role in regional specification. Mice homozygous for a targeted mutation that deletes the homeobox were viable and showed no obvious defects in embryonic development. This may be due to functional redundancy of En-2 and the related En-1 gene product during embryogenesis. Consistent with this hypothesis, the mutant mice showed abnormal foliation in the adult cerebellum, where En-2, and not En-1, is normally expressed.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Joyner, A L -- Herrup, K -- Auerbach, B A -- Davis, C A -- Rossant, J -- HD25334/HD/NICHD NIH HHS/ -- NS18381/NS/NINDS NIH HHS/ -- NS20591/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1991 Mar 8;251(4998):1239-43.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Samuel Lunenfeld Research Institute, Mount Sinai Hospital, Toronto, Ontario, Canada.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1672471" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Blastocyst ; Cell Line ; Cerebellum/*anatomy & histology/embryology/pathology ; Chimera ; *Chromosome Deletion ; Female ; *Genes, Homeobox ; Male ; Mice ; Mice, Inbred BALB C ; Mice, Inbred C57BL ; Nervous System/embryology ; Phenotype
    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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  • 4
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    Regulation of a transcription factor network required for differentiation and metabolism (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-07-31
    Description: Hepatocyte nuclear factors (HNFs) are a heterogeneous class of evolutionarily conserved transcription factors that are required for cellular differentiation and metabolism. Mutations in HNF-1alphaand HNF-4alpha genes impair insulin secretion and cause type 2 diabetes. Regulation of HNF-4/HNF-1 expression by HNF-3alpha and HNF-3beta was studied in embryoid bodies in which one or both HNF-3alpha or HNF-3beta alleles were inactivated. HNF-3beta positively regulated the expression of HNF-4alpha/HNF-1alpha and their downstream targets, implicating a role in diabetes. HNF-3beta was also necessary for expression of HNF-3alpha. In contrast, HNF-3alpha acts as a negative regulator of HNF-4alpha/HNF-1alpha demonstrating that HNF-3alpha and HNF-3beta have antagonistic transcriptional regulatory functions in vivo. HNF-3alpha does not appear to act as a classic biochemical repressor but rather exerts its negative effect by competing for HNF-3 binding sites with the more efficient activator HNF-3beta. In addition, the HNF-3alpha/HNF-3beta ratio is modulated by the presence of insulin, providing evidence that the HNF network may have important roles in mediating the action of insulin.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Duncan, S A -- Navas, M A -- Dufort, D -- Rossant, J -- Stoffel, M -- New York, N.Y. -- Science. 1998 Jul 31;281(5377):692-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratories of Molecular Cell Biology and Metabolic Diseases, Rockefeller University, New York, NY 10021, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9685261" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Basic Helix-Loop-Helix Leucine Zipper Transcription Factors ; Cell Differentiation ; Clone Cells ; DNA-Binding Proteins/genetics/*metabolism ; Diabetes Mellitus, Type 2/genetics/metabolism ; Embryonic and Fetal Development ; Endoderm/cytology/*metabolism ; *Gene Expression Regulation ; *Gene Expression Regulation, Developmental ; Gene Targeting ; Glucose/metabolism ; Hepatocyte Nuclear Factor 1 ; Hepatocyte Nuclear Factor 1-alpha ; Hepatocyte Nuclear Factor 1-beta ; Hepatocyte Nuclear Factor 3-alpha ; Hepatocyte Nuclear Factor 3-beta ; Hepatocyte Nuclear Factor 4 ; Insulin/pharmacology ; Mice ; Mutation ; Nuclear Proteins/genetics/*metabolism ; Phenotype ; Phosphoproteins/genetics ; Stem Cells ; Transcription Factors/genetics/*metabolism ; Up-Regulation
    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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    Control of effector CD8+ T cell function by the transcription factor Eomesodermin (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-11-08
    Description: Activated CD8+ T cells play a critical role in host defense against viruses, intracellular microbes, and tumors. It is not clear if a key regulatory transcription factor unites the effector functions of CD8+ T cells. We now show that Eomesodermin (Eomes), a paralogue of T-bet, is induced in effector CD8+ T cells in vitro and in vivo. Ectopic expression of Eomes was sufficient to invoke attributes of effector CD8+ T cells, including interferon-gamma (IFN-gamma), perforin, and granzyme B. Loss-of-function analysis suggests Eomes may also be necessary for full effector differentiation of CD8+ T cells. We suggest that Eomesodermin is likely to complement the actions of T-bet and act as a key regulatory gene in the development of cell-mediated immunity.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pearce, Erika L -- Mullen, Alan C -- Martins, Gislaine A -- Krawczyk, Connie M -- Hutchins, Anne S -- Zediak, Valerie P -- Banica, Monica -- DiCioccio, Catherine B -- Gross, Darrick A -- Mao, Chai-An -- Shen, Hao -- Cereb, Nezih -- Yang, Soo Y -- Lindsten, Tullia -- Rossant, Janet -- Hunter, Christopher A -- Reiner, Steven L -- AI-042370/AI/NIAID NIH HHS/ -- GM-07229/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2003 Nov 7;302(5647):1041-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Abramson Family Cancer Research Institute, and Department of Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/14605368" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Arenaviridae Infections/immunology ; Base Sequence ; CD8-Positive T-Lymphocytes/*immunology/physiology ; Cell Differentiation ; Cytotoxicity, Immunologic ; Gene Expression Regulation ; Granzymes ; Interferon-gamma/biosynthesis ; Lymphocyte Activation ; Lymphocytic choriomeningitis virus/immunology ; Membrane Glycoproteins/biosynthesis/genetics ; Mice ; Mice, Inbred BALB C ; Mice, Inbred C57BL ; Molecular Sequence Data ; Perforin ; Pore Forming Cytotoxic Proteins ; RNA, Messenger/genetics/metabolism ; Serine Endopeptidases/biosynthesis/genetics ; T-Box Domain Proteins/chemistry/genetics/*physiology ; Th2 Cells/immunology/physiology ; Transcription Factors/chemistry/genetics/physiology
    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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  • 6
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    Cardiac malformation in neonatal mice lacking connexin43 (1995)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1995-03-24
    Description: Gap junctions are made up of connexin proteins, which comprise a multigene family in mammals. Targeted mutagenesis of connexin43 (Cx43), one of the most prevalent connexin proteins, showed that its absence was compatible with survival of mouse embryos to term, even though mutant cell lines showed reduced dye coupling in vitro. However, mutant embryos died at birth, as a result of a failure in pulmonary gas exchange caused by a swelling and blockage of the right ventricular outflow tract from the heart. This finding suggests that Cx43 plays an essential role in heart development but that there is functional compensation among connexins in other parts of the developing fetus.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Reaume, A G -- de Sousa, P A -- Kulkarni, S -- Langille, B L -- Zhu, D -- Davies, T C -- Juneja, S C -- Kidder, G M -- Rossant, J -- New York, N.Y. -- Science. 1995 Mar 24;267(5205):1831-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Samuel Lunenfeld Research Institute, Mount Sinai Hospital, Toronto, Ontario, Canada.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7892609" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Line ; Connexin 43/*genetics/*physiology ; Embryo, Mammalian/cytology ; Heart Defects, Congenital/*genetics/pathology ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Respiratory Transport/genetics ; Stem Cells ; Ventricular Outflow Obstruction/congenital/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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