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  • Mice  (169)
  • 2005-2009  (169)
  • 1965-1969
  • 1940-1944
  • 2007  (169)
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  • 2005-2009  (169)
  • 1965-1969
  • 1940-1944
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  • 1
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2007-12-22
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cibelli, Jose -- New York, N.Y. -- Science. 2007 Dec 21;318(5858):1879-80.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Animal Sciences, Cellular Reprogramming Laboratory, Michigan State University, East Lansing, MI 48824, USA. cibelli@msu.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18096796" target="_blank"〉PubMed〈/a〉
    Keywords: Anemia, Sickle Cell/therapy ; Animals ; Cell Dedifferentiation ; Cell Differentiation ; *Cellular Reprogramming ; Embryonic Stem Cells/cytology ; Fibroblasts/*cytology ; Gene Transfer Techniques ; Genetic Vectors ; Hematopoietic Stem Cells/cytology ; Humans ; Mice ; *Nuclear Transfer Techniques ; Pluripotent Stem Cells/*cytology ; Primates ; Transcription Factors/*genetics/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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  • 2
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2007-12-15
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Miller, Greg -- New York, N.Y. -- Science. 2007 Dec 14;318(5857):1710-1.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18079374" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Astrocytes/physiology ; Brain/*growth & development/metabolism ; Complement C1q/genetics/*metabolism ; Glaucoma/immunology/metabolism/pathology ; Mice ; Neurodegenerative Diseases/immunology/metabolism/pathology ; Neurons/*metabolism ; Retina/growth & development/metabolism ; Synapses/*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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  • 3
    Publication Date: 2007-12-15
    Description: Kelly et al. (Brevia, 20 July 2007, p. 337) questioned xenotransplant experiments supporting the cancer stem cell (CSC) hypothesis because they found a high frequency of leukemia-initiating cells (L-IC) in some transgenic mouse models. However, the CSC hypothesis depends on prospective purification of cells with tumor-initiating capacity, irrespective of frequency. Moreover, we found similar L-IC frequencies in genetically comparable leukemias using syngeneic or xenogeneic models.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kennedy, James A -- Barabe, Frederic -- Poeppl, Armando G -- Wang, Jean C Y -- Dick, John E -- New York, N.Y. -- Science. 2007 Dec 14;318(5857):1722; author reply 1722.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Cell and Molecular Biology, University Health Network, Toronto, Canada.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18079385" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Bone Marrow Cells/pathology ; Bone Marrow Transplantation ; Cell Separation ; Disease Models, Animal ; Humans ; Leukemia/*pathology/physiopathology ; Leukemia, Myeloid, Acute/pathology/physiopathology ; Mice ; Mice, Transgenic ; Neoplasm Transplantation ; Neoplastic Stem Cells/pathology/*physiology ; Precursor Cell Lymphoblastic Leukemia-Lymphoma/pathology/physiopathology ; Transplantation, Heterologous
    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
    Publication Date: 2007-12-08
    Description: It has recently been demonstrated that mouse and human fibroblasts can be reprogrammed into an embryonic stem cell-like state by introducing combinations of four transcription factors. However, the therapeutic potential of such induced pluripotent stem (iPS) cells remained undefined. By using a humanized sickle cell anemia mouse model, we show that mice can be rescued after transplantation with hematopoietic progenitors obtained in vitro from autologous iPS cells. This was achieved after correction of the human sickle hemoglobin allele by gene-specific targeting. Our results provide proof of principle for using transcription factor-induced reprogramming combined with gene and cell therapy for disease treatment in mice. The problems associated with using retroviruses and oncogenes for reprogramming need to be resolved before iPS cells can be considered for human therapy.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hanna, Jacob -- Wernig, Marius -- Markoulaki, Styliani -- Sun, Chiao-Wang -- Meissner, Alexander -- Cassady, John P -- Beard, Caroline -- Brambrink, Tobias -- Wu, Li-Chen -- Townes, Tim M -- Jaenisch, Rudolf -- 2-R01-HL057619/HL/NHLBI NIH HHS/ -- 5-R37-CA084198/CA/NCI NIH HHS/ -- 5-RO1-CA087869/CA/NCI NIH HHS/ -- 5-RO1-HDO45022/PHS HHS/ -- New York, N.Y. -- Science. 2007 Dec 21;318(5858):1920-3. Epub 2007 Dec 6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Whitehead Institute for Biomedical Research, Cambridge, MA 02142, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18063756" target="_blank"〉PubMed〈/a〉
    Keywords: Anemia, Sickle Cell/blood/physiopathology/*therapy ; Animals ; Cell Differentiation ; Cells, Cultured ; *Cellular Reprogramming ; DNA-Binding Proteins/genetics ; Disease Models, Animal ; Embryonic Stem Cells/cytology ; Erythrocyte Count ; Fibroblasts/*cytology ; Genes, myc ; Globins/genetics ; Hematopoiesis ; *Hematopoietic Stem Cell Transplantation ; Hematopoietic Stem Cells/*cytology ; Hemoglobin A/analysis ; Hemoglobin, Sickle/analysis ; Humans ; Kidney Concentrating Ability ; Kruppel-Like Transcription Factors/genetics ; Male ; Mice ; Octamer Transcription Factor-3/genetics ; Pluripotent Stem Cells/*cytology ; SOXB1 Transcription Factors ; Trans-Activators/genetics ; Transduction, Genetic
    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
    Publication Date: 2007-12-08
    Description: Abuse of the dissociative anesthetic ketamine can lead to a syndrome indistinguishable from schizophrenia. In animals, repetitive exposure to this N-methyl-d-aspartate-receptor antagonist induces the dysfunction of a subset of cortical fast-spiking inhibitory interneurons, with loss of expression of parvalbumin and the gamma-aminobutyric acid-producing enzyme GAD67. We show here that exposure of mice to ketamine induced a persistent increase in brain superoxide due to activation in neurons of reduced nicotinamide adenine dinucleotide phosphate (NADPH) oxidase. Decreasing superoxide production prevented the effects of ketamine on inhibitory interneurons in the prefrontal cortex. These results suggest that NADPH oxidase may represent a novel target for the treatment of ketamine-induced psychosis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Behrens, M Margarita -- Ali, Sameh S -- Dao, Diep N -- Lucero, Jacinta -- Shekhtman, Grigoriy -- Quick, Kevin L -- Dugan, Laura L -- New York, N.Y. -- Science. 2007 Dec 7;318(5856):1645-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine, Division of Geriatric Medicine, University of California San Diego, La Jolla, CA 92093-0746, USA. mbehrens@ucsd.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18063801" target="_blank"〉PubMed〈/a〉
    Keywords: Acetophenones/pharmacology ; Animals ; Brain/*drug effects/enzymology/metabolism ; Cells, Cultured ; Enzyme Activation ; Enzyme Inhibitors/pharmacology ; Glutamate Decarboxylase/metabolism ; Interneurons/*drug effects/enzymology/*metabolism ; Ketamine/*pharmacology ; Male ; Membrane Glycoproteins/*metabolism ; Mice ; Mice, Inbred C57BL ; NADPH Oxidase/*metabolism ; Oxidation-Reduction ; Parvalbumins/metabolism ; Receptors, N-Methyl-D-Aspartate/antagonists & inhibitors/metabolism ; Superoxides/*metabolism ; Synaptic Transmission/drug effects ; Synaptosomes/metabolism
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    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 6
    Publication Date: 2007-12-08
    Description: Mammalian dosage compensation involves silencing of one of the two X chromosomes in females and is controlled by the X-inactivation center (Xic). The Xic, which includes Xist and its antisense transcription unit Tsix/Xite, somehow senses the number of X chromosomes and triggers Xist up-regulation from one of the two X chromosomes in females. We found that a segment of the mouse Xic lying several hundred kilobases upstream of Xist brings the two Xics together before the onset of X inactivation. This region can autonomously drive Xic trans-interactions even as an ectopic single-copy transgene. Its introduction into male embryonic stem cells is strongly selected against, consistent with a possible role in trans-activating Xist. We propose that homologous associations driven by this novel X-pairing region (Xpr) of the Xic enable a cell to sense that more than one X chromosome is present and coordinate reciprocal Xist/Tsix expression.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Augui, S -- Filion, G J -- Huart, S -- Nora, E -- Guggiari, M -- Maresca, M -- Stewart, A F -- Heard, E -- New York, N.Y. -- Science. 2007 Dec 7;318(5856):1632-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉CNRS UMR218, Curie Institute, 26 rue d'Ulm, Paris 75005, France.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18063799" target="_blank"〉PubMed〈/a〉
    Keywords: Alleles ; Animals ; Cell Differentiation ; Cell Line ; *Chromosome Pairing ; Chromosomes, Artificial, Bacterial ; Down-Regulation ; Embryonic Stem Cells ; Female ; Mice ; Mice, Transgenic ; RNA, Long Noncoding ; RNA, Untranslated/genetics/metabolism ; S Phase ; Transfection ; Transgenes ; Up-Regulation ; X Chromosome/*genetics/physiology ; *X Chromosome Inactivation
    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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  • 7
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2007-12-01
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Dorin, Julia R -- Jackson, Ian J -- MC_U127527200/Medical Research Council/United Kingdom -- MC_U127527201/Medical Research Council/United Kingdom -- New York, N.Y. -- Science. 2007 Nov 30;318(5855):1395.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉MRC Human Genetics Unit, Western General Hospital, Crewe Road, Edinburgh EH4 2XU, UK. ian.jackson@hgu.mrc.ac.uk〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18048676" target="_blank"〉PubMed〈/a〉
    Keywords: Agouti Signaling Protein/genetics/metabolism ; Animals ; Dogs/*genetics/metabolism ; Female ; Hair Color/*genetics ; Haplotypes ; Humans ; Male ; Mice ; Mice, Transgenic ; Mutation ; Polymorphism, Genetic ; Receptor, Melanocortin, Type 1/*metabolism ; Sequence Deletion ; Signal Transduction ; Skin/metabolism ; beta-Defensins/chemistry/*genetics/*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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  • 8
    Publication Date: 2007-12-01
    Description: JAM-C is an adhesion molecule that is expressed on cells within the vascular compartment and epithelial cells and, to date, has been largely studied in the context of inflammatory events. Using immunolabeling procedures in conjunction with confocal and electron microscopy, we show here that JAM-C is also expressed in peripheral nerves and that this expression is localized to Schwann cells at junctions between adjoining myelin end loops. Sciatic nerves from JAM-C-deficient [having the JAM-C gene knocked out (KO)] mice exhibited loss of integrity of the myelin sheath and defective nerve conduction as indicated by morphological and electrophysiological studies, respectively. In addition, behavioral tests showed motor abnormalities in the KO animals. JAM-C was also expressed in human sural nerves with an expression profile similar to that seen in mice. These results demonstrate that JAM-C is a component of the autotypic junctional attachments of Schwann cells and plays an important role in maintaining the integrity and function of myelinated peripheral nerves.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3299566/" 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/PMC3299566/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Scheiermann, Christoph -- Meda, Paolo -- Aurrand-Lions, Michel -- Madani, Rime -- Yiangou, Yiangos -- Coffey, Peter -- Salt, Thomas E -- Ducrest-Gay, Dominique -- Caille, Dorothee -- Howell, Owain -- Reynolds, Richard -- Lobrinus, Alexander -- Adams, Ralf H -- Yu, Alan S L -- Anand, Praveen -- Imhof, Beat A -- Nourshargh, Sussan -- 064920/Wellcome Trust/United Kingdom -- PG/03/123/16102/British Heart Foundation/United Kingdom -- R01 DK062283/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 2007 Nov 30;318(5855):1472-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉National Heart and Lung Institute, Imperial College London, London, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18048693" target="_blank"〉PubMed〈/a〉
    Keywords: Action Potentials ; Animals ; Cell Adhesion Molecules/*metabolism ; Humans ; Immunoglobulins/*metabolism ; Intercellular Junctions/metabolism ; Membrane Proteins/*metabolism ; Mice ; Mice, Knockout ; Myelin Sheath/metabolism/*physiology/ultrastructure ; Nerve Fibers, Myelinated/metabolism/*physiology/ultrastructure ; Neural Conduction ; Peripheral Nerves/*metabolism/physiology ; Peripheral Nervous System Diseases/metabolism/pathology/physiopathology ; Schwann Cells/*metabolism ; Sciatic Nerve/metabolism/physiology/ultrastructure ; Sural Nerve/metabolism/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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  • 9
    Publication Date: 2007-11-24
    Description: Inositol pyrophosphates are recognized components of cellular processes that regulate vesicle trafficking, telomere length, and apoptosis. We observed that pancreatic beta cells maintain high basal concentrations of the pyrophosphate diphosphoinositol pentakisphosphate (InsP7 or IP7). Inositol hexakisphosphate kinases (IP6Ks) that can generate IP7 were overexpressed. This overexpression stimulated exocytosis of insulin-containing granules from the readily releasable pool. Exogenously applied IP7 dose-dependently enhanced exocytosis at physiological concentrations. We determined that IP6K1 and IP6K2 were present in beta cells. RNA silencing of IP6K1, but not IP6K2, inhibited exocytosis, which suggests that IP6K1 is the critical endogenous kinase. Maintenance of high concentrations of IP7 in the pancreatic beta cell may enhance the immediate exocytotic capacity and consequently allow rapid adjustment of insulin secretion in response to increased demand.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Illies, Christopher -- Gromada, Jesper -- Fiume, Roberta -- Leibiger, Barbara -- Yu, Jia -- Juhl, Kirstine -- Yang, Shao-Nian -- Barma, Deb K -- Falck, John R -- Saiardi, Adolfo -- Barker, Christopher J -- Berggren, Per-Olof -- GM31278/GM/NIGMS NIH HHS/ -- MC_U122680443/Medical Research Council/United Kingdom -- New York, N.Y. -- Science. 2007 Nov 23;318(5854):1299-302.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Rolf Luft Research Center for Diabetes and Endocrinology, Karolinska Institutet, SE-171 76, Stockholm, Sweden.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18033884" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Line ; Cricetinae ; Electric Capacitance ; *Exocytosis ; Inositol Phosphates/*metabolism ; Insulin/*secretion ; Insulin-Secreting Cells/*metabolism/secretion ; Islets of Langerhans/metabolism ; Mice ; Patch-Clamp Techniques ; Phosphotransferases (Phosphate Group Acceptor)/genetics/metabolism ; Phytic Acid/metabolism ; RNA Interference ; Rats ; Secretory Vesicles/*metabolism ; Transfection
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 10
    Publication Date: 2007-11-24
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Vogel, Gretchen -- Holden, Constance -- New York, N.Y. -- Science. 2007 Nov 23;318(5854):1224-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18033853" target="_blank"〉PubMed〈/a〉
    Keywords: Adult ; Aged ; Animals ; *Cell Line ; *Cellular Reprogramming ; *Cloning, Organism ; Embryonic Stem Cells/*cytology ; Female ; Gene Transfer Techniques ; Humans ; Macaca mulatta ; Male ; Mice ; Pluripotent Stem Cells/*cytology ; Skin/*cytology/embryology
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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