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  • Articles  (214)
  • Mice  (214)
  • 2000-2004  (214)
  • 2004  (214)
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  • Articles  (214)
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  • 2000-2004  (214)
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  • 1
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    Neuroscience. The mice that don't miss mom: love and the mu-opioid receptor (2004)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2004-06-26
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Beckman, Mary -- New York, N.Y. -- Science. 2004 Jun 25;304(5679):1888-9.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15218114" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Animals, Newborn ; Bedding and Linens ; *Behavior, Animal ; Female ; Male ; *Maternal Deprivation ; Mice ; *Mothers ; Mutation ; *Object Attachment ; Odors ; Receptors, Opioid, mu/genetics/*physiology ; Vocalization, Animal
    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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    Medicine. Bone marrow cells: the source of gastric cancer? (2004)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2004-11-30
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Marx, Jean -- New York, N.Y. -- Science. 2004 Nov 26;306(5701):1455-7.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15567822" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Bone Marrow Cells/*cytology ; Bone Marrow Transplantation ; Cell Differentiation ; Cell Fusion ; Disease Progression ; Female ; Gastric Mucosa/chemistry/pathology ; Gastritis/microbiology/*pathology ; Helicobacter Infections/*pathology ; *Helicobacter felis ; Male ; Mice ; Mice, Inbred C57BL ; Stem Cells/*cytology ; Stomach Neoplasms/*pathology
    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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  • 3
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    Neuroscience. NAD to the rescue (2004)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2004-08-18
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bedalov, Antonio -- Simon, Julian A -- New York, N.Y. -- Science. 2004 Aug 13;305(5686):954-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Clinical Research Division and J. A. Simon is in the Clinical Research and Human Biology Divisions, Fred Hutchinson Cancer Research Center, Seattle, WA 98109, USA. abedalov@fhcrc.org〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15310883" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Axons/*physiology ; Cell Nucleus/metabolism ; Cell Survival ; Cells, Cultured ; Ganglia, Spinal/cytology ; Mice ; Mutation ; NAD/biosynthesis/*metabolism ; Nerve Tissue Proteins/genetics/*metabolism ; Neurodegenerative Diseases/drug therapy/physiopathology ; Neuroprotective Agents/therapeutic use ; Nicotinamide-Nucleotide Adenylyltransferase/metabolism ; RNA, Small Interfering ; Sirtuin 1 ; Sirtuins/metabolism ; Ubiquitin-Protein Ligases/metabolism ; Wallerian Degeneration/metabolism/*physiopathology
    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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    Cancer research. Inflammation and cancer: the link grows stronger (2004)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2004-11-06
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Marx, Jean -- New York, N.Y. -- Science. 2004 Nov 5;306(5698):966-8.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15528423" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cyclooxygenase 2 ; Humans ; Inflammation/*complications/immunology ; Isoenzymes/metabolism ; Macrophage Colony-Stimulating Factor/physiology ; Macrophages/immunology ; Membrane Proteins ; Mice ; NF-kappa B/physiology ; Neoplasms/*etiology/immunology ; Prostaglandin-Endoperoxide Synthases/metabolism ; Risk Factors
    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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    Regulation of cytokine receptors by Golgi N-glycan processing and endocytosis (2004)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2004-10-02
    Description: The Golgi enzyme beta1,6 N-acetylglucosaminyltransferase V (Mgat5) is up-regulated in carcinomas and promotes the substitution of N-glycan with poly N-acetyllactosamine, the preferred ligand for galectin-3 (Gal-3). Here, we report that expression of Mgat5 sensitized mouse cells to multiple cytokines. Gal-3 cross-linked Mgat5-modified N-glycans on epidermal growth factor and transforming growth factor-beta receptors at the cell surface and delayed their removal by constitutive endocytosis. Mgat5 expression in mammary carcinoma was rate limiting for cytokine signaling and consequently for epithelial-mesenchymal transition, cell motility, and tumor metastasis. Mgat5 also promoted cytokine-mediated leukocyte signaling, phagocytosis, and extravasation in vivo. Thus, conditional regulation of N-glycan processing drives synchronous modification of cytokine receptors, which balances their surface retention against loss via endocytosis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Partridge, Emily A -- Le Roy, Christine -- Di Guglielmo, Gianni M -- Pawling, Judy -- Cheung, Pam -- Granovsky, Maria -- Nabi, Ivan R -- Wrana, Jeffrey L -- Dennis, James W -- New York, N.Y. -- Science. 2004 Oct 1;306(5693):120-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Samuel Lunenfeld Research Institute, Mount Sinai Hospital, 600 University Avenue, Toronto, ON M5G 1X5, Canada.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15459394" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Line, Tumor ; Cell Membrane/metabolism ; Cell Movement ; Cell Transformation, Neoplastic ; *Endocytosis ; Galectin 3/metabolism ; Genetic Vectors ; Glycosylation ; Golgi Apparatus/enzymology ; Growth Substances/metabolism/pharmacology ; Macrophages, Peritoneal/physiology ; Mammary Neoplasms, Animal/metabolism/pathology ; Mice ; Mice, Transgenic ; N-Acetylglucosaminyltransferases/genetics/*metabolism ; Neoplasm Metastasis ; Phagocytosis ; Polysaccharides/*metabolism ; Receptor, Epidermal Growth Factor/*metabolism ; Receptors, Cytokine/*metabolism ; Receptors, Transforming Growth Factor beta/*metabolism ; Signal Transduction
    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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    In vivo activation of the p53 pathway by small-molecule antagonists of MDM2 (2004)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2004-01-06
    Description: MDM2 binds the p53 tumor suppressor protein with high affinity and negatively modulates its transcriptional activity and stability. Overexpression of MDM2, found in many human tumors, effectively impairs p53 function. Inhibition of MDM2-p53 interaction can stabilize p53 and may offer a novel strategy for cancer therapy. Here, we identify potent and selective small-molecule antagonists of MDM2 and confirm their mode of action through the crystal structures of complexes. These compounds bind MDM2 in the p53-binding pocket and activate the p53 pathway in cancer cells, leading to cell cycle arrest, apoptosis, and growth inhibition of human tumor xenografts in nude mice.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Vassilev, Lyubomir T -- Vu, Binh T -- Graves, Bradford -- Carvajal, Daisy -- Podlaski, Frank -- Filipovic, Zoran -- Kong, Norman -- Kammlott, Ursula -- Lukacs, Christine -- Klein, Christian -- Fotouhi, Nader -- Liu, Emily A -- New York, N.Y. -- Science. 2004 Feb 6;303(5659):844-8. Epub 2004 Jan 2.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Discovery Oncology, Roche Research Center, Hoffmann-La Roche, Inc., Nutley, NJ 07110, USA. lyubomir.vassilev@roche.com〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/14704432" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Apoptosis/*drug effects ; Binding Sites ; Cell Cycle/drug effects ; Cell Division/*drug effects ; Cell Line ; Cell Line, Tumor ; Cell Survival/drug effects ; Crystallization ; Crystallography, X-Ray ; Cyclin-Dependent Kinase Inhibitor p21 ; Cyclins/metabolism ; Dose-Response Relationship, Drug ; Gene Expression ; Genes, p53 ; Humans ; Hydrophobic and Hydrophilic Interactions ; Imidazoles/chemistry/metabolism/*pharmacology ; Mice ; Mice, Nude ; Models, Molecular ; Molecular Weight ; NIH 3T3 Cells ; Neoplasm Transplantation ; Neoplasms, Experimental/drug therapy/metabolism/*pathology ; *Nuclear Proteins ; Phosphorylation ; Piperazines/chemistry/metabolism/*pharmacology ; Protein Conformation ; Proto-Oncogene Proteins/*antagonists & inhibitors/chemistry/metabolism ; Proto-Oncogene Proteins c-mdm2 ; Stereoisomerism ; Transplantation, Heterologous ; Tumor Suppressor Protein p53/*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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  • 7
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    Cell biology. "Pumping" iron: the proteins (2004)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2004-12-18
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Beutler, Ernest -- New York, N.Y. -- Science. 2004 Dec 17;306(5704):2051-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular and Experimental Medicine, Scripps Research Institute, La Jolla, CA 92037, USA. beutler@scripps.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15604397" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antimicrobial Cationic Peptides/*metabolism ; Biological Transport ; Cation Transport Proteins/genetics/*metabolism ; Enterocytes/metabolism ; Erythropoiesis ; Erythropoietin/genetics/metabolism ; Gene Expression Regulation ; Hemochromatosis/genetics ; Hepatocytes/metabolism ; Hepcidins ; Histocompatibility Antigens Class I/genetics ; Homeostasis ; Iron/*metabolism ; Iron Regulatory Protein 1/*metabolism ; Iron Regulatory Protein 2/*metabolism ; Membrane Proteins/genetics ; Mice ; Models, Biological ; Mutation ; Nitric Oxide/metabolism ; Oxygen/physiology ; Response Elements ; Signal Transduction ; Transcription, 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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  • 8
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    Jun turnover is controlled through JNK-dependent phosphorylation of the E3 ligase Itch (2004)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2004-09-11
    Description: The turnover of Jun proteins, like that of other transcription factors, is regulated through ubiquitin-dependent proteolysis. Usually, such processes are regulated by extracellular stimuli through phosphorylation of the target protein, which allows recognition by F box-containing E3 ubiquitin ligases. In the case of c-Jun and JunB, we found that extracellular stimuli also modulate protein turnover by regulating the activity of an E3 ligase by means of its phosphorylation. Activation of the Jun amino-terminal kinase (JNK) mitogen-activated protein kinase cascade after T cell stimulation accelerated degradation of c-Jun and JunB through phosphorylation-dependent activation of the E3 ligase Itch. This pathway modulates cytokine production by effector T cells.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gao, Min -- Labuda, Tord -- Xia, Ying -- Gallagher, Ewen -- Fang, Deyu -- Liu, Yun-Cai -- Karin, Michael -- AI43477/AI/NIAID NIH HHS/ -- ES04151/ES/NIEHS NIH HHS/ -- ES06376/ES/NIEHS NIH HHS/ -- R21AI48542/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 2004 Oct 8;306(5694):271-5. Epub 2004 Sep 9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Gene Regulation and Signal Transduction, Department of Pharmacology, School of Medicine, University of California, San Diego, 9500 Gilman Drive, La Jolla, CA 92093-0723, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15358865" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, CD28/immunology ; CD4-Positive T-Lymphocytes/immunology/*metabolism ; Interferon-gamma/metabolism ; Interleukins/metabolism ; Lymphocyte Activation ; *MAP Kinase Kinase Kinase 1 ; MAP Kinase Kinase Kinases/genetics/metabolism ; Mice ; Mitogen-Activated Protein Kinase 8 ; Mitogen-Activated Protein Kinase 9 ; Mitogen-Activated Protein Kinases/*metabolism ; Phosphorylation ; Proto-Oncogene Proteins c-jun/genetics/*metabolism ; RNA, Messenger/genetics/metabolism ; Receptors, Antigen, T-Cell/immunology ; Recombinant Fusion Proteins/metabolism ; T-Lymphocytes/immunology/*metabolism ; Th2 Cells/cytology/immunology/metabolism ; Ubiquitin/metabolism ; Ubiquitin-Protein Ligases/*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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    The Gs-linked receptor GPR3 maintains meiotic arrest in mammalian oocytes (2004)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2004-12-14
    Description: Mammalian oocytes are held in prophase arrest by an unknown signal from the surrounding somatic cells. Here we show that the orphan Gs-linked receptor GPR3, which is localized in the oocyte, maintains this arrest. Oocytes from Gpr3 knockout mice resume meiosis within antral follicles, independently of an increase in luteinizing hormone, and this phenotype can be reversed by injection of Gpr3 RNA into the oocytes. Thus, the GPR3 receptor is a link in communication between the somatic cells and oocyte of the ovarian follicle and is crucial for the regulation of meiosis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Mehlmann, Lisa M -- Saeki, Yoshinaga -- Tanaka, Shigeru -- Brennan, Thomas J -- Evsikov, Alexei V -- Pendola, Frank L -- Knowles, Barbara B -- Eppig, John J -- Jaffe, Laurinda A -- New York, N.Y. -- Science. 2004 Dec 10;306(5703):1947-50.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cell Biology, University of Connecticut Health Center (UCHC), Farmington, CT 06032, USA. lmehlmann@neuron.uchc.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15591206" target="_blank"〉PubMed〈/a〉
    Keywords: Adenylyl Cyclases/metabolism ; Animals ; Chondroitin Sulfate Proteoglycans/genetics/metabolism ; Expressed Sequence Tags ; Female ; Granulosa Cells/physiology ; Heterotrimeric GTP-Binding Proteins/*metabolism ; In Situ Hybridization ; Lectins, C-Type ; Ligands ; Luteinizing Hormone/metabolism ; *Meiosis ; Metaphase ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Mitosis ; Oocytes/*physiology ; Ovarian Follicle/*physiology ; RNA/genetics/metabolism ; Receptors, G-Protein-Coupled/genetics/*physiology ; Versicans
    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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  • 10
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    Cancer research. Proposed leukemia stem cell encounters a blast of scrutiny (2004)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2004-08-18
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Couzin, Jennifer -- New York, N.Y. -- Science. 2004 Aug 13;305(5686):929.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15310869" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Blast Crisis/*pathology ; Cell Differentiation ; Cell Division ; Cells, Cultured ; Cytoskeletal Proteins/metabolism ; Granulocytes/cytology ; Humans ; Leukemia, Myelogenous, Chronic, BCR-ABL Positive/blood/*pathology ; Macrophages/cytology ; Mice ; Myeloid Progenitor Cells/pathology/*physiology ; Stem Cells/physiology ; Trans-Activators/metabolism ; beta Catenin
    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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