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  • Cells, Cultured  (18)
  • American Association for the Advancement of Science (AAAS)  (18)
  • American Geophysical Union
  • Springer
  • 2005-2009  (11)
  • 1985-1989  (7)
  • 2005  (11)
  • 1987  (7)
Collection
Publisher
  • American Association for the Advancement of Science (AAAS)  (18)
  • American Geophysical Union
  • Springer
Years
  • 2005-2009  (11)
  • 1985-1989  (7)
Year
  • 1
    Publication Date: 2005-02-26
    Description: We identified axonal defects in mouse models of Alzheimer's disease that preceded known disease-related pathology by more than a year; we observed similar axonal defects in the early stages of Alzheimer's disease in humans. Axonal defects consisted of swellings that accumulated abnormal amounts of microtubule-associated and molecular motor proteins, organelles, and vesicles. Impairing axonal transport by reducing the dosage of a kinesin molecular motor protein enhanced the frequency of axonal defects and increased amyloid-beta peptide levels and amyloid deposition. Reductions in microtubule-dependent transport may stimulate proteolytic processing of beta-amyloid precursor protein, resulting in the development of senile plaques and Alzheimer's disease.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Stokin, Gorazd B -- Lillo, Concepcion -- Falzone, Tomas L -- Brusch, Richard G -- Rockenstein, Edward -- Mount, Stephanie L -- Raman, Rema -- Davies, Peter -- Masliah, Eliezer -- Williams, David S -- Goldstein, Lawrence S B -- EY12598/EY/NEI NIH HHS/ -- EY13408/EY/NEI NIH HHS/ -- P50 AG05131/AG/NIA NIH HHS/ -- R01 EY007042/EY/NEI NIH HHS/ -- R01 EY007042-19/EY/NEI NIH HHS/ -- R01 EY013408/EY/NEI NIH HHS/ -- R01 EY013408-02/EY/NEI NIH HHS/ -- New York, N.Y. -- Science. 2005 Feb 25;307(5713):1282-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute and Department of Cellular and Molecular Medicine, School of Medicine, University of California San Diego (UCSD), 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/15731448" target="_blank"〉PubMed〈/a〉
    Keywords: Aged ; Aged, 80 and over ; Alzheimer Disease/genetics/*metabolism/*pathology ; Amyloid beta-Peptides/metabolism ; Amyloid beta-Protein Precursor/metabolism ; Animals ; *Axonal Transport ; Axons/*pathology/physiology ; Basal Nucleus of Meynert/pathology ; Brain/*metabolism/*pathology ; Cells, Cultured ; Cytoplasmic Vesicles/ultrastructure ; Female ; Hippocampus ; Humans ; Kinesin/metabolism ; Male ; Mice ; Mice, Inbred C3H ; Mice, Inbred C57BL ; Microtubule-Associated Proteins/genetics/metabolism ; Neurons/metabolism ; Organelles/ultrastructure ; Plaque, Amyloid/pathology ; Time 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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  • 2
    Publication Date: 2005-02-05
    Description: Variants of NOD2, an intracellular sensor of bacteria-derived muramyl dipeptide (MDP), increase susceptibility to Crohn's disease (CD). These variants are thought to be defective in activation of nuclear factor kappaB (NF-kappaB) and antibacterial defenses, but CD clinical specimens display elevated NF-kappaB activity. To illuminate the pathophysiological function of NOD2, we introduced such a variant to the mouse Nod2 locus. Mutant mice exhibited elevated NF-kappaB activation in response to MDP and more efficient processing and secretion of the cytokine interleukin-1beta (IL-1beta). These effects are linked to increased susceptibility to bacterial-induced intestinal inflammation and identify NOD2 as a positive regulator of NF-kappaB activation and IL-1beta secretion.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Maeda, Shin -- Hsu, Li-Chung -- Liu, Hongjun -- Bankston, Laurie A -- Iimura, Mitsutoshi -- Kagnoff, Martin F -- Eckmann, Lars -- Karin, Michael -- AI43477/AI/NIAID NIH HHS/ -- AI56075/AI/NIAID NIH HHS/ -- DK07202/DK/NIDDK NIH HHS/ -- DK35108/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 2005 Feb 4;307(5710):734-8.〈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/15692052" target="_blank"〉PubMed〈/a〉
    Keywords: Acetylmuramyl-Alanyl-Isoglutamine/immunology ; Animals ; Anti-Bacterial Agents/pharmacology ; Apoptosis ; Bacteria/immunology ; Cells, Cultured ; Colitis/immunology/pathology ; Colon/*immunology/microbiology ; Crohn Disease/genetics/*immunology ; Cytokines/biosynthesis/genetics ; Dextran Sulfate/pharmacology ; Interleukin-1/*metabolism ; Intestinal Mucosa/immunology ; Intracellular Signaling Peptides and Proteins/*genetics/*physiology ; Lipopolysaccharides/immunology ; Macrophage Activation ; Macrophages/*immunology/metabolism ; Mice ; Mutation ; NF-kappa B/*metabolism ; Nod2 Signaling Adaptor Protein ; Peptidoglycan/immunology ; 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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  • 3
    Publication Date: 2005-11-19
    Description: Nodes of Ranvier are regularly placed, nonmyelinated axon segments along myelinated nerves. Here we show that nodal membranes isolated from the central nervous system (CNS) of mammals restricted neurite outgrowth of cultured neurons. Proteomic analysis of these membranes revealed several inhibitors of neurite outgrowth, including the oligodendrocyte myelin glycoprotein (OMgp). In rat spinal cord, OMgp was not localized to compact myelin, as previously thought, but to oligodendroglia-like cells, whose processes converge to form a ring that completely encircles the nodes. In OMgp-null mice, CNS nodes were abnormally wide and collateral sprouting was observed. Nodal ensheathment in the CNS may stabilize the node and prevent axonal sprouting.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Huang, Jeffrey K -- Phillips, Greg R -- Roth, Alejandro D -- Pedraza, Liliana -- Shan, Weisong -- Belkaid, Wiam -- Mi, Sha -- Fex-Svenningsen, Asa -- Florens, Laurence -- Yates, John R 3rd -- Colman, David R -- NS20147/NS/NINDS NIH HHS/ -- P41 RR11823/RR/NCRR NIH HHS/ -- New York, N.Y. -- Science. 2005 Dec 16;310(5755):1813-7. Epub 2005 Nov 17.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Fishberg Department of Neuroscience, Mount Sinai School of Medicine, One Gustave L. Levy Place, New York, NY 10029, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16293723" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens/analysis ; Axons/*physiology/ultrastructure ; Cattle ; Cell Surface Extensions/chemistry/*physiology/ultrastructure ; Cells, Cultured ; GPI-Linked Proteins ; Ganglia, Spinal/physiology/ultrastructure ; Humans ; Mice ; Myelin Proteins ; Myelin Sheath/chemistry ; Myelin-Associated Glycoprotein/analysis ; Myelin-Oligodendrocyte Glycoprotein ; Neurites/*physiology/ultrastructure ; Neuroglia/chemistry/*physiology/*ultrastructure ; Oligodendroglia/chemistry/physiology/ultrastructure ; Proteoglycans/analysis ; Proteomics ; Ranvier's Nodes/chemistry/*physiology/ultrastructure ; Rats ; Spinal Cord/cytology
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 4
    Publication Date: 2005-07-30
    Description: It is generally reasoned that lethal infections caused by opportunistic pathogens develop permissively by invading a host that is both physiologically stressed and immunologically compromised. However, an alternative hypothesis might be that opportunistic pathogens actively sense alterations in host immune function and respond by enhancing their virulence phenotype. We demonstrate that interferon-gamma binds to an outer membrane protein in Pseudomonas aeruginosa, OprF, resulting in the expression of a quorum-sensing dependent virulence determinant, the PA-I lectin. These observations provide details of the mechanisms by which prokaryotic organisms are directly signaled by immune activation in their eukaryotic host.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wu, Licheng -- Estrada, Oscar -- Zaborina, Olga -- Bains, Manjeet -- Shen, Le -- Kohler, Jonathan E -- Patel, Nachiket -- Musch, Mark W -- Chang, Eugene B -- Fu, Yang-Xin -- Jacobs, Michael A -- Nishimura, Michael I -- Hancock, Robert E W -- Turner, Jerrold R -- Alverdy, John C -- 2-RO1 GM062344-05/GM/NIGMS NIH HHS/ -- DK-38510/DK/NIDDK NIH HHS/ -- DK-47722/DK/NIDDK NIH HHS/ -- R01DK61931/DK/NIDDK NIH HHS/ -- R01DK68271/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 2005 Jul 29;309(5735):774-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Surgery, University of Chicago, Pritzker School of Medicine, Chicago, IL 60637, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16051797" target="_blank"〉PubMed〈/a〉
    Keywords: Adhesins, Bacterial/*biosynthesis ; Animals ; Cell Line ; Cell Line, Tumor ; Cells, Cultured ; Cytokines/immunology/metabolism/pharmacology ; Humans ; Interferon-gamma/immunology/*metabolism/pharmacology ; Lectins/*biosynthesis ; Lymphocyte Activation ; Porins/isolation & purification/*metabolism ; Protein Binding ; Pseudomonas aeruginosa/growth & development/*immunology/metabolism/*pathogenicity ; Pyocyanine/biosynthesis ; Recombinant Proteins/pharmacology ; Signal Transduction ; T-Lymphocytes/*immunology ; Up-Regulation ; Virulence
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 5
    Publication Date: 2005-11-29
    Description: Drug-dependent neural plasticity related to drug addiction and schizophrenia can be modeled in animals as behavioral sensitization, which is induced by repeated noncontingent or self-administration of many drugs of abuse. Molecular mechanisms that are critical for behavioral sensitization have yet to be specified. Long-term depression (LTD) of alpha-amino-3-hydroxy-5-methyl-isoxazole-4-propionic acid receptor (AMPAR)-mediated synaptic transmission in the brain has been proposed as a cellular substrate for learning and memory. The expression of LTD in the nucleus accumbens (NAc) required clathrin-dependent endocytosis of postsynaptic AMPARs. NAc LTD was blocked by a dynamin-derived peptide that inhibited clathrin-mediated endocytosis or by a GluR2-derived peptide that blocked regulated AMPAR endocytosis. Systemic or intra-NAc infusion of the membrane-permeable GluR2 peptide prevented the expression of amphetamine-induced behavioral sensitization in the rat.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Brebner, Karen -- Wong, Tak Pan -- Liu, Lidong -- Liu, Yitao -- Campsall, Paul -- Gray, Sarah -- Phelps, Lindsay -- Phillips, Anthony G -- Wang, Yu Tian -- New York, N.Y. -- Science. 2005 Nov 25;310(5752):1340-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Brain Research Centre, University of British Columbia, Vancouver, British Columbia V6T 2B5, Canada.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16311338" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Behavior, Addictive ; Behavior, Animal/*drug effects ; Cells, Cultured ; Clathrin/physiology ; Dextroamphetamine/*administration & dosage/pharmacology ; Dynamins/pharmacology ; Endocytosis ; Excitatory Postsynaptic Potentials ; *Long-Term Synaptic Depression/drug effects ; Male ; Membrane Potentials ; Models, Animal ; Motor Activity/*drug effects ; Nucleus Accumbens/drug effects/*physiology ; Patch-Clamp Techniques ; Peptides/pharmacology ; Random Allocation ; Rats ; Rats, Sprague-Dawley ; Receptors, AMPA/metabolism ; Recombinant Fusion Proteins/pharmacology ; Stereotyped Behavior/*drug effects ; Synaptic Transmission/drug effects ; Ventral Tegmental Area/drug effects/physiology
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  • 6
    Publication Date: 1987-08-21
    Description: The genome of the human immunodeficiency virus HIV-1 contains at least eight genes, of which three (sor, R, and 3' orf) have no known function. In this study, the role of the sor gene was examined by constructing a series of proviral genomes of HIV-1 that either lacked the coding sequences for sor or contained point mutations in sor. Analysis of four such mutants revealed that although each clone could generate morphologically normal virus particles upon transfection, the mutant viruses were limited in their capacity to establish stable infection. Virus derived from transfection of Cos-1 cells (OKT4-) with sor mutant proviral DNA's was resistant to transmission to OKT4+ "susceptible" cells under cell-free conditions, and was transmitted poorly by coculture. In contrast, virus derived from clones with an intact sor frame was readily propagated by either approach. Normal amounts of gag-, env-, and pol-derived proteins were produced by all four mutants and assays in both lymphoid and nonlymphoid cells indicated that their trans-activating capacity was intact and comparable with wild type. Thus the sor gene, although not absolutely required in HIV virion formation, influences virus transmission in vitro and is crucial in the efficient generation of infectious virus. The data also suggest that sor influences virus replication at a novel, post-translational stage and that its action is independent of the regulatory genes tat and trs.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Fisher, A G -- Ensoli, B -- Ivanoff, L -- Chamberlain, M -- Petteway, S -- Ratner, L -- Gallo, R C -- Wong-Staal, F -- New York, N.Y. -- Science. 1987 Aug 21;237(4817):888-93.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3497453" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Communication ; Cells, Cultured ; Cercopithecus aethiops ; Cytopathogenic Effect, Viral ; Genes, Viral ; HIV/*genetics ; T-Lymphocytes/microbiology ; Viral Proteins/*physiology ; *Virus Replication
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  • 7
    Publication Date: 2005-09-17
    Description: A small number of mammalian signaling pathways mediate a myriad of distinct physiological responses to diverse cellular stimuli. Temporal control of the signaling module that contains IkappaB kinase (IKK), its substrate inhibitor of NF-kappaB (IkappaB), and the key inflammatory transcription factor NF-kappaB can allow for selective gene activation. We have demonstrated that different inflammatory stimuli induce distinct IKK profiles, and we examined the underlying molecular mechanisms. Although tumor necrosis factor-alpha (TNFalpha)-induced IKK activity was rapidly attenuated by negative feedback, lipopolysaccharide (LPS) signaling and LPS-specific gene expression programs were dependent on a cytokine-mediated positive feedback mechanism. Thus, the distinct biological responses to LPS and TNFalpha depend on signaling pathway-specific mechanisms that regulate the temporal profile of IKK activity.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Werner, Shannon L -- Barken, Derren -- Hoffmann, Alexander -- GM071573/GM/NIGMS NIH HHS/ -- GM72024/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2005 Sep 16;309(5742):1857-61.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Signaling Systems Laboratory, Department of Chemistry and Biochemistry, 9500 Gilman Drive, Mailcode 0375, La Jolla, CA 92093-0375, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16166517" target="_blank"〉PubMed〈/a〉
    Keywords: Algorithms ; Animals ; Autocrine Communication ; Cell Line ; Cells, Cultured ; Computer Simulation ; Cytokines/genetics ; Feedback, Physiological ; Gene Expression Profiling ; *Gene Expression Regulation ; I-kappa B Kinase ; I-kappa B Proteins/metabolism ; Lipopolysaccharides/immunology/metabolism/pharmacology ; Mice ; Models, Biological ; NF-kappa B/deficiency/metabolism ; Oligonucleotide Array Sequence Analysis ; Protein-Serine-Threonine Kinases/*metabolism ; Receptors, Immunologic/metabolism ; Signal Transduction ; Toll-Like Receptor 4 ; Transcriptional Activation ; Tumor Necrosis Factor-alpha/deficiency/immunology/metabolism/pharmacology
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 8
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2005-07-16
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Fetler, Luc -- Amigorena, Sebastian -- New York, N.Y. -- Science. 2005 Jul 15;309(5733):392-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratoire Physico-Chimie Curie, CNRS UMR 168, Institut Curie, Paris, France. luc.fetler@curie.fr〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16020721" target="_blank"〉PubMed〈/a〉
    Keywords: Adenosine Triphosphate/metabolism ; Animals ; Astrocytes/metabolism ; Brain/blood supply/*cytology/pathology/*physiology ; Brain Injuries/immunology/pathology/*physiopathology ; Capillaries/injuries ; Cell Surface Extensions/physiology/ultrastructure ; Cells, Cultured ; Mice ; Mice, Transgenic ; Microglia/cytology/*physiology/*ultrastructure ; Microscopy/methods ; Movement ; Phagocytosis ; Photons ; Receptors, Purinergic P2/metabolism
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 9
    Publication Date: 2005-11-19
    Description: The immunological synapse is a specialized cell-cell junction that is defined by large-scale spatial patterns of receptors and signaling molecules yet remains largely enigmatic in terms of formation and function. We used supported bilayer membranes and nanometer-scale structures fabricated onto the underlying substrate to impose geometric constraints on immunological synapse formation. Analysis of the resulting alternatively patterned synapses revealed a causal relation between the radial position of T cell receptors (TCRs) and signaling activity, with prolonged signaling from TCR microclusters that had been mechanically trapped in the peripheral regions of the synapse. These results are consistent with a model of the synapse in which spatial translocation of TCRs represents a direct mechanism of signal regulation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Mossman, Kaspar D -- Campi, Gabriele -- Groves, Jay T -- Dustin, Michael L -- GM64900/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2005 Nov 18;310(5751):1191-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Biophysics Graduate Group, University of California, Berkeley, CA 94720, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16293763" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Motifs ; Animals ; Antigen-Presenting Cells/metabolism ; Cells, Cultured ; Lipid Bilayers ; Mice ; Models, Immunological ; Receptors, Antigen, T-Cell/chemistry/*metabolism ; *Signal Transduction ; Structure-Activity Relationship ; T-Lymphocytes/immunology/*metabolism
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 10
    Publication Date: 2005-03-12
    Description: Antigen-presenting cells (APCs) internalize antigens and present antigen-derived peptides to T cells. Although APCs have been thought to exhibit a well-developed capacity for lysosomal proteolysis, here we found that they can exhibit two distinct strategies upon antigen encounter. Whereas macrophages contained high levels of lysosomal proteases and rapidly degraded internalized proteins, dendritic cells (DCs) and B lymphocytes were protease-poor, resulting in a limited capacity for lysosomal degradation. Consistent with these findings, DCs in vivo degraded internalized antigens slowly and thus retained antigen in lymphoid organs for extended periods. Limited lysosomal proteolysis also favored antigen presentation. These results help explain why DCs are able to efficiently accumulate, process, and disseminate antigens and microbes systemically for purposes of tolerance and immunity.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Delamarre, Lelia -- Pack, Margit -- Chang, Henry -- Mellman, Ira -- Trombetta, E Sergio -- R37-AI34098/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 2005 Mar 11;307(5715):1630-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cell Biology and Department of Immunobiology, Ludwig Institute for Cancer Research, Yale University School of Medicine, 333 Cedar Street, Post Office Box 208002, New Haven, CT 06520-8002, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15761154" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Antigen Presentation ; Antigen-Presenting Cells/*enzymology/*immunology/metabolism ; Antigens/*metabolism ; B-Lymphocytes/enzymology/immunology/metabolism ; Cells, Cultured ; Dendritic Cells/*enzymology/immunology/metabolism ; Endocytosis ; Green Fluorescent Proteins/immunology/metabolism ; Histocompatibility Antigens Class II/immunology ; Horseradish Peroxidase/immunology/metabolism ; Lymphoid Tissue/cytology/enzymology/immunology ; Lysosome-Associated Membrane Glycoproteins ; Lysosomes/*enzymology/ultrastructure ; Macrophages/enzymology/immunology/metabolism ; Membrane Glycoproteins/metabolism ; Mice ; Mice, Inbred C3H ; Peptide Hydrolases/*metabolism ; Ribonuclease, Pancreatic/immunology/metabolism ; Ribonucleases/immunology/metabolism
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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