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  • Articles  (30)
  • Cells, Cultured
  • 2005-2009  (30)
  • 1980-1984
  • 2006  (30)
  • Computer Science  (30)
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  • Articles  (30)
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Keywords
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  • 2005-2009  (30)
  • 1980-1984
Year
Journal
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  • 1
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    American Society for Cell Biology. Sprayed-on growth factors guide stem cells (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-12-23
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Leslie, Mitch -- New York, N.Y. -- Science. 2006 Dec 22;314(5807):1865.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17185579" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Bone Morphogenetic Proteins/*pharmacology ; Bone and Bones/*cytology ; Cell Differentiation ; Cell Lineage ; Cells, Cultured ; Extracellular Matrix ; Myoblasts/cytology ; Rats ; Stem Cells/*cytology
    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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    Generation of gut-homing IgA-secreting B cells by intestinal dendritic cells (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-11-18
    Description: Normal intestinal mucosa contains abundant immunoglobulin A (IgA)-secreting cells, which are generated from B cells in gut-associated lymphoid tissues (GALT). We show that dendritic cells (DC) from GALT induce T cell-independent expression of IgA and gut-homing receptors on B cells. GALT-DC-derived retinoic acid (RA) alone conferred gut tropism but could not promote IgA secretion. However, RA potently synergized with GALT-DC-derived interleukin-6 (IL-6) or IL-5 to induce IgA secretion. Consequently, mice deficient in the RA precursor vitamin A lacked IgA-secreting cells in the small intestine. Thus, GALT-DC shape mucosal immunity by modulating B cell migration and effector activity through synergistically acting mediators.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Mora, J Rodrigo -- Iwata, Makoto -- Eksteen, Bertus -- Song, Si-Young -- Junt, Tobias -- Senman, Balimkiz -- Otipoby, Kevin L -- Yokota, Aya -- Takeuchi, Hajime -- Ricciardi-Castagnoli, Paola -- Rajewsky, Klaus -- Adams, David H -- von Andrian, Ulrich H -- AI-061663/AI/NIAID NIH HHS/ -- G0601816/Medical Research Council/United Kingdom -- HL54936/HL/NHLBI NIH HHS/ -- HL56949/HL/NHLBI NIH HHS/ -- HL62524/HL/NHLBI NIH HHS/ -- R37 AI054636/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 2006 Nov 17;314(5802):1157-60.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉CBR Institute for Biomedical Research and Department of Pathology, Harvard Medical School, Boston, MA 02115, USA. mora@cbr.med.harvard.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17110582" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; B-Lymphocytes/*immunology/secretion ; Cell Movement ; Cells, Cultured ; Chemotaxis, Leukocyte ; Dendritic Cells/*immunology ; Immunity, Mucosal ; Immunoglobulin A/*biosynthesis/immunology ; Interleukin-5/immunology ; Interleukin-6/immunology ; Intestinal Mucosa/immunology ; Intestines/cytology/*immunology ; Lymphoid Tissue/cytology/immunology ; Mice ; Mice, Inbred C57BL ; Receptors, Antigen, B-Cell/biosynthesis ; Tretinoin/immunology ; Vitamin A/physiology ; Vitamin A Deficiency/immunology ; Vitamins/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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    Cell biology. Tools to tamper with phosphoinositides (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-11-11
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉McLaughlin, Stuart -- New York, N.Y. -- Science. 2006 Dec 1;314(5804):1402-3. Epub 2006 Nov 9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Physiology, Stony Brook University, Stony Brook, NY 11794-8661, USA. smclaughlin@notes.cc.sunysb.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17095656" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Membrane/chemistry/*metabolism ; Cells, Cultured ; GTP Phosphohydrolases/*metabolism ; Inositol 1,4,5-Trisphosphate/metabolism ; *Ion Channel Gating ; KCNQ Potassium Channels/*metabolism ; Models, Biological ; Phosphatidylinositol 4,5-Diphosphate/*metabolism ; Phosphatidylinositol Phosphates/*metabolism ; Phosphoric Monoester Hydrolases/metabolism ; Second Messenger Systems ; Type C Phospholipases/metabolism ; ras 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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  • 4
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    The polarity protein Par-3 directly interacts with p75NTR to regulate myelination (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-11-04
    Description: Cell polarity is critical in various cellular processes ranging from cell migration to asymmetric cell division and axon and dendrite specification. Similarly, myelination by Schwann cells is polarized, but the mechanisms involved remain unclear. Here, we show that the polarity protein Par-3 localizes asymmetrically in Schwann cells at the axon-glial junction and that disruption of Par-3 localization, by overexpression and knockdown, inhibits myelination. Additionally, we show that Par-3 directly associates and recruits the p75 neurotrophin receptor to the axon-glial junction, forming a complex necessary for myelination. Together, these results point to a critical role in the establishment of cell polarity for myelination.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chan, Jonah R -- Jolicoeur, Christine -- Yamauchi, Junji -- Elliott, Jimmy -- Fawcett, James P -- Ng, Benjamin K -- Cayouette, Michel -- New York, N.Y. -- Science. 2006 Nov 3;314(5800):832-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cell and Neurobiology, Zilkha Neurogenetic Institute, Keck School of Medicine, University of Southern California, Los Angeles 90089, USA. jonah.chan@usc.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17082460" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Motifs ; Animals ; Axons/chemistry/ultrastructure ; Brain-Derived Neurotrophic Factor/physiology ; Carrier Proteins/analysis/chemistry/genetics/*metabolism ; *Cell Polarity ; Cells, Cultured ; Coculture Techniques ; Ganglia, Spinal/ultrastructure ; Intercellular Junctions/chemistry ; Mice ; Myelin Sheath/*physiology ; Nerve Tissue Proteins/chemistry/*metabolism ; Protein Structure, Tertiary ; Rats ; Receptors, Growth Factor/chemistry/*metabolism ; Schwann Cells/cytology/*physiology/ultrastructure
    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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    Functional delivery of a cytosolic tRNA into mutant mitochondria of human cells (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-10-21
    Description: Many maternally inherited and incurable neuromyopathies are caused by mutations in mitochondrial (mt) transfer RNA (tRNA) genes. Kinetoplastid protozoa, including Leishmania, have evolved specialized systems for importing nucleus-encoded tRNAs into mitochondria. We found that the Leishmania RNA import complex (RIC) could enter human cells by a caveolin-1-dependent pathway, where it induced import of endogenous cytosolic tRNAs, including tRNA(Lys), and restored mitochondrial function in a cybrid harboring a mutant mt tRNA(Lys) (MT-TK) gene. The use of protein complexes to modulate mitochondrial function may help in the management of such genetic disorders.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Mahata, Bidesh -- Mukherjee, Saikat -- Mishra, Sumita -- Bandyopadhyay, Arun -- Adhya, Samit -- New York, N.Y. -- Science. 2006 Oct 20;314(5798):471-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Genetic Engineering, Indian Institute of Chemical Biology, 4 Raja S. C. Mullick Road, Calcutta 700032, India.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17053148" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Caveolin 1/metabolism ; Cell Line, Tumor ; Cell Proliferation ; Cell Respiration ; Cells, Cultured ; Cytosol/*metabolism ; Electron Transport Complex IV/metabolism ; Endocytosis ; Humans ; Kearns-Sayre Syndrome/metabolism ; *Leishmania tropica ; MERRF Syndrome/metabolism ; Mitochondria/genetics/*metabolism ; Mitochondrial Proteins/*metabolism ; Mutation ; Oxygen Consumption ; Protein Biosynthesis ; Protozoan Proteins/*metabolism ; RNA, Transfer, Lys/genetics/*metabolism ; RNA-Binding Proteins/*metabolism ; Transfection
    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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    RIG-I-mediated antiviral responses to single-stranded RNA bearing 5'-phosphates (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-10-14
    Description: Double-stranded RNA (dsRNA) produced during viral replication is believed to be the critical trigger for activation of antiviral immunity mediated by the RNA helicase enzymes retinoic acid-inducible gene I (RIG-I) and melanoma differentiation-associated gene 5 (MDA5). We showed that influenza A virus infection does not generate dsRNA and that RIG-I is activated by viral genomic single-stranded RNA (ssRNA) bearing 5'-phosphates. This is blocked by the influenza protein nonstructured protein 1 (NS1), which is found in a complex with RIG-I in infected cells. These results identify RIG-I as a ssRNA sensor and potential target of viral immune evasion and suggest that its ability to sense 5'-phosphorylated RNA evolved in the innate immune system as a means of discriminating between self and nonself.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pichlmair, Andreas -- Schulz, Oliver -- Tan, Choon Ping -- Naslund, Tanja I -- Liljestrom, Peter -- Weber, Friedemann -- Reis e Sousa, Caetano -- New York, N.Y. -- Science. 2006 Nov 10;314(5801):997-1001. Epub 2006 Oct 12.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Immunobiology Laboratory, Cancer Research UK, London Research Institute, London WC2A 3PX, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17038589" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Line ; Cells, Cultured ; Cytoplasm/metabolism/virology ; DEAD-box RNA Helicases/genetics/*metabolism ; Dendritic Cells/virology ; Encephalomyocarditis virus/genetics/immunology/metabolism ; Genome, Viral ; Humans ; *Immunity, Innate ; Influenza A virus/*genetics/*immunology/metabolism/physiology ; Interferon-alpha/biosynthesis ; Interferon-beta/biosynthesis ; Mice ; Mice, Inbred C57BL ; Phosphates/metabolism ; Phosphorylation ; RNA Caps/metabolism ; RNA, Double-Stranded/metabolism ; RNA, Viral/chemistry/genetics/*metabolism ; Recombinant Fusion Proteins/metabolism ; Transfection ; Vesicular stomatitis Indiana virus/genetics/immunology/metabolism ; Viral Nonstructural Proteins/genetics/metabolism ; Virus Replication
    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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    5'-Triphosphate RNA is the ligand for RIG-I (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-10-14
    Description: The structural basis for the distinction of viral RNA from abundant self RNA in the cytoplasm of virally infected cells is largely unknown. We demonstrated that the 5'-triphosphate end of RNA generated by viral polymerases is responsible for retinoic acid-inducible protein I (RIG-I)-mediated detection of RNA molecules. Detection of 5'-triphosphate RNA is abrogated by capping of the 5'-triphosphate end or by nucleoside modification of RNA, both occurring during posttranscriptional RNA processing in eukaryotes. Genomic RNA prepared from a negative-strand RNA virus and RNA prepared from virus-infected cells (but not from noninfected cells) triggered a potent interferon-alpha response in a phosphatase-sensitive manner. 5'-triphosphate RNA directly binds to RIG-I. Thus, uncapped 5'-triphosphate RNA (now termed 3pRNA) present in viruses known to be recognized by RIG-I, but absent in viruses known to be detected by MDA-5 such as the picornaviruses, serves as the molecular signature for the detection of viral infection by RIG-I.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hornung, Veit -- Ellegast, Jana -- Kim, Sarah -- Brzozka, Krzysztof -- Jung, Andreas -- Kato, Hiroki -- Poeck, Hendrik -- Akira, Shizuo -- Conzelmann, Karl-Klaus -- Schlee, Martin -- Endres, Stefan -- Hartmann, Gunther -- New York, N.Y. -- Science. 2006 Nov 10;314(5801):994-7. Epub 2006 Oct 12.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Clinical Pharmacology, Department of Internal Medicine, University of Munich, 80336 Munich, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17038590" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Line ; Cells, Cultured ; Cytosol/metabolism/virology ; DEAD-box RNA Helicases/*metabolism ; DNA-Directed RNA Polymerases/metabolism ; Humans ; Interferon-alpha/biosynthesis ; Interferon-beta/biosynthesis ; Ligands ; Mice ; Monocytes/metabolism ; Oligoribonucleotides/metabolism ; Phosphates/metabolism ; Phosphorylation ; RNA/chemistry/*metabolism ; RNA Caps/metabolism ; RNA, Double-Stranded/chemistry/metabolism ; RNA, Viral/chemistry/*metabolism ; Rabies virus/genetics/immunology/physiology ; Transcription, Genetic ; Transfection ; Viral Proteins/metabolism ; Virus Replication
    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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    Activity- and mTOR-dependent suppression of Kv1.1 channel mRNA translation in dendrites (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-10-07
    Description: Mammalian target of rapamycin (mTOR) is implicated in synaptic plasticity and local translation in dendrites. We found that the mTOR inhibitor, rapamycin, increased the Kv1.1 voltage-gated potassium channel protein in hippocampal neurons and promoted Kv1.1 surface expression on dendrites without altering its axonal expression. Moreover, endogenous Kv1.1 mRNA was detected in dendrites. Using Kv1.1 fused to the photoconvertible fluorescence protein Kaede as a reporter for local synthesis, we observed Kv1.1 synthesis in dendrites upon inhibition of mTOR or the N-methyl-d-aspartate (NMDA) glutamate receptor. Thus, synaptic excitation may cause local suppression of dendritic Kv1 channels by reducing their local synthesis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Raab-Graham, Kimberly F -- Haddick, Patrick C G -- Jan, Yuh Nung -- Jan, Lily Yeh -- MH13010/MH/NIMH NIH HHS/ -- MH65334/MH/NIMH NIH HHS/ -- New York, N.Y. -- Science. 2006 Oct 6;314(5796):144-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Departments of Physiology and Biochemistry, University of California, San Francisco, CA 94158, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17023663" target="_blank"〉PubMed〈/a〉
    Keywords: 3' Untranslated Regions ; Animals ; Cells, Cultured ; Dendrites/drug effects/*metabolism ; Excitatory Postsynaptic Potentials ; Hippocampus/drug effects/*metabolism ; In Vitro Techniques ; Kv1.1 Potassium Channel/*biosynthesis/*genetics ; Neuronal Plasticity ; Neurons/metabolism/virology ; Oligonucleotide Array Sequence Analysis ; Phosphorylation ; Protein Biosynthesis ; Protein Kinase Inhibitors/pharmacology ; Protein Kinases/*physiology ; RNA, Messenger/genetics/metabolism ; Rats ; Rats, Sprague-Dawley ; Receptors, N-Methyl-D-Aspartate/antagonists & inhibitors/metabolism ; Recombinant Fusion Proteins/metabolism ; Sindbis Virus/physiology ; Sirolimus/pharmacology ; Synapses/physiology ; TOR Serine-Threonine Kinases
    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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  • 9
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    Microbiology. Malaria's stealth shuttle (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-09-02
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cowman, Alan F -- Kappe, Stefan H I -- New York, N.Y. -- Science. 2006 Sep 1;313(5791):1245-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Walter and Eliza Hall Institute of Medical Research, Melbourne, Victoria 3050, Australia. cowman@wehi.edu.au〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16946056" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Calcium/metabolism ; Cell Adhesion ; Cell Death ; Cell Membrane/metabolism ; Cells, Cultured ; Cellular Structures/*parasitology/ultrastructure ; Endothelial Cells/parasitology ; Erythrocytes/parasitology ; Hepatocytes/*parasitology/physiology/ultrastructure ; Liver/blood supply/parasitology ; Malaria/*parasitology ; Mice ; Phagocytosis ; Phosphatidylserines/metabolism ; Plasmodium berghei/growth & development/*pathogenicity ; Sporozoites/growth & development ; Vacuoles/parasitology/ultrastructure
    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 regression in patients after transfer of genetically engineered lymphocytes (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-09-02
    Description: Through the adoptive transfer of lymphocytes after host immunodepletion, it is possible to mediate objective cancer regression in human patients with metastatic melanoma. However, the generation of tumor-specific T cells in this mode of immunotherapy is often limiting. Here we report the ability to specifically confer tumor recognition by autologous lymphocytes from peripheral blood by using a retrovirus that encodes a T cell receptor. Adoptive transfer of these transduced cells in 15 patients resulted in durable engraftment at levels exceeding 10% of peripheral blood lymphocytes for at least 2 months after the infusion. We observed high sustained levels of circulating, engineered cells at 1 year after infusion in two patients who both demonstrated objective regression of metastatic melanoma lesions. This study suggests the therapeutic potential of genetically engineered cells for the biologic therapy of cancer.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2267026/" 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/PMC2267026/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Morgan, Richard A -- Dudley, Mark E -- Wunderlich, John R -- Hughes, Marybeth S -- Yang, James C -- Sherry, Richard M -- Royal, Richard E -- Topalian, Suzanne L -- Kammula, Udai S -- Restifo, Nicholas P -- Zheng, Zhili -- Nahvi, Azam -- de Vries, Christiaan R -- Rogers-Freezer, Linda J -- Mavroukakis, Sharon A -- Rosenberg, Steven A -- Z01 BC010763-01/Intramural NIH HHS/ -- Z01 SC003811-32/Intramural NIH HHS/ -- Z99 CA999999/Intramural NIH HHS/ -- New York, N.Y. -- Science. 2006 Oct 6;314(5796):126-9. Epub 2006 Aug 31.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Surgery Branch, Center for Cancer Research, National Cancer Institute, National Institutes of Health, 10 Center Drive, Bethesda, MD 20892, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16946036" target="_blank"〉PubMed〈/a〉
    Keywords: *Adoptive Transfer ; Adult ; Antigens, Neoplasm/*immunology ; CD8-Positive T-Lymphocytes/*immunology ; Cancer Vaccines/therapeutic use ; Cells, Cultured ; Electroporation ; Female ; Genetic Engineering ; *Genetic Therapy ; HLA-A Antigens/immunology ; HLA-A2 Antigen ; Humans ; Interleukin-2/immunology/therapeutic use ; MART-1 Antigen ; Male ; Melanoma/immunology/secondary/*therapy ; Middle Aged ; Neoplasm Proteins/*immunology ; Receptors, Antigen, T-Cell, alpha-beta/*genetics/*immunology ; Transduction, Genetic ; Transgenes
    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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