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  • Cells, Cultured
  • American Association for the Advancement of Science (AAAS)  (30)
  • 2005-2009  (30)
  • 2007  (30)
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  • 2005-2009  (30)
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  • 1
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    Muscular thin films for building actuators and powering devices (2007)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2007-09-08
    Description: We demonstrate the assembly of biohybrid materials from engineered tissues and synthetic polymer thin films. The constructs were built by culturing neonatal rat ventricular cardiomyocytes on polydimethylsiloxane thin films micropatterned with extracellular matrix proteins to promote spatially ordered, two-dimensional myogenesis. The constructs, termed muscular thin films, adopted functional, three-dimensional conformations when released from a thermally sensitive polymer substrate and were designed to perform biomimetic tasks by varying tissue architecture, thin-film shape, and electrical-pacing protocol. These centimeter-scale constructs perform functions as diverse as gripping, pumping, walking, and swimming with fine spatial and temporal control and generating specific forces as high as 4 millinewtons per square millimeter.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Feinberg, Adam W -- Feigel, Alex -- Shevkoplyas, Sergey S -- Sheehy, Sean -- Whitesides, George M -- Parker, Kevin Kit -- New York, N.Y. -- Science. 2007 Sep 7;317(5843):1366-70.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Disease Biophysics Group, School of Engineering and Applied Sciences, Harvard University, Cambridge, MA 02138, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17823347" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Anisotropy ; Cell Culture Techniques ; Cells, Cultured ; Dimethylpolysiloxanes ; Microscopy, Fluorescence ; Motion ; Muscle Contraction ; *Myocardium ; Myocytes, Cardiac ; Rats ; Rats, Sprague-Dawley ; Robotics ; Silicones ; *Tissue Engineering
    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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    Regulation of hepatic stellate cell differentiation by the neurotrophin receptor p75NTR (2007)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2007-03-31
    Description: Differentiation of hepatic stellate cells (HSCs) to extracellular matrix- and growth factor-producing cells supports liver regeneration through promotion of hepatocyte proliferation. We show that the neurotrophin receptor p75NTR, a tumor necrosis factor receptor superfamily member expressed in HSCs after fibrotic and cirrhotic liver injury in humans, is a regulator of liver repair. In mice, depletion of p75NTR exacerbated liver pathology and inhibited hepatocyte proliferation in vivo. p75NTR-/- HSCs failed to differentiate to myofibroblasts and did not support hepatocyte proliferation. Moreover, inhibition of p75NTR signaling to the small guanosine triphosphatase Rho resulted in impaired HSC differentiation. Our results identify signaling from p75NTR to Rho as a mechanism for the regulation of HSC differentiation to regeneration-promoting cells that support hepatocyte proliferation in the diseased liver.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Passino, Melissa A -- Adams, Ryan A -- Sikorski, Shoana L -- Akassoglou, Katerina -- 5T32-GM07752/GM/NIGMS NIH HHS/ -- NS051470/NS/NINDS NIH HHS/ -- P30-NS047101/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 2007 Mar 30;315(5820):1853-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pharmacology, University of California, San Diego (UCSD), La Jolla, CA 92093-0636, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17395831" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Cell Differentiation ; Cell Proliferation ; Cells, Cultured ; Disease Progression ; Extracellular Matrix/metabolism ; Fibroblasts/*cytology ; Hepatocyte Growth Factor/metabolism ; Hepatocytes/*cytology ; Liver/*cytology/metabolism/pathology/physiology ; Liver Diseases/metabolism/*pathology ; *Liver Regeneration ; Mice ; Nerve Growth Factor/pharmacology ; Receptors, Nerve Growth Factor/genetics/*metabolism ; Signal Transduction ; rho GTP-Binding 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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  • 3
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    Mosaic organization of neural stem cells in the adult brain (2007)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2007-07-07
    Description: The in vivo potential of neural stem cells in the postnatal mouse brain is not known, but because they produce many different types of neurons, they must be either very versatile or very diverse. By specifically targeting stem cells and following their progeny in vivo, we showed that postnatal stem cells in different regions produce different types of neurons, even when heterotopically grafted or grown in culture. This suggests that rather than being plastic and homogeneous, neural stem cells are a restricted and diverse population of progenitors.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Merkle, Florian T -- Mirzadeh, Zaman -- Alvarez-Buylla, Arturo -- New York, N.Y. -- Science. 2007 Jul 20;317(5836):381-4. Epub 2007 Jul 5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurosurgery and Developmental and Stem Cell Biology Program, University of California, San Francisco, San Francisco, CA 94143-0525, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17615304" target="_blank"〉PubMed〈/a〉
    Keywords: Adult Stem Cells/*cytology ; Animals ; Animals, Newborn ; Astrocytes/cytology ; Brain/*cytology ; Cell Differentiation ; Cells, Cultured ; Interneurons/cytology ; Lateral Ventricles/cytology ; Mice ; Neuroglia/cytology ; Neurons/*cytology ; Olfactory Bulb/cytology ; Stem Cell Transplantation ; Transplantation, Heterotopic
    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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    Molecular basis for the nerve dependence of limb regeneration in an adult vertebrate (2007)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2007-11-03
    Description: The limb blastemal cells of an adult salamander regenerate the structures distal to the level of amputation, and the surface protein Prod 1 is a critical determinant of their proximodistal identity. The anterior gradient protein family member nAG is a secreted ligand for Prod 1 and a growth factor for cultured newt blastemal cells. nAG is sequentially expressed after amputation in the regenerating nerve and the wound epidermis-the key tissues of the stem cell niche-and its expression in both locations is abrogated by denervation. The local expression of nAG after electroporation is sufficient to rescue a denervated blastema and regenerate the distal structures. Our analysis brings together the positional identity of the blastema and the classical nerve dependence of limb regeneration.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2696928/" 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/PMC2696928/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kumar, Anoop -- Godwin, James W -- Gates, Phillip B -- Garza-Garcia, A Acely -- Brockes, Jeremy P -- G0600229/Medical Research Council/United Kingdom -- G0600229(77696)/Medical Research Council/United Kingdom -- G9537983/Medical Research Council/United Kingdom -- G9537983(56733)/Medical Research Council/United Kingdom -- MC_U117574559/Medical Research Council/United Kingdom -- New York, N.Y. -- Science. 2007 Nov 2;318(5851):772-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biochemistry and Molecular Biology, University College London, Gower Street, London WC1E 6BT, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17975060" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, CD59/*physiology ; COS Cells ; Cells, Cultured ; Cercopithecus aethiops ; Denervation ; Extremities/innervation ; Glycosylphosphatidylinositols/physiology ; Growth Substances ; Intercellular Signaling Peptides and Proteins/isolation & ; purification/*physiology/secretion ; Ligands ; Mice ; Notophthalmus viridescens ; Peripheral Nerves/*physiology ; Regeneration/*physiology ; Stem Cells/*cytology ; Two-Hybrid System Techniques
    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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    Protein kinase C beta and prolyl isomerase 1 regulate mitochondrial effects of the life-span determinant p66Shc (2007)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2007-02-03
    Description: The 66-kilodalton isoform of the growth factor adapter Shc (p66Shc) translates oxidative damage into cell death by acting as reactive oxygen species (ROS) producer within mitochondria. However, the signaling link between cellular stress and mitochondrial proapoptotic activity of p66Shc was not known. We demonstrate that protein kinase C beta, activated by oxidative conditions in the cell, induces phosphorylation of p66Shc and triggers mitochondrial accumulation of the protein after it is recognized by the prolyl isomerase Pin1. Once imported, p66Shc causes alterations of mitochondrial Ca2+ responses and three-dimensional structure, thus inducing apoptosis. These data identify a signaling route that activates an apoptotic inducer shortening the life span and could be a potential target of pharmacological approaches to inhibit aging.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pinton, Paolo -- Rimessi, Alessandro -- Marchi, Saverio -- Orsini, Francesca -- Migliaccio, Enrica -- Giorgio, Marco -- Contursi, Cristina -- Minucci, Saverio -- Mantovani, Fiamma -- Wieckowski, Mariusz R -- Del Sal, Giannino -- Pelicci, Pier Giuseppe -- Rizzuto, Rosario -- GGP05284/Telethon/Italy -- New York, N.Y. -- Science. 2007 Feb 2;315(5812):659-63.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Experimental and Diagnostic Medicine, Section of General Pathology and Interdisciplinary Center for the Study of Inflammation (ICSI), University of Ferrara, Ferrera, Italy.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17272725" target="_blank"〉PubMed〈/a〉
    Keywords: Adaptor Proteins, Signal Transducing/genetics/*metabolism ; Adenosine Triphosphate/metabolism/pharmacology ; Animals ; *Apoptosis ; Calcium/metabolism ; Calcium Signaling ; *Cell Aging ; Cell Survival ; Cells, Cultured ; Cyclosporine/pharmacology ; Hydrogen Peroxide/metabolism/pharmacology ; Mice ; Mitochondria/*metabolism/ultrastructure ; Mutation ; Oxidative Stress ; Peptidylprolyl Isomerase/*metabolism ; Permeability ; Phosphorylation ; Protein Kinase C/antagonists & inhibitors/genetics/*metabolism ; Protein Kinase C beta ; Reactive Oxygen Species/metabolism ; Recombinant Fusion Proteins/metabolism ; Shc Signaling Adaptor Proteins ; *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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    Apoptosis initiated when BH3 ligands engage multiple Bcl-2 homologs, not Bax or Bak (2007)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2007-02-10
    Description: A central issue in the regulation of apoptosis by the Bcl-2 family is whether its BH3-only members initiate apoptosis by directly binding to the essential cell-death mediators Bax and Bak, or whether they can act indirectly, by engaging their pro-survival Bcl-2-like relatives. Contrary to the direct-activation model, we show that Bax and Bak can mediate apoptosis without discernable association with the putative BH3-only activators (Bim, Bid, and Puma), even in cells with no Bim or Bid and reduced Puma. Our results indicate that BH3-only proteins induce apoptosis at least primarily by engaging the multiple pro-survival relatives guarding Bax and Bak.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Willis, Simon N -- Fletcher, Jamie I -- Kaufmann, Thomas -- van Delft, Mark F -- Chen, Lin -- Czabotar, Peter E -- Ierino, Helen -- Lee, Erinna F -- Fairlie, W Douglas -- Bouillet, Philippe -- Strasser, Andreas -- Kluck, Ruth M -- Adams, Jerry M -- Huang, David C S -- CA43540/CA/NCI NIH HHS/ -- CA80188/CA/NCI NIH HHS/ -- Wellcome Trust/United Kingdom -- New York, N.Y. -- Science. 2007 Feb 9;315(5813):856-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Walter and Eliza Hall Institute of Medical Research, 1G Royal Parade, Parkville, Victoria 3050, Australia.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17289999" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Apoptosis ; Apoptosis Regulatory Proteins/chemistry/genetics/*metabolism ; BH3 Interacting Domain Death Agonist Protein/chemistry/genetics/*metabolism ; Cell Line ; Cells, Cultured ; Humans ; Ligands ; Membrane Proteins/chemistry/genetics/*metabolism ; Mice ; Mice, Knockout ; Models, Biological ; Mutation ; Myeloid Cell Leukemia Sequence 1 Protein ; Neoplasm Proteins/metabolism ; Protein Structure, Tertiary ; Proteins/metabolism ; Proto-Oncogene Proteins/chemistry/genetics/*metabolism ; Proto-Oncogene Proteins c-bcl-2/*metabolism ; Tumor Suppressor Proteins/genetics/metabolism ; bcl-2 Homologous Antagonist-Killer Protein/metabolism ; bcl-2-Associated X Protein/chemistry/*metabolism ; bcl-Associated Death Protein/metabolism ; bcl-X Protein/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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    Hardwiring the brain: endocannabinoids shape neuronal connectivity (2007)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2007-05-26
    Description: The roles of endocannabinoid signaling during central nervous system development are unknown. We report that CB(1) cannabinoid receptors (CB(1)Rs) are enriched in the axonal growth cones of gamma-aminobutyric acid-containing (GABAergic) interneurons in the rodent cortex during late gestation. Endocannabinoids trigger CB(1)R internalization and elimination from filopodia and induce chemorepulsion and collapse of axonal growth cones of these GABAergic interneurons by activating RhoA. Similarly, endocannabinoids diminish the galvanotropism of Xenopus laevis spinal neurons. These findings, together with the impaired target selection of cortical GABAergic interneurons lacking CB(1)Rs, identify endocannabinoids as axon guidance cues and demonstrate that endocannabinoid signaling regulates synaptogenesis and target selection in vivo.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Berghuis, Paul -- Rajnicek, Ann M -- Morozov, Yury M -- Ross, Ruth A -- Mulder, Jan -- Urban, Gabriella M -- Monory, Krisztina -- Marsicano, Giovanni -- Matteoli, Michela -- Canty, Alison -- Irving, Andrew J -- Katona, Istvan -- Yanagawa, Yuchio -- Rakic, Pasko -- Lutz, Beat -- Mackie, Ken -- Harkany, Tibor -- DA00286/DA/NIDA NIH HHS/ -- DA015916/DA/NIDA NIH HHS/ -- DA11322/DA/NIDA NIH HHS/ -- New York, N.Y. -- Science. 2007 May 25;316(5828):1212-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Molecular Neurobiology, Department of Medical Biochemistry and Biophysics, Karolinska Institutet, S-17177 Stockholm, Sweden.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17525344" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Axons/physiology ; Cannabinoid Receptor Modulators/metabolism/*physiology ; Cell Movement ; Cells, Cultured ; Cerebral Cortex/cytology/embryology/ultrastructure ; *Endocannabinoids ; Growth Cones/physiology/ultrasonography ; In Situ Hybridization ; Interneurons/metabolism/*physiology/ultrasonography ; Mice ; Mice, Inbred C57BL ; Microscopy, Confocal ; Rats ; Rats, Sprague-Dawley ; Receptor, Cannabinoid, CB1/agonists/*physiology ; Signal Transduction ; Stem Cells/metabolism ; Synapses/physiology/ultrasonography ; Xenopus Proteins/physiology ; Xenopus laevis ; gamma-Aminobutyric Acid/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
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    Dynamic visualization of thrombopoiesis within bone marrow (2007)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2007-09-22
    Description: Platelets are generated from megakaryocytes (MKs) in mammalian bone marrow (BM) by mechanisms that remain poorly understood. Here we describe the use of multiphoton intravital microscopy in intact BM to visualize platelet generation in mice. MKs were observed as sessile cells that extended dynamic proplatelet-like protrusions into microvessels. These intravascular extensions appeared to be sheared from their transendothelial stems by flowing blood, resulting in the appearance of proplatelets in peripheral blood. In vitro, proplatelet production from differentiating MKs was enhanced by fluid shear. These results confirm the concept of proplatelet formation in vivo and are consistent with the possibility that blood flow-induced hydrodynamic shear stress is a biophysical determinant of thrombopoiesis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Junt, Tobias -- Schulze, Harald -- Chen, Zhao -- Massberg, Steffen -- Goerge, Tobias -- Krueger, Andreas -- Wagner, Denisa D -- Graf, Thomas -- Italiano, Joseph E Jr -- Shivdasani, Ramesh A -- von Andrian, Ulrich H -- HL068130/HL/NHLBI NIH HHS/ -- HL56949/HL/NHLBI NIH HHS/ -- HL63143/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 2007 Sep 21;317(5845):1767-70.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Immune Disease Institute and Department of Pathology, Harvard Medical School, Boston, MA 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17885137" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Bacterial Proteins ; Blood Platelets/*cytology ; Bone Marrow/*physiology ; Cells, Cultured ; Luminescent Proteins ; Megakaryocytes/*cytology ; Mice ; Microscopy, Fluorescence, Multiphoton ; Platelet Membrane Glycoprotein IIb ; Shear Strength ; Thrombopoiesis/*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
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    Cell signaling. mTOR, unleashed (2007)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2007-11-10
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Proud, Christopher G -- New York, N.Y. -- Science. 2007 Nov 9;318(5852):926-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biochemistry and Molecular Biology, University of British Columbia, 2350 Health Sciences Mall, Vancouver, British Columbia V6T 1Z3, Canada.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17991850" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acids/metabolism ; Cells, Cultured ; Guanosine Triphosphate/metabolism ; Humans ; Insulin/metabolism ; Models, Biological ; Monomeric GTP-Binding Proteins/*metabolism ; Multiprotein Complexes ; Neuropeptides/*metabolism ; Protein Binding ; Protein Kinases/*metabolism ; Proteins ; *Signal Transduction ; Sirolimus/metabolism/pharmacology ; TOR Serine-Threonine Kinases ; Tacrolimus Binding Protein 1A/metabolism ; Tacrolimus Binding Proteins/antagonists & inhibitors/*metabolism ; Transcription Factors/*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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  • 10
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    Host immune system gene targeting by a viral miRNA (2007)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2007-07-21
    Description: Virally encoded microRNAs (miRNAs) have recently been discovered in herpesviruses. However, their biological roles are mostly unknown. We developed an algorithm for the prediction of miRNA targets and applied it to human cytomegalovirus miRNAs, resulting in the identification of the major histocompatibility complex class I-related chain B (MICB) gene as a top candidate target of hcmv-miR-UL112. MICB is a stress-induced ligand of the natural killer (NK) cell activating receptor NKG2D and is critical for the NK cell killing of virus-infected cells and tumor cells. We show that hcmv-miR-UL112 specifically down-regulates MICB expression during viral infection, leading to decreased binding of NKG2D and reduced killing by NK cells. Our results reveal a miRNA-based immunoevasion mechanism that appears to be exploited by human cytomegalovirus.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4283197/" 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/PMC4283197/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Stern-Ginossar, Noam -- Elefant, Naama -- Zimmermann, Albert -- Wolf, Dana G -- Saleh, Nivin -- Biton, Moshe -- Horwitz, Elad -- Prokocimer, Zafnat -- Prichard, Mark -- Hahn, Gabriele -- Goldman-Wohl, Debra -- Greenfield, Caryn -- Yagel, Simcha -- Hengel, Hartmut -- Altuvia, Yael -- Margalit, Hanah -- Mandelboim, Ofer -- N01 AI030049/AI/NIAID NIH HHS/ -- N01 AI30049/AI/NIAID NIH HHS/ -- N01-30049/PHS HHS/ -- New York, N.Y. -- Science. 2007 Jul 20;317(5836):376-81.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Lautenberg Center for General and Tumor Immunology, Hebrew University Hadassah Medical School, Jerusalem, Israel.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17641203" target="_blank"〉PubMed〈/a〉
    Keywords: 3' Untranslated Regions/metabolism ; Algorithms ; Binding Sites ; Cell Line, Tumor ; Cells, Cultured ; Cytomegalovirus/genetics/*immunology/*pathogenicity ; Cytotoxicity, Immunologic ; Down-Regulation ; Histocompatibility Antigens Class I/*genetics/metabolism ; Humans ; Killer Cells, Natural/immunology ; Ligands ; MicroRNAs/genetics/*metabolism ; NK Cell Lectin-Like Receptor Subfamily K ; RNA, Viral/*metabolism ; Receptors, Immunologic/metabolism ; Receptors, Natural Killer Cell ; Transduction, Genetic
    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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