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  • American Association for the Advancement of Science (AAAS)  (113)
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  • 1
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    Medicine. The blood stem cell Holy Grail? (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-09-11
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sauvageau, Guy -- Humphries, R Keith -- New York, N.Y. -- Science. 2010 Sep 10;329(5997):1291-2. doi: 10.1126/science.1195173.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Molecular Genetics of Stem Cells Laboratory, Institute of Research in Immunology and Cancer, University of Montreal, Montreal, QC H3C 3J7, Canada. guy.sauvageau@umontreal.ca〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20829472" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, CD34/analysis ; Cell Lineage ; Cell Proliferation ; Cells, Cultured ; Fetal Blood/cytology ; *Hematopoiesis ; Hematopoietic Stem Cell Transplantation ; Hematopoietic Stem Cells/*cytology/*drug effects/physiology ; Humans ; Mice ; Purines/chemistry/metabolism/*pharmacology ; Receptors, Aryl Hydrocarbon/*antagonists & inhibitors/metabolism ; Small Molecule Libraries ; Species Specificity
    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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    Developmental biology. Microenvironment mimicry (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-08-28
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bhatia, Mickie -- New York, N.Y. -- Science. 2010 Aug 27;329(5995):1024-5. doi: 10.1126/science.1194919.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Stem Cell and Cancer Research Institute, McMaster University, Hamilton, Ontario L8N 3Z5, Canada. mbhatia@mcmaster.ca〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20798306" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Culture Techniques/*methods ; Cell Differentiation ; Cell Division ; Cells, Cultured ; Elasticity ; Humans ; Hydrogels ; Mice ; Muscle Fibers, Skeletal/*cytology/physiology ; Myoblasts, Skeletal/cytology/physiology ; Regeneration ; Stem Cell Niche/*physiology ; Stem Cell Transplantation ; Stem Cells/*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
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    Astrocytes control breathing through pH-dependent release of ATP (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-07-22
    Description: Astrocytes provide structural and metabolic support for neuronal networks, but direct evidence demonstrating their active role in complex behaviors is limited. Central respiratory chemosensitivity is an essential mechanism that, via regulation of breathing, maintains constant levels of blood and brain pH and partial pressure of CO2. We found that astrocytes of the brainstem chemoreceptor areas are highly chemosensitive. They responded to physiological decreases in pH with vigorous elevations in intracellular Ca2+ and release of adenosine triphosphate (ATP). ATP propagated astrocytic Ca2+ excitation, activated chemoreceptor neurons, and induced adaptive increases in breathing. Mimicking pH-evoked Ca2+ responses by means of optogenetic stimulation of astrocytes expressing channelrhodopsin-2 activated chemoreceptor neurons via an ATP-dependent mechanism and triggered robust respiratory responses in vivo. This demonstrates a potentially crucial role for brain glial cells in mediating a fundamental physiological reflex.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3160742/" 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/PMC3160742/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gourine, Alexander V -- Kasymov, Vitaliy -- Marina, Nephtali -- Tang, Feige -- Figueiredo, Melina F -- Lane, Samantha -- Teschemacher, Anja G -- Spyer, K Michael -- Deisseroth, Karl -- Kasparov, Sergey -- 079040/Wellcome Trust/United Kingdom -- PG/09/064/27886/British Heart Foundation/United Kingdom -- British Heart Foundation/United Kingdom -- New York, N.Y. -- Science. 2010 Jul 30;329(5991):571-5. doi: 10.1126/science.1190721. Epub 2010 Jul 15.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Neuroscience, Physiology, and Pharmacology, University College London, London WC1E 6BT, UK. a.gourine@ucl.ac.uk〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20647426" target="_blank"〉PubMed〈/a〉
    Keywords: Adenosine Triphosphate/*metabolism ; Animals ; Astrocytes/*physiology ; Brain Stem/cytology/*physiology ; Calcium/metabolism ; Carbon Dioxide/analysis/blood ; Cells, Cultured ; Chemoreceptor Cells/*physiology ; Exocytosis ; Gap Junctions/metabolism ; Hydrogen-Ion Concentration ; In Vitro Techniques ; Light ; Medulla Oblongata/cytology/*physiology ; Membrane Potentials ; Rats ; Rats, Sprague-Dawley ; Receptors, Purinergic P2/metabolism ; *Respiration ; Rhodopsin/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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  • 4
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    Platelets amplify inflammation in arthritis via collagen-dependent microparticle production (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-01-30
    Description: In addition to their pivotal role in thrombosis and wound repair, platelets participate in inflammatory responses. We investigated the role of platelets in the autoimmune disease rheumatoid arthritis. We identified platelet microparticles--submicrometer vesicles elaborated by activated platelets--in joint fluid from patients with rheumatoid arthritis and other forms of inflammatory arthritis, but not in joint fluid from patients with osteoarthritis. Platelet microparticles were proinflammatory, eliciting cytokine responses from synovial fibroblasts via interleukin-1. Consistent with these findings, depletion of platelets attenuated murine inflammatory arthritis. Using both pharmacologic and genetic approaches, we identified the collagen receptor glycoprotein VI as a key trigger for platelet microparticle generation in arthritis pathophysiology. Thus, these findings demonstrate a previously unappreciated role for platelets and their activation-induced microparticles in inflammatory joint diseases.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2927861/" 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/PMC2927861/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Boilard, Eric -- Nigrovic, Peter A -- Larabee, Katherine -- Watts, Gerald F M -- Coblyn, Jonathan S -- Weinblatt, Michael E -- Massarotti, Elena M -- Remold-O'Donnell, Eileen -- Farndale, Richard W -- Ware, Jerry -- Lee, David M -- G0500707/Medical Research Council/United Kingdom -- HL091269/HL/NHLBI NIH HHS/ -- HL50545/HL/NHLBI NIH HHS/ -- K08AR051321/AR/NIAMS NIH HHS/ -- P01 AI065858/AI/NIAID NIH HHS/ -- R01 HL050545/HL/NHLBI NIH HHS/ -- R01 HL050545-16/HL/NHLBI NIH HHS/ -- R01 HL050545-18/HL/NHLBI NIH HHS/ -- R21 HL091269/HL/NHLBI NIH HHS/ -- R21 HL091269-01A2/HL/NHLBI NIH HHS/ -- RG/09/003/27122/British Heart Foundation/United Kingdom -- British Heart Foundation/United Kingdom -- Medical Research Council/United Kingdom -- New York, N.Y. -- Science. 2010 Jan 29;327(5965):580-3. doi: 10.1126/science.1181928.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Rheumatology, Immunology and Allergy, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20110505" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Arthritis/blood/immunology ; Arthritis, Rheumatoid/*blood/*immunology/physiopathology ; Blood Platelets/cytology/*physiology/ultrastructure ; Cell-Derived Microparticles/metabolism/*physiology ; Cells, Cultured ; Collagen/*metabolism ; Cytokines/*metabolism ; Extracellular Matrix/metabolism ; Fibroblasts/immunology/metabolism ; Humans ; Interleukin-1/metabolism ; Mice ; Mice, Transgenic ; Platelet Activation ; Platelet Membrane Glycoproteins/metabolism ; Receptors, Collagen/metabolism ; Synovial Fluid/cytology/*immunology ; Synovial Membrane/cytology/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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  • 5
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    Substrate elasticity regulates skeletal muscle stem cell self-renewal in culture (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-07-22
    Description: Stem cells that naturally reside in adult tissues, such as muscle stem cells (MuSCs), exhibit robust regenerative capacity in vivo that is rapidly lost in culture. Using a bioengineered substrate to recapitulate key biophysical and biochemical niche features in conjunction with a highly automated single-cell tracking algorithm, we show that substrate elasticity is a potent regulator of MuSC fate in culture. Unlike MuSCs on rigid plastic dishes (approximately 10(6) kilopascals), MuSCs cultured on soft hydrogel substrates that mimic the elasticity of muscle (12 kilopascals) self-renew in vitro and contribute extensively to muscle regeneration when subsequently transplanted into mice and assayed histologically and quantitatively by noninvasive bioluminescence imaging. Our studies provide novel evidence that by recapitulating physiological tissue rigidity, propagation of adult muscle stem cells is possible, enabling future cell-based therapies for muscle-wasting diseases.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2929271/" 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/PMC2929271/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gilbert, P M -- Havenstrite, K L -- Magnusson, K E G -- Sacco, A -- Leonardi, N A -- Kraft, P -- Nguyen, N K -- Thrun, S -- Lutolf, M P -- Blau, H M -- 2 T32 HD007249/HD/NICHD NIH HHS/ -- 52005886/Howard Hughes Medical Institute/ -- AG009521/AG/NIA NIH HHS/ -- AG020961/AG/NIA NIH HHS/ -- CA09151/CA/NCI NIH HHS/ -- HL096113/HL/NHLBI NIH HHS/ -- R01 AG009521/AG/NIA NIH HHS/ -- R01 AG009521-25/AG/NIA NIH HHS/ -- R01 AG020961/AG/NIA NIH HHS/ -- R01 AG020961-06A2/AG/NIA NIH HHS/ -- R01 AG020961-07/AG/NIA NIH HHS/ -- R01 HL096113/HL/NHLBI NIH HHS/ -- R01 HL096113-03/HL/NHLBI NIH HHS/ -- T32 CA009151/CA/NCI NIH HHS/ -- T32 CA009151-35/CA/NCI NIH HHS/ -- T32 HD007249/HD/NICHD NIH HHS/ -- T32 HD007249-25/HD/NICHD NIH HHS/ -- U01 HL100397/HL/NHLBI NIH HHS/ -- U01 HL100397-01/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 2010 Aug 27;329(5995):1078-81. doi: 10.1126/science.1191035. Epub 2010 Jul 15.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Baxter Laboratory for Stem Cell Biology, Department of Microbiology and Immunology, Institute for Stem Cell Biology and Regenerative Medicine, Stanford University School of Medicine, Stanford, CA 94305, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20647425" target="_blank"〉PubMed〈/a〉
    Keywords: Algorithms ; Animals ; Cell Count ; Cell Culture Techniques/*methods ; Cell Death ; Cell Differentiation ; Cell Division ; Cell Lineage ; Cell Separation ; Cell Survival ; Cells, Cultured ; Elastic Modulus ; Hydrogels ; Mice ; Mice, Inbred C57BL ; Mice, Inbred NOD ; Mice, SCID ; Mice, Transgenic ; Muscle Fibers, Skeletal/*cytology/physiology ; Muscle, Skeletal/*cytology ; Polyethylene Glycols ; Regeneration ; Satellite Cells, Skeletal Muscle/cytology ; Stem Cell Niche/*physiology ; Stem Cell Transplantation ; Stem Cells/cytology/*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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  • 6
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    Loss of Rap1 induces telomere recombination in the absence of NHEJ or a DNA damage signal (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-03-27
    Description: Shelterin is an essential telomeric protein complex that prevents DNA damage signaling and DNA repair at mammalian chromosome ends. Here we report on the role of the TRF2-interacting factor Rap1, a conserved shelterin subunit of unknown function. We removed Rap1 from mouse telomeres either through gene deletion or by replacing TRF2 with a mutant that does not bind Rap1. Rap1 was dispensable for the essential functions of TRF2--repression of ATM kinase signaling and nonhomologous end joining (NHEJ)--and mice lacking telomeric Rap1 were viable and fertile. However, Rap1 was critical for the repression of homology-directed repair (HDR), which can alter telomere length. The data reveal that HDR at telomeres can take place in the absence of DNA damage foci and underscore the functional compartmentalization within shelterin.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2864730/" 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/PMC2864730/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sfeir, Agnel -- Kabir, Shaheen -- van Overbeek, Megan -- Celli, Giulia B -- de Lange, Titia -- AG016642/AG/NIA NIH HHS/ -- GM049046/GM/NIGMS NIH HHS/ -- R01 AG016642/AG/NIA NIH HHS/ -- R01 AG016642-01/AG/NIA NIH HHS/ -- R01 AG016642-02/AG/NIA NIH HHS/ -- R01 AG016642-03/AG/NIA NIH HHS/ -- R01 AG016642-04/AG/NIA NIH HHS/ -- R01 AG016642-05/AG/NIA NIH HHS/ -- R01 AG016642-06/AG/NIA NIH HHS/ -- R01 AG016642-07/AG/NIA NIH HHS/ -- R01 AG016642-08/AG/NIA NIH HHS/ -- R01 AG016642-09/AG/NIA NIH HHS/ -- R01 AG016642-10/AG/NIA NIH HHS/ -- R01 AG016642-11/AG/NIA NIH HHS/ -- R01 GM049046/GM/NIGMS NIH HHS/ -- R01 GM049046-07/GM/NIGMS NIH HHS/ -- R01 GM049046-08/GM/NIGMS NIH HHS/ -- R01 GM049046-09/GM/NIGMS NIH HHS/ -- R01 GM049046-10/GM/NIGMS NIH HHS/ -- R01 GM049046-11/GM/NIGMS NIH HHS/ -- R01 GM049046-12/GM/NIGMS NIH HHS/ -- R37 GM049046/GM/NIGMS NIH HHS/ -- R37 GM049046-13/GM/NIGMS NIH HHS/ -- R37 GM049046-14/GM/NIGMS NIH HHS/ -- R37 GM049046-15/GM/NIGMS NIH HHS/ -- R37 GM049046-16/GM/NIGMS NIH HHS/ -- R37 GM049046-17/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2010 Mar 26;327(5973):1657-61. doi: 10.1126/science.1185100.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉The Rockefeller University, 1230 York Avenue, New York, NY 10065, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20339076" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Ataxia Telangiectasia Mutated Proteins ; Cell Cycle Proteins/metabolism ; Cell Proliferation ; Cells, Cultured ; Checkpoint Kinase 2 ; *DNA Damage ; *DNA Repair ; DNA-Binding Proteins/metabolism ; Gene Deletion ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Molecular Sequence Data ; Protein-Serine-Threonine Kinases/metabolism ; Recombination, Genetic ; Signal Transduction ; Sister Chromatid Exchange ; Telomere/*genetics/metabolism ; Telomere-Binding Proteins/chemistry/*genetics/*metabolism ; Telomeric Repeat Binding Protein 2/genetics/metabolism ; Tumor Suppressor 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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  • 7
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    Alpha-synuclein promotes SNARE-complex assembly in vivo and in vitro (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-08-28
    Description: Presynaptic nerve terminals release neurotransmitters repeatedly, often at high frequency, and in relative isolation from neuronal cell bodies. Repeated release requires cycles of soluble N-ethylmaleimide-sensitive factor attachment protein receptor (SNARE)-complex assembly and disassembly, with continuous generation of reactive SNARE-protein intermediates. Although many forms of neurodegeneration initiate presynaptically, only few pathogenic mechanisms are known, and the functions of presynaptic proteins linked to neurodegeneration, such as alpha-synuclein, remain unclear. Here, we show that maintenance of continuous presynaptic SNARE-complex assembly required a nonclassical chaperone activity mediated by synucleins. Specifically, alpha-synuclein directly bound to the SNARE-protein synaptobrevin-2/vesicle-associated membrane protein 2 (VAMP2) and promoted SNARE-complex assembly. Moreover, triple-knockout mice lacking synucleins developed age-dependent neurological impairments, exhibited decreased SNARE-complex assembly, and died prematurely. Thus, synucleins may function to sustain normal SNARE-complex assembly in a presynaptic terminal during aging.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3235365/" 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/PMC3235365/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Burre, Jacqueline -- Sharma, Manu -- Tsetsenis, Theodoros -- Buchman, Vladimir -- Etherton, Mark R -- Sudhof, Thomas C -- 075615/Wellcome Trust/United Kingdom -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2010 Sep 24;329(5999):1663-7. doi: 10.1126/science.1195227. Epub 2010 Aug 26.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular and Cellular Physiology, and Howard Hughes Medical Institute, Stanford University, 1050 Arastradero Road, Palo Alto, CA 94304-5543, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20798282" target="_blank"〉PubMed〈/a〉
    Keywords: *Aging ; Animals ; Cell Line ; Cells, Cultured ; HSP40 Heat-Shock Proteins/metabolism ; Humans ; Membrane Fusion ; Membrane Proteins/metabolism ; Mice ; Mice, Knockout ; Mice, Transgenic ; Nerve Degeneration/*metabolism ; Neurons/*metabolism ; Presynaptic Terminals/*metabolism ; Protein Binding ; Rats ; Recombinant Fusion Proteins/metabolism ; SNARE Proteins/*metabolism ; Vesicle-Associated Membrane Protein 2/metabolism ; alpha-Synuclein/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
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    Inhibition of NF-kappaB signaling by A20 through disruption of ubiquitin enzyme complexes (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-02-27
    Description: A20 negatively regulates inflammation by inhibiting the nuclear factor kappaB (NF-kappaB) transcription factor in the tumor necrosis factor-receptor (TNFR) and Toll-like receptor (TLR) pathways. A20 contains deubiquitinase and E3 ligase domains and thus has been proposed to function as a ubiquitin-editing enzyme downstream of TNFR1 by inactivating ubiquitinated RIP1. However, it remains unclear how A20 terminates NF-kappaB signaling downstream of TLRs. We have shown that A20 inhibited the E3 ligase activities of TRAF6, TRAF2, and cIAP1 by antagonizing interactions with the E2 ubiquitin conjugating enzymes Ubc13 and UbcH5c. A20, together with the regulatory molecule TAX1BP1, interacted with Ubc13 and UbcH5c and triggered their ubiquitination and proteasome-dependent degradation. These findings suggest mechanism of A20 action in the inhibition of inflammatory signaling pathways.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3025292/" 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/PMC3025292/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Shembade, Noula -- Ma, Averil -- Harhaj, Edward W -- R01 CA135362/CA/NCI NIH HHS/ -- R01 CA135362-04/CA/NCI NIH HHS/ -- R01 DK071939/DK/NIDDK NIH HHS/ -- R01 DK071939-07/DK/NIDDK NIH HHS/ -- R01 GM083143/GM/NIGMS NIH HHS/ -- R01 GM083143-03/GM/NIGMS NIH HHS/ -- R01CA135362/CA/NCI NIH HHS/ -- R01GM083143/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2010 Feb 26;327(5969):1135-9. doi: 10.1126/science.1182364.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Microbiology and Immunology, Sylvester Comprehensive Cancer Center, The University of Miami, Miller School of Medicine, Miami, FL 33136, USA. nshembade@med.miami.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20185725" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Motifs ; Animals ; Cells, Cultured ; Cysteine Endopeptidases/chemistry/genetics/*metabolism ; Gene Products, tax/metabolism ; Inflammation/*metabolism ; Inhibitor of Apoptosis Proteins/antagonists & inhibitors/metabolism ; Interleukin-1/immunology/metabolism ; Intracellular Signaling Peptides and Proteins/chemistry/genetics/*metabolism ; Mice ; NF-kappa B/*metabolism ; Neoplasm Proteins/metabolism ; Proteasome Endopeptidase Complex/metabolism ; Protein Binding ; Receptor-Interacting Protein Serine-Threonine Kinases/metabolism ; Receptors, Tumor Necrosis Factor, Type I/metabolism ; *Signal Transduction ; TNF Receptor-Associated Factor 2/antagonists & inhibitors/metabolism ; TNF Receptor-Associated Factor 6/antagonists & inhibitors/metabolism ; Tumor Necrosis Factor-alpha/immunology/metabolism ; Ubiquitin-Conjugating Enzymes/*metabolism ; Ubiquitin-Protein Ligases/*antagonists & inhibitors/metabolism ; Ubiquitinated Proteins/metabolism ; Ubiquitination ; Zinc Fingers
    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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    FCHo proteins are nucleators of clathrin-mediated endocytosis (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-05-08
    Description: Clathrin-mediated endocytosis, the major pathway for ligand internalization into eukaryotic cells, is thought to be initiated by the clustering of clathrin and adaptors around receptors destined for internalization. However, here we report that the membrane-sculpting F-BAR domain-containing Fer/Cip4 homology domain-only proteins 1 and 2 (FCHo1/2) were required for plasma membrane clathrin-coated vesicle (CCV) budding and marked sites of CCV formation. Changes in FCHo1/2 expression levels correlated directly with numbers of CCV budding events, ligand endocytosis, and synaptic vesicle marker recycling. FCHo1/2 proteins bound specifically to the plasma membrane and recruited the scaffold proteins eps15 and intersectin, which in turn engaged the adaptor complex AP2. The FCHo F-BAR membrane-bending activity was required, leading to the proposal that FCHo1/2 sculpt the initial bud site and recruit the clathrin machinery for CCV formation.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2883440/" 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/PMC2883440/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Henne, William Mike -- Boucrot, Emmanuel -- Meinecke, Michael -- Evergren, Emma -- Vallis, Yvonne -- Mittal, Rohit -- McMahon, Harvey T -- MC_U105178795/Medical Research Council/United Kingdom -- U.1051.02.007(78795)/Medical Research Council/United Kingdom -- Medical Research Council/United Kingdom -- New York, N.Y. -- Science. 2010 Jun 4;328(5983):1281-4. doi: 10.1126/science.1188462. Epub 2010 May 6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Medical Research Council, Laboratory of Molecular Biology (MRC-LMB), Hills Road, Cambridge CB2 0QH, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20448150" target="_blank"〉PubMed〈/a〉
    Keywords: Adaptor Protein Complex 2/metabolism ; Adaptor Proteins, Signal Transducing ; Adaptor Proteins, Vesicular Transport/metabolism ; Animals ; Calcium-Binding Proteins/metabolism ; Cell Line ; Cell Membrane/metabolism ; Cells, Cultured ; Clathrin/*metabolism ; Clathrin-Coated Vesicles/*metabolism ; *Endocytosis ; HeLa Cells ; Humans ; Intracellular Signaling Peptides and Proteins/metabolism ; Membrane Proteins ; Mice ; Models, Molecular ; Neurons/cytology/metabolism ; Phosphoproteins/metabolism ; Protein Multimerization ; Protein Structure, Tertiary ; Proteins/chemistry/*metabolism ; RNA Interference ; Rats ; Rats, Sprague-Dawley ; Recombinant Fusion Proteins/metabolism ; Synaptic Vesicles/metabolism
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  • 10
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    A critical role for LTA4H in limiting chronic pulmonary neutrophilic inflammation (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-09-04
    Description: Leukotriene A(4) hydrolase (LTA(4)H) is a proinflammatory enzyme that generates the inflammatory mediator leukotriene B(4) (LTB(4)). LTA(4)H also possesses aminopeptidase activity with unknown substrate and physiological importance; we identified the neutrophil chemoattractant proline-glycine-proline (PGP) as this physiological substrate. PGP is a biomarker for chronic obstructive pulmonary disease (COPD) and is implicated in neutrophil persistence in the lung. In acute neutrophil-driven inflammation, PGP was degraded by LTA(4)H, which facilitated the resolution of inflammation. In contrast, cigarette smoke, a major risk factor for the development of COPD, selectively inhibited LTA(4)H aminopeptidase activity, which led to the accumulation of PGP and neutrophils. These studies imply that therapeutic strategies inhibiting LTA(4)H to prevent LTB(4) generation may not reduce neutrophil recruitment because of elevated levels of PGP.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3072752/" 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/PMC3072752/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Snelgrove, Robert J -- Jackson, Patricia L -- Hardison, Matthew T -- Noerager, Brett D -- Kinloch, Andrew -- Gaggar, Amit -- Shastry, Suresh -- Rowe, Steven M -- Shim, Yun M -- Hussell, Tracy -- Blalock, J Edwin -- 082727/Z/07/Z/Wellcome Trust/United Kingdom -- 1K23DK075788/DK/NIDDK NIH HHS/ -- 1R03DK084110-01/DK/NIDDK NIH HHS/ -- G0400795/Medical Research Council/United Kingdom -- G0802752/Medical Research Council/United Kingdom -- HL07783/HL/NHLBI NIH HHS/ -- HL087824/HL/NHLBI NIH HHS/ -- HL090999/HL/NHLBI NIH HHS/ -- HL102371-A1/HL/NHLBI NIH HHS/ -- K08HL091127/HL/NHLBI NIH HHS/ -- P171/03/C1/048/Medical Research Council/United Kingdom -- P30 DK079337/DK/NIDDK NIH HHS/ -- P30AR050948/AR/NIAMS NIH HHS/ -- P30CA13148/CA/NCI NIH HHS/ -- P50 AT00477/AT/NCCIH NIH HHS/ -- R01 HL077783/HL/NHLBI NIH HHS/ -- R01 HL077783-05/HL/NHLBI NIH HHS/ -- R01 HL087824/HL/NHLBI NIH HHS/ -- R01 HL087824-02/HL/NHLBI NIH HHS/ -- R01 HL090999/HL/NHLBI NIH HHS/ -- R01 HL090999-02S1/HL/NHLBI NIH HHS/ -- R01 HL090999-04/HL/NHLBI NIH HHS/ -- R01 HL102371/HL/NHLBI NIH HHS/ -- RR19231/RR/NCRR NIH HHS/ -- U54CA100949/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 2010 Oct 1;330(6000):90-4. doi: 10.1126/science.1190594. Epub 2010 Sep 2.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Pulmonary, Allergy and Critical Care Medicine, University of Alabama at Birmingham Lung Health Center, Department of Medicine, University of Alabama at Birmingham, Birmingham, AL 35294, USA. rjs198@imperial.ac.uk〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20813919" target="_blank"〉PubMed〈/a〉
    Keywords: Acetylation ; Animals ; Bronchoalveolar Lavage Fluid/chemistry ; Cells, Cultured ; Chemokines, CXC/metabolism ; Chemotaxis, Leukocyte ; Epoxide Hydrolases/antagonists & inhibitors/isolation & purification/*metabolism ; Female ; Humans ; Inflammation ; Leukotriene B4/metabolism ; Lung/*immunology/metabolism/pathology ; Mice ; Mice, Inbred BALB C ; Mice, Inbred C57BL ; Neutrophils/enzymology/immunology/*physiology ; Oligopeptides/*metabolism ; Orthomyxoviridae Infections/immunology/metabolism/pathology ; Pneumococcal Infections/immunology/metabolism/pathology ; Pneumonia/*immunology/metabolism/pathology/therapy ; Proline/*analogs & derivatives/metabolism ; Pulmonary Disease, Chronic Obstructive/immunology/metabolism/pathology ; *Smoke ; Tobacco
    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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  • 11
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    Signaling kinase AMPK activates stress-promoted transcription via histone H2B phosphorylation (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-07-22
    Description: The mammalian adenosine monophosphate-activated protein kinase (AMPK) is a serine-threonine kinase protein complex that is a central regulator of cellular energy homeostasis. However, the mechanisms by which AMPK mediates cellular responses to metabolic stress remain unclear. We found that AMPK activates transcription through direct association with chromatin and phosphorylation of histone H2B at serine 36. AMPK recruitment and H2B Ser36 phosphorylation colocalized within genes activated by AMPK-dependent pathways, both in promoters and in transcribed regions. Ectopic expression of H2B in which Ser36 was substituted by alanine reduced transcription and RNA polymerase II association to AMPK-dependent genes, and lowered cell survival in response to stress. Our results place AMPK-dependent H2B Ser36 phosphorylation in a direct transcriptional and chromatin regulatory pathway leading to cellular adaptation to stress.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3922052/" 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/PMC3922052/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bungard, David -- Fuerth, Benjamin J -- Zeng, Ping-Yao -- Faubert, Brandon -- Maas, Nancy L -- Viollet, Benoit -- Carling, David -- Thompson, Craig B -- Jones, Russell G -- Berger, Shelley L -- CA078831/CA/NCI NIH HHS/ -- CA09171/CA/NCI NIH HHS/ -- CA105463/CA/NCI NIH HHS/ -- MC_U120027537/Medical Research Council/United Kingdom -- MOP-93799/Canadian Institutes of Health Research/Canada -- P01 AG031862/AG/NIA NIH HHS/ -- P01 CA104838/CA/NCI NIH HHS/ -- R01 CA078831/CA/NCI NIH HHS/ -- R01 CA105463/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 2010 Sep 3;329(5996):1201-5. doi: 10.1126/science.1191241. Epub 2010 Jul 15.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cellular and Developmental Biology, University of Pennsylvania Medical School, Philadelphia, PA 19104, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20647423" target="_blank"〉PubMed〈/a〉
    Keywords: AMP-Activated Protein Kinases/chemistry/*metabolism ; Adaptation, Physiological ; Amino Acid Motifs ; Amino Acid Substitution ; Animals ; Cell Line ; Cell Line, Tumor ; Cell Survival ; Cells, Cultured ; Chromatin/*metabolism ; Chromatin Immunoprecipitation ; Enzyme Activation ; Gene Expression Regulation ; Histones/chemistry/*metabolism ; Humans ; Mice ; Phosphorylation ; Promoter Regions, Genetic ; Protein-Serine-Threonine Kinases/genetics/metabolism ; Serine/metabolism ; Signal Transduction ; *Stress, Physiological ; *Transcription, Genetic ; Tumor Suppressor Protein p53/metabolism
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  • 12
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    Immunology. Double TIP-ping (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-08-21
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Singh, Harinder -- Demarco, Ignacio A -- New York, N.Y. -- Science. 2010 Aug 20;329(5994):914-5. doi: 10.1126/science.1194316.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Discovery Immunology, Genentech, San Francisco, CA 94080, USA. singh.harinder@gene.com〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20724627" target="_blank"〉PubMed〈/a〉
    Keywords: Acetylation ; Animals ; Antibody Specificity/*genetics ; B-Lymphocytes/*immunology ; Carrier Proteins/genetics/*physiology ; Cells, Cultured ; Chromatin/metabolism ; Cytidine Deaminase/*metabolism ; Dna ; DNA Breaks, Double-Stranded ; DNA Modification Methylases/metabolism ; Histone-Lysine N-Methyltransferase/genetics ; Histones/metabolism ; Immunoglobulin Class Switching/genetics/*physiology ; Immunoglobulin Switch Region ; Lymphocyte Activation ; Methylation ; Mice ; Mice, Knockout ; Nuclear Proteins/genetics/*physiology ; Promoter Regions, Genetic ; Recombination, Genetic ; Transcriptional Activation
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 13
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    Immunology. A guardian of T cell fate (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-07-03
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Di Santo, James P -- R01 AR060723/AR/NIAMS NIH HHS/ -- New York, N.Y. -- Science. 2010 Jul 2;329(5987):44-5. doi: 10.1126/science.1191664.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Innate Immunity Unit, Institut Pasteur, Paris F-75724, France. james.di-santo@pasteur.fr〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20595605" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Lineage ; Cells, Cultured ; Cytokines/metabolism ; Gene Deletion ; Gene Expression Regulation ; Interleukin-7/physiology ; Killer Cells, Natural/cytology/immunology/*physiology ; *Lymphopoiesis/genetics ; Mice ; Models, Biological ; Precursor Cells, T-Lymphoid/cytology/physiology ; Repressor Proteins/*genetics/*metabolism ; Signal Transduction ; T-Lymphocytes/cytology/immunology/*physiology ; Tumor Suppressor Proteins/*genetics/*metabolism
    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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  • 14
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    Reconstituting organ-level lung functions on a chip (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-06-26
    Description: Here, we describe a biomimetic microsystem that reconstitutes the critical functional alveolar-capillary interface of the human lung. This bioinspired microdevice reproduces complex integrated organ-level responses to bacteria and inflammatory cytokines introduced into the alveolar space. In nanotoxicology studies, this lung mimic revealed that cyclic mechanical strain accentuates toxic and inflammatory responses of the lung to silica nanoparticles. Mechanical strain also enhances epithelial and endothelial uptake of nanoparticulates and stimulates their transport into the underlying microvascular channel. Similar effects of physiological breathing on nanoparticle absorption are observed in whole mouse lung. Mechanically active "organ-on-a-chip" microdevices that reconstitute tissue-tissue interfaces critical to organ function may therefore expand the capabilities of cell culture models and provide low-cost alternatives to animal and clinical studies for drug screening and toxicology applications.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Huh, Dongeun -- Matthews, Benjamin D -- Mammoto, Akiko -- Montoya-Zavala, Martin -- Hsin, Hong Yuan -- Ingber, Donald E -- R01-ES016665/ES/NIEHS NIH HHS/ -- New York, N.Y. -- Science. 2010 Jun 25;328(5986):1662-8. doi: 10.1126/science.1188302.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Wyss Institute for Biologically Inspired Engineering at Harvard University, Boston, MA 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20576885" target="_blank"〉PubMed〈/a〉
    Keywords: Air ; Animals ; *Biomimetic Materials ; Blood-Air Barrier ; Capillaries/*physiology ; Capillary Permeability ; Cells, Cultured ; Endothelial Cells/*physiology ; Escherichia coli/immunology ; Humans ; Immunity, Innate ; Inflammation ; Lung/blood supply/physiology ; Mice ; *Microfluidic Analytical Techniques ; Microtechnology ; Nanoparticles/toxicity ; Neutrophil Infiltration ; Oxidative Stress ; Pneumocytes/*physiology ; Pulmonary Alveoli/*blood supply/cytology/immunology/*physiology ; Respiration ; Silicon Dioxide/toxicity ; Stress, Mechanical
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  • 15
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    BID, BIM, and PUMA are essential for activation of the BAX- and BAK-dependent cell death program (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-12-04
    Description: Although the proteins BAX and BAK are required for initiation of apoptosis at the mitochondria, how BAX and BAK are activated remains unsettled. We provide in vivo evidence demonstrating an essential role of the proteins BID, BIM, and PUMA in activating BAX and BAK. Bid, Bim, and Puma triple-knockout mice showed the same developmental defects that are associated with deficiency of Bax and Bak, including persistent interdigital webs and imperforate vaginas. Genetic deletion of Bid, Bim, and Puma prevented the homo-oligomerization of BAX and BAK, and thereby cytochrome c-mediated activation of caspases in response to diverse death signals in neurons and T lymphocytes, despite the presence of other BH3-only molecules. Thus, many forms of apoptosis require direct activation of BAX and BAK at the mitochondria by a member of the BID, BIM, or PUMA family of proteins.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3163443/" 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/PMC3163443/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ren, Decheng -- Tu, Ho-Chou -- Kim, Hyungjin -- Wang, Gary X -- Bean, Gregory R -- Takeuchi, Osamu -- Jeffers, John R -- Zambetti, Gerard P -- Hsieh, James J-D -- Cheng, Emily H-Y -- P30CA21765/CA/NCI NIH HHS/ -- R01 CA125562/CA/NCI NIH HHS/ -- R01 CA125562-02/CA/NCI NIH HHS/ -- R01 CA125562-03/CA/NCI NIH HHS/ -- R01 CA125562-04/CA/NCI NIH HHS/ -- R01CA125562/CA/NCI NIH HHS/ -- R01GM083159/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2010 Dec 3;330(6009):1390-3. doi: 10.1126/science.1190217.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Molecular Oncology, Department of Medicine, Washington University School of Medicine, St. Louis, MO 63110, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21127253" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Apoptosis ; Apoptosis Regulatory Proteins/deficiency/genetics/*metabolism ; BH3 Interacting Domain Death Agonist Protein/deficiency/genetics/*metabolism ; Caspases/metabolism ; Cells, Cultured ; Cerebellum/cytology ; Cytochromes c/metabolism ; Intracellular Membranes/metabolism ; Membrane Proteins/deficiency/genetics/*metabolism ; Mice ; Mice, Knockout ; Mitochondria/metabolism ; Models, Biological ; Neurons/*physiology ; Permeability ; Protein Multimerization ; Proto-Oncogene Proteins/deficiency/genetics/*metabolism ; Stress, Physiological ; T-Lymphocytes/physiology ; Tumor Suppressor Proteins/deficiency/genetics/*metabolism ; bcl-2 Homologous Antagonist-Killer Protein/chemistry/genetics/*metabolism ; bcl-2-Associated X Protein/chemistry/genetics/*metabolism
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  • 16
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    Molecular biology. Mixing or not mixing (2010)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2010-04-03
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ray-Gallet, Dominique -- Almouzni, Genevieve -- New York, N.Y. -- Science. 2010 Apr 2;328(5974):56-7. doi: 10.1126/science.1188653.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Nuclear Dynamics and Genome Plasticity, UMR218 CNRS/Institut Curie, 26 rue d'Ulm, 75248 Paris Cedex 05, France.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20360101" target="_blank"〉PubMed〈/a〉
    Keywords: Cell Cycle ; Cells, Cultured ; Chromatin/*metabolism ; Chromatin Assembly and Disassembly ; DNA Replication ; Histones/*chemistry/*metabolism ; Humans ; Nucleosomes/*metabolism ; Protein Multimerization
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  • 17
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    An early T cell lineage commitment checkpoint dependent on the transcription factor Bcl11b (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-07-03
    Description: The identities of the regulators that mediate commitment of hematopoietic precursors to the T lymphocyte lineage have been unknown. The last stage of T lineage commitment in vivo involves mechanisms to suppress natural killer cell potential, to suppress myeloid and dendritic cell potential, and to silence the stem cell or progenitor cell regulatory functions that initially provide T cell receptor-independent self-renewal capability. The zinc finger transcription factor Bcl11b is T cell-specific in expression among hematopoietic cell types and is first expressed in precursors immediately before T lineage commitment. We found that Bcl11b is necessary for T lineage commitment in mice and is specifically required both to repress natural killer cell-associated genes and to down-regulate a battery of stem cell or progenitor cell genes at the pivotal stage of commitment.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2935300/" 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/PMC2935300/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Li, Long -- Leid, Mark -- Rothenberg, Ellen V -- F06 TW002367/TW/FIC NIH HHS/ -- F06 TW002367-01A1/TW/FIC NIH HHS/ -- R01 GM060852/GM/NIGMS NIH HHS/ -- R01 GM060852-04/GM/NIGMS NIH HHS/ -- R01 GM60852/GM/NIGMS NIH HHS/ -- R33 HL089123/HL/NHLBI NIH HHS/ -- R33 HL089123-03/HL/NHLBI NIH HHS/ -- RC2 CA148278/CA/NCI NIH HHS/ -- RC2 CA148278-02/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 2010 Jul 2;329(5987):89-93. doi: 10.1126/science.1188989.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Biology 156-29, California Institute of Technology, Pasadena, CA 91125, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20595614" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Differentiation ; *Cell Lineage ; Cells, Cultured ; Down-Regulation ; Gene Expression Profiling ; *Gene Expression Regulation, Developmental ; Genes, T-Cell Receptor delta ; Genes, T-Cell Receptor gamma ; Killer Cells, Natural/cytology/physiology ; *Lymphopoiesis/genetics ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Precursor Cells, T-Lymphoid/cytology/immunology/*physiology ; Receptors, Antigen, T-Cell, gamma-delta/metabolism ; Receptors, Notch/metabolism ; Repressor Proteins/deficiency/genetics/*metabolism ; Signal Transduction ; T-Lymphocytes/cytology/metabolism/*physiology ; Transcription Factors/genetics/metabolism ; Tumor Suppressor Proteins/deficiency/genetics/*metabolism
    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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  • 18
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    Reprogramming of T cells to natural killer-like cells upon Bcl11b deletion (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-06-12
    Description: T cells develop in the thymus and are critical for adaptive immunity. Natural killer (NK) lymphocytes constitute an essential component of the innate immune system in tumor surveillance, reproduction, and defense against microbes and viruses. Here, we show that the transcription factor Bcl11b was expressed in all T cell compartments and was indispensable for T lineage development. When Bcl11b was deleted, T cells from all developmental stages acquired NK cell properties and concomitantly lost or decreased T cell-associated gene expression. These induced T-to-natural killer (ITNK) cells, which were morphologically and genetically similar to conventional NK cells, killed tumor cells in vitro, and effectively prevented tumor metastasis in vivo. Therefore, ITNKs may represent a new cell source for cell-based therapies.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3628452/" 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/PMC3628452/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Li, Peng -- Burke, Shannon -- Wang, Juexuan -- Chen, Xiongfeng -- Ortiz, Mariaestela -- Lee, Song-Choon -- Lu, Dong -- Campos, Lia -- Goulding, David -- Ng, Bee Ling -- Dougan, Gordon -- Huntly, Brian -- Gottgens, Bertie -- Jenkins, Nancy A -- Copeland, Neal G -- Colucci, Francesco -- Liu, Pentao -- 076962/Wellcome Trust/United Kingdom -- 077186/Wellcome Trust/United Kingdom -- G0501150/Medical Research Council/United Kingdom -- G0800784/Medical Research Council/United Kingdom -- G116/187/Medical Research Council/United Kingdom -- Biotechnology and Biological Sciences Research Council/United Kingdom -- Wellcome Trust/United Kingdom -- Medical Research Council/United Kingdom -- New York, N.Y. -- Science. 2010 Jul 2;329(5987):85-9. doi: 10.1126/science.1188063. Epub 2010 Jun 10.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Wellcome Trust Sanger Institute, Hinxton, Cambridge CB10 1HH, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20538915" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Line, Tumor ; *Cell Lineage ; Cells, Cultured ; Coculture Techniques ; Cytotoxicity, Immunologic ; Gene Deletion ; Gene Expression Profiling ; Gene Expression Regulation, Developmental ; Gene Knock-In Techniques ; Genes, T-Cell Receptor beta ; Killer Cells, Natural/cytology/immunology/*physiology ; *Lymphopoiesis/genetics ; Melanoma, Experimental/immunology/therapy ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Oligonucleotide Array Sequence Analysis ; Precursor Cells, T-Lymphoid/cytology/physiology ; Receptors, Antigen, T-Cell, alpha-beta/metabolism ; Repressor Proteins/*genetics/*metabolism ; Signal Transduction ; Stromal Cells/cytology/physiology ; T-Lymphocytes/cytology/immunology/*physiology/transplantation ; Tamoxifen/analogs & derivatives/pharmacology ; Tumor Suppressor Proteins/*genetics/*metabolism
    Print ISSN: 0036-8075
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    GE Prize-winning essay. A new approach to fluorescence microscopy (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-12-04
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bates, Mark -- New York, N.Y. -- Science. 2010 Dec 3;330(6009):1334-5. doi: 10.1126/science.1200252.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of NanoBiophotonics, Max Planck Institute for Biophysical Chemistry, 37077 Gottingen, Germany. mbates@ggweg.de〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21127240" target="_blank"〉PubMed〈/a〉
    Keywords: Awards and Prizes ; *Carbocyanines/chemistry ; Cells, Cultured ; Coated Pits, Cell-Membrane/*ultrastructure ; *Fluorescent Dyes/chemistry ; Image Processing, Computer-Assisted ; Imaging, Three-Dimensional/*methods ; Microscopy, Fluorescence/*methods ; Microtubules/*ultrastructure ; Ultraviolet Rays
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Three-dimensional, flexible nanoscale field-effect transistors as localized bioprobes (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-08-14
    Description: Nanoelectronic devices offer substantial potential for interrogating biological systems, although nearly all work has focused on planar device designs. We have overcome this limitation through synthetic integration of a nanoscale field-effect transistor (nanoFET) device at the tip of an acute-angle kinked silicon nanowire, where nanoscale connections are made by the arms of the kinked nanostructure, and remote multilayer interconnects allow three-dimensional (3D) probe presentation. The acute-angle probe geometry was designed and synthesized by controlling cis versus trans crystal conformations between adjacent kinks, and the nanoFET was localized through modulation doping. 3D nanoFET probes exhibited conductance and sensitivity in aqueous solution, independent of large mechanical deflections, and demonstrated high pH sensitivity. Additionally, 3D nanoprobes modified with phospholipid bilayers can enter single cells to allow robust recording of intracellular potentials.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3149824/" 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/PMC3149824/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Tian, Bozhi -- Cohen-Karni, Tzahi -- Qing, Quan -- Duan, Xiaojie -- Xie, Ping -- Lieber, Charles M -- 5DP1OD003900/OD/NIH HHS/ -- DP1 OD003900/OD/NIH HHS/ -- DP1 OD003900-04/OD/NIH HHS/ -- New York, N.Y. -- Science. 2010 Aug 13;329(5993):830-4. doi: 10.1126/science.1192033.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Chemistry and Chemical Biology, Harvard University, Cambridge, MA 02138, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20705858" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Biosensing Techniques/instrumentation/methods ; Cell Line ; Cells, Cultured ; Chick Embryo ; Electric Conductivity ; Electrophysiological Phenomena ; Equipment Design ; Hydrogen-Ion Concentration ; Lipid Bilayers ; Membrane Potentials ; Mice ; Microfluidics ; Myocytes, Cardiac/*physiology ; *Nanowires ; Sensitivity and Specificity ; Sodium Chloride ; *Transistors, Electronic
    Print ISSN: 0036-8075
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  • 21
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    Bifurcation of Toll-like receptor 9 signaling by adaptor protein 3 (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-09-18
    Description: Endosomal Toll-like receptors (TLRs) 7 and 9 recognize viral pathogens and induce signals leading to the activation of nuclear factor kappaB (NF-kappaB)-dependent proinflammatory cytokines and interferon regulatory factor 7 (IRF7)-dependent type I interferons (IFNs). Recognition of viral nucleic acids by TLR9 requires its cleavage in the endolysosomal compartment. Here, we show that TLR9 signals leading to the activation of type I IFN, but not proinflammatory cytokine genes, require TLR9 trafficking from endosomes to a specialized lysosome-related organelle. Furthermore, we identify adapter protein-3 as the protein complex responsible for the trafficking of TLR9 to this subcellular compartment. Our results reveal an intracellular mechanism for bifurcation of TLR9 signals by selective receptor trafficking within the endosomal system.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3063333/" 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/PMC3063333/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sasai, Miwa -- Linehan, Melissa M -- Iwasaki, Akiko -- AI054359/AI/NIAID NIH HHS/ -- AI064705/AI/NIAID NIH HHS/ -- AI081884/AI/NIAID NIH HHS/ -- R01 AI054359/AI/NIAID NIH HHS/ -- R01 AI054359-07/AI/NIAID NIH HHS/ -- R01 AI064705/AI/NIAID NIH HHS/ -- R01 AI064705-06/AI/NIAID NIH HHS/ -- R01 AI081884/AI/NIAID NIH HHS/ -- R01 AI081884-01A2/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 2010 Sep 17;329(5998):1530-4. doi: 10.1126/science.1187029.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Immunobiology, Yale University School of Medicine, New Haven, CT 06520, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20847273" target="_blank"〉PubMed〈/a〉
    Keywords: Adaptor Protein Complex 3/genetics/*metabolism ; Adaptor Protein Complex beta Subunits ; Animals ; Cells, Cultured ; Cytokines/genetics/immunology/metabolism ; Cytoplasmic Vesicles/metabolism ; Dendritic Cells/*immunology/metabolism ; Endosomes/metabolism ; Interferon Regulatory Factor-7/metabolism ; Interferon Type I/genetics/immunology/metabolism ; Lysosomal-Associated Membrane Protein 2/metabolism ; Macrophages/immunology ; Membrane Transport Proteins/metabolism ; Mice ; Mice, Inbred C57BL ; Myeloid Differentiation Factor 88/metabolism ; Oligodeoxyribonucleotides/immunology ; Protein Transport ; Recombinant Fusion Proteins/immunology/metabolism ; Signal Transduction ; TNF Receptor-Associated Factor 3/metabolism ; Toll-Like Receptor 9/immunology/*metabolism ; Transcriptional Activation ; Vesicle-Associated Membrane Protein 3/metabolism
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    Long noncoding RNA as modular scaffold of histone modification complexes (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-07-10
    Description: Long intergenic noncoding RNAs (lincRNAs) regulate chromatin states and epigenetic inheritance. Here, we show that the lincRNA HOTAIR serves as a scaffold for at least two distinct histone modification complexes. A 5' domain of HOTAIR binds polycomb repressive complex 2 (PRC2), whereas a 3' domain of HOTAIR binds the LSD1/CoREST/REST complex. The ability to tether two distinct complexes enables RNA-mediated assembly of PRC2 and LSD1 and coordinates targeting of PRC2 and LSD1 to chromatin for coupled histone H3 lysine 27 methylation and lysine 4 demethylation. Our results suggest that lincRNAs may serve as scaffolds by providing binding surfaces to assemble select histone modification enzymes, thereby specifying the pattern of histone modifications on target genes.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2967777/" 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/PMC2967777/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Tsai, Miao-Chih -- Manor, Ohad -- Wan, Yue -- Mosammaparast, Nima -- Wang, Jordon K -- Lan, Fei -- Shi, Yang -- Segal, Eran -- Chang, Howard Y -- R01 CA118750/CA/NCI NIH HHS/ -- R01 CA119176/CA/NCI NIH HHS/ -- R01 CA119176-05/CA/NCI NIH HHS/ -- R01-CA118487/CA/NCI NIH HHS/ -- R01-HG004361/HG/NHGRI NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2010 Aug 6;329(5992):689-93. doi: 10.1126/science.1192002. Epub 2010 Jul 8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute and Program in Epithelial Biology, Stanford University School of Medicine, Stanford, CA 94305, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20616235" target="_blank"〉PubMed〈/a〉
    Keywords: Binding Sites ; Carrier Proteins/metabolism ; Cell Line ; Cells, Cultured ; Chromatin/*metabolism ; Chromatin Immunoprecipitation ; Co-Repressor Proteins ; DNA-Binding Proteins/*metabolism ; HeLa Cells ; Histone Demethylases/*metabolism ; Histones/*metabolism ; Humans ; Methylation ; Mutation ; Nerve Tissue Proteins/metabolism ; Nuclear Proteins/metabolism ; Nucleic Acid Conformation ; Polycomb Repressive Complex 2 ; Polycomb-Group Proteins ; Promoter Regions, Genetic ; Protein Binding ; RNA Interference ; RNA, Untranslated/chemistry/*metabolism ; Repressor Proteins/*metabolism ; Transcription Factors/*metabolism ; Transcription, Genetic
    Print ISSN: 0036-8075
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    Aryl hydrocarbon receptor antagonists promote the expansion of human hematopoietic stem cells (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-08-07
    Description: Although practiced clinically for more than 40 years, the use of hematopoietic stem cell (HSC) transplants remains limited by the ability to expand these cells ex vivo. An unbiased screen with primary human HSCs identified a purine derivative, StemRegenin 1 (SR1), that promotes the ex vivo expansion of CD34+ cells. Culture of HSCs with SR1 led to a 50-fold increase in cells expressing CD34 and a 17-fold increase in cells that retain the ability to engraft immunodeficient mice. Mechanistic studies show that SR1 acts by antagonizing the aryl hydrocarbon receptor (AHR). The identification of SR1 and AHR modulation as a means to induce ex vivo HSC expansion should facilitate the clinical use of HSC therapy.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3033342/" 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/PMC3033342/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Boitano, Anthony E -- Wang, Jian -- Romeo, Russell -- Bouchez, Laure C -- Parker, Albert E -- Sutton, Sue E -- Walker, John R -- Flaveny, Colin A -- Perdew, Gary H -- Denison, Michael S -- Schultz, Peter G -- Cooke, Michael P -- ES004869/ES/NIEHS NIH HHS/ -- ES007685/ES/NIEHS NIH HHS/ -- ES04699/ES/NIEHS NIH HHS/ -- P42 ES004699/ES/NIEHS NIH HHS/ -- P42 ES004699-24/ES/NIEHS NIH HHS/ -- R01 ES004869/ES/NIEHS NIH HHS/ -- R01 ES004869-23/ES/NIEHS NIH HHS/ -- R01 ES007685/ES/NIEHS NIH HHS/ -- R01 ES007685-11/ES/NIEHS NIH HHS/ -- New York, N.Y. -- Science. 2010 Sep 10;329(5997):1345-8. doi: 10.1126/science.1191536. Epub 2010 Aug 5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Chemistry, The Scripps Research Institute, 10550 North Torrey Pines Road, La Jolla, CA 92037, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20688981" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, CD/analysis ; Antigens, CD34/analysis ; Aryl Hydrocarbon Hydroxylases/genetics/metabolism ; Cell Count ; Cell Lineage ; Cell Proliferation ; Cells, Cultured ; Cytochrome P-450 CYP1B1 ; Cytokines/pharmacology ; Glycoproteins/analysis ; Hematopoiesis ; *Hematopoietic Stem Cell Transplantation ; Hematopoietic Stem Cells/cytology/drug effects/metabolism/*physiology ; Humans ; Mice ; Mice, Inbred NOD ; Mice, SCID ; Multipotent Stem Cells/cytology/drug effects/physiology ; Peptides/analysis ; Purines/*metabolism/*pharmacology ; Receptors, Aryl Hydrocarbon/*antagonists & inhibitors/metabolism ; Signal Transduction ; Small Molecule Libraries ; Species Specificity ; Tetrachlorodibenzodioxin/pharmacology
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    Stem cells for sale (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-11-27
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Vogel, Gretchen -- New York, N.Y. -- Science. 2010 Nov 26;330(6008):1173. doi: 10.1126/science.330.6008.1173.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21109646" target="_blank"〉PubMed〈/a〉
    Keywords: Biotechnology/*economics ; Cells, Cultured ; *Commerce ; Embryonic Stem Cells/cytology/physiology ; Humans ; *Induced Pluripotent Stem Cells/cytology ; *Myocytes, Cardiac/cytology/physiology
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    Cbln1 is a ligand for an orphan glutamate receptor delta2, a bidirectional synapse organizer (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-04-17
    Description: Cbln1, secreted from cerebellar granule cells, and the orphan glutamate receptor delta2 (GluD2), expressed by Purkinje cells, are essential for synapse integrity between these neurons in adult mice. Nevertheless, no endogenous binding partners for these molecules have been identified. We found that Cbln1 binds directly to the N-terminal domain of GluD2. GluD2 expression by postsynaptic cells, combined with exogenously applied Cbln1, was necessary and sufficient to induce new synapses in vitro and in the adult cerebellum in vivo. Further, beads coated with recombinant Cbln1 directly induced presynaptic differentiation and indirectly caused clustering of postsynaptic molecules via GluD2. These results indicate that the Cbln1-GluD2 complex is a unique synapse organizer that acts bidirectionally on both pre- and postsynaptic components.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Matsuda, Keiko -- Miura, Eriko -- Miyazaki, Taisuke -- Kakegawa, Wataru -- Emi, Kyoichi -- Narumi, Sakae -- Fukazawa, Yugo -- Ito-Ishida, Aya -- Kondo, Tetsuro -- Shigemoto, Ryuichi -- Watanabe, Masahiko -- Yuzaki, Michisuke -- New York, N.Y. -- Science. 2010 Apr 16;328(5976):363-8. doi: 10.1126/science.1185152.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Physiology, School of Medicine, Keio University, Tokyo 160-8582, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20395510" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Binding Sites ; Cell Line ; Cells, Cultured ; Cerebellum/cytology/*physiology ; Coculture Techniques ; Excitatory Postsynaptic Potentials ; Humans ; Ligands ; Mice ; Nerve Tissue Proteins/*metabolism ; Presynaptic Terminals/physiology ; Protein Binding ; Protein Interaction Domains and Motifs ; Protein Precursors/*metabolism ; Purkinje Cells/metabolism/*physiology ; Rats ; Receptors, Glutamate/chemistry/*metabolism ; Recombinant Fusion Proteins/metabolism ; Synapses/*physiology ; Synaptic Membranes/metabolism
    Print ISSN: 0036-8075
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    PML regulates apoptosis at endoplasmic reticulum by modulating calcium release (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-10-30
    Description: The promyelocytic leukemia (PML) tumor suppressor is a pleiotropic modulator of apoptosis. However, the molecular basis for such a diverse proapoptotic role is currently unknown. We show that extranuclear Pml was specifically enriched at the endoplasmic reticulum (ER) and at the mitochondria-associated membranes, signaling domains involved in ER-to-mitochondria calcium ion (Ca(2+)) transport and in induction of apoptosis. We found Pml in complexes of large molecular size with the inositol 1,4,5-trisphosphate receptor (IP(3)R), protein kinase Akt, and protein phosphatase 2a (PP2a). Pml was essential for Akt- and PP2a-dependent modulation of IP(3)R phosphorylation and in turn for IP(3)R-mediated Ca(2+) release from ER. Our findings provide a mechanistic explanation for the pleiotropic role of Pml in apoptosis and identify a pharmacological target for the modulation of Ca(2+) signals.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3017677/" 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/PMC3017677/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Giorgi, Carlotta -- Ito, Keisuke -- Lin, Hui-Kuan -- Santangelo, Clara -- Wieckowski, Mariusz R -- Lebiedzinska, Magdalena -- Bononi, Angela -- Bonora, Massimo -- Duszynski, Jerzy -- Bernardi, Rosa -- Rizzuto, Rosario -- Tacchetti, Carlo -- Pinton, Paolo -- Pandolfi, Pier Paolo -- GGP05284/Telethon/Italy -- K99 CA139009/CA/NCI NIH HHS/ -- K99 CA139009-01A1/CA/NCI NIH HHS/ -- K99 CA139009-02/CA/NCI NIH HHS/ -- R01 CA071692/CA/NCI NIH HHS/ -- R01 CA071692-04S1/CA/NCI NIH HHS/ -- R01 CA102142/CA/NCI NIH HHS/ -- R01 CA102142-07/CA/NCI NIH HHS/ -- R01 CA142874/CA/NCI NIH HHS/ -- R01 CA142874-01/CA/NCI NIH HHS/ -- R01 CA142874-02/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 2010 Nov 26;330(6008):1247-51. doi: 10.1126/science.1189157. Epub 2010 Oct 28.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Experimental and Diagnostic Medicine, Section of General Pathology, Interdisciplinary Center for the Study of Inflammation (ICSI), Emilia Romagna Laboratory BioPharmaNet, and Laboratory for Technologies of Advanced Therapies (LTTA) University of Ferrara, Ferrara, Italy.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21030605" target="_blank"〉PubMed〈/a〉
    Keywords: Adenosine Triphosphate/metabolism ; Animals ; *Apoptosis ; Calcium/*metabolism ; *Calcium Signaling ; Cell Line ; Cell Nucleus/metabolism ; Cells, Cultured ; Cytosol/metabolism ; Endoplasmic Reticulum/*metabolism ; Homeostasis ; Humans ; Inositol 1,4,5-Trisphosphate/metabolism ; Inositol 1,4,5-Trisphosphate Receptors/metabolism ; Intracellular Membranes/metabolism ; Mice ; Mitochondria/metabolism ; Nuclear Proteins/genetics/*metabolism ; Phosphorylation ; Protein Phosphatase 2/metabolism ; Proto-Oncogene Proteins c-akt/metabolism ; Recombinant Fusion Proteins/metabolism ; Stress, Physiological ; Transcription Factors/genetics/*metabolism ; Tumor Suppressor Proteins/genetics/*metabolism
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    Doc2b is a high-affinity Ca2+ sensor for spontaneous neurotransmitter release (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-02-13
    Description: Synaptic vesicle fusion in brain synapses occurs in phases that are either tightly coupled to action potentials (synchronous), immediately following action potentials (asynchronous), or as stochastic events in the absence of action potentials (spontaneous). Synaptotagmin-1, -2, and -9 are vesicle-associated Ca2+ sensors for synchronous release. Here we found that double C2 domain (Doc2) proteins act as Ca2+ sensors to trigger spontaneous release. Although Doc2 proteins are cytosolic, they function analogously to synaptotagmin-1 but with a higher Ca2+ sensitivity. Doc2 proteins bound to N-ethylmaleimide-sensitive factor attachment receptor (SNARE) complexes in competition with synaptotagmin-1. Thus, different classes of multiple C2 domain-containing molecules trigger synchronous versus spontaneous fusion, which suggests a general mechanism for synaptic vesicle fusion triggered by the combined actions of SNAREs and multiple C2 domain-containing proteins.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2846320/" 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/PMC2846320/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Groffen, Alexander J -- Martens, Sascha -- Diez Arazola, Rocio -- Cornelisse, L Niels -- Lozovaya, Natalia -- de Jong, Arthur P H -- Goriounova, Natalia A -- Habets, Ron L P -- Takai, Yoshimi -- Borst, J Gerard -- Brose, Nils -- McMahon, Harvey T -- Verhage, Matthijs -- MC_U105178795/Medical Research Council/United Kingdom -- U.1051.02.007(78795)/Medical Research Council/United Kingdom -- Medical Research Council/United Kingdom -- New York, N.Y. -- Science. 2010 Mar 26;327(5973):1614-8. doi: 10.1126/science.1183765. Epub 2010 Feb 11.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Functional Genomics, CNCR, Neuroscience Campus Amsterdam, VU University and VU Medical Center, Amsterdam, 1081 HV, Netherlands. sander.groffen@cncr.vu.nl〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20150444" target="_blank"〉PubMed〈/a〉
    Keywords: Action Potentials ; Animals ; Binding Sites ; Calcium/*metabolism ; Calcium-Binding Proteins/chemistry/genetics/*metabolism ; Cells, Cultured ; Excitatory Postsynaptic Potentials ; Hippocampus/cytology ; Inhibitory Postsynaptic Potentials ; Membrane Fusion ; Mice ; Mice, Knockout ; Mutant Proteins/genetics/metabolism ; Nerve Tissue Proteins/chemistry/genetics/*metabolism ; Neurons/physiology ; Neurotransmitter Agents/*metabolism ; Patch-Clamp Techniques ; Protein Structure, Tertiary ; Purkinje Cells/physiology ; Rats ; SNARE Proteins/metabolism ; *Synaptic Transmission ; Synaptic Vesicles/*physiology ; Synaptotagmin I/metabolism
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    Lysosomal pathology and osteopetrosis upon loss of H+-driven lysosomal Cl- accumulation (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-05-01
    Description: During lysosomal acidification, proton-pump currents are thought to be shunted by a chloride ion (Cl-) channel, tentatively identified as ClC-7. Surprisingly, recent data suggest that ClC-7 instead mediates Cl-/proton (H+) exchange. We generated mice carrying a point mutation converting ClC-7 into an uncoupled (unc) Cl- conductor. Despite maintaining lysosomal conductance and normal lysosomal pH, these Clcn7(unc/unc) mice showed lysosomal storage disease like mice lacking ClC-7. However, their osteopetrosis was milder, and they lacked a coat color phenotype. Thus, only some roles of ClC-7 Cl-/H+ exchange can be taken over by a Cl- conductance. This conductance was even deleterious in Clcn7(+/unc) mice. Clcn7(-/-) and Clcn7(unc/unc) mice accumulated less Cl- in lysosomes than did wild-type mice. Thus, lowered lysosomal chloride may underlie their common phenotypes.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Weinert, Stefanie -- Jabs, Sabrina -- Supanchart, Chayarop -- Schweizer, Michaela -- Gimber, Niclas -- Richter, Martin -- Rademann, Jorg -- Stauber, Tobias -- Kornak, Uwe -- Jentsch, Thomas J -- New York, N.Y. -- Science. 2010 Jun 11;328(5984):1401-3. doi: 10.1126/science.1188072.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Leibniz-Institut fur Molekulare Pharmakologie (FMP), 13125 Berlin, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20430974" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Bone and Bones/pathology ; Cells, Cultured ; Chloride Channels/genetics/*metabolism ; Chlorides/*metabolism ; Gene Knock-In Techniques ; Hair Color ; Hippocampus/pathology ; Hydrogen-Ion Concentration ; Lysosomal Storage Diseases/metabolism/pathology ; Lysosomes/*metabolism ; Membrane Potentials ; Membrane Proteins/genetics/metabolism ; Mice ; Mutant Proteins/metabolism ; Osteoclasts/metabolism/pathology ; Osteopetrosis/*metabolism/pathology ; Phenotype ; Point Mutation ; *Protons
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    Local and long-range reciprocal regulation of cAMP and cGMP in axon/dendrite formation (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-01-30
    Description: Cytosolic cyclic adenosine monophosphate (cAMP) and cyclic guanosine monophosphate (cGMP) often mediate antagonistic cellular actions of extracellular factors, from the regulation of ion channels to cell volume control and axon guidance. We found that localized cAMP and cGMP activities in undifferentiated neurites of cultured hippocampal neurons promote and suppress axon formation, respectively, and exert opposite effects on dendrite formation. Fluorescence resonance energy transfer imaging showed that alterations of the amount of cAMP resulted in opposite changes in the amount of cGMP, and vice versa, through the activation of specific phosphodiesterases and protein kinases. Local elevation of cAMP in one neurite resulted in cAMP reduction in all other neurites of the same neuron. Thus, local and long-range reciprocal regulation of cAMP and cGMP together ensures coordinated development of one axon and multiple dendrites.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Shelly, Maya -- Lim, Byung Kook -- Cancedda, Laura -- Heilshorn, Sarah C -- Gao, Hongfeng -- Poo, Mu-ming -- NS-22764/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 2010 Jan 29;327(5965):547-52. doi: 10.1126/science.1179735.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Neurobiology, Department of Molecular and Cell Biology, Helen Wills Neuroscience Institute, University of California, Berkeley, CA 94720, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20110498" target="_blank"〉PubMed〈/a〉
    Keywords: Adenylyl Cyclase Inhibitors ; Adenylyl Cyclases/metabolism ; Animals ; Axons/metabolism/*physiology ; Cell Differentiation ; Cell Line ; Cell Polarity ; Cells, Cultured ; Cyclic AMP/*metabolism ; Cyclic AMP-Dependent Protein Kinases/antagonists & inhibitors/metabolism ; Cyclic GMP/*metabolism ; Dendrites/metabolism/*physiology ; Enzyme Inhibitors/pharmacology ; Fluorescence Resonance Energy Transfer ; Guanylate Cyclase/antagonists & inhibitors/metabolism ; Hippocampus/*cytology ; Humans ; Neurites/metabolism/physiology ; Neurons/cytology/*physiology ; Phosphodiesterase Inhibitors/pharmacology ; Phosphoric Diester Hydrolases/metabolism ; Phosphorylation ; Rats ; Signal Transduction ; Transfection
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    Tau reduction prevents Abeta-induced defects in axonal transport (2010)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2010-09-11
    Description: Amyloid-beta (Abeta) peptides, derived from the amyloid precursor protein, and the microtubule-associated protein tau are key pathogenic factors in Alzheimer's disease (AD). How exactly they impair cognitive functions is unknown. We assessed the effects of Abeta and tau on axonal transport of mitochondria and the neurotrophin receptor TrkA, cargoes that are critical for neuronal function and survival and whose distributions are altered in AD. Abeta oligomers rapidly inhibited axonal transport of these cargoes in wild-type neurons. Lowering tau levels prevented these defects without affecting baseline axonal transport. Thus, Abeta requires tau to impair axonal transport, and tau reduction protects against Abeta-induced axonal transport defects.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3024010/" 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/PMC3024010/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Vossel, Keith A -- Zhang, Kai -- Brodbeck, Jens -- Daub, Aaron C -- Sharma, Punita -- Finkbeiner, Steven -- Cui, Bianxiao -- Mucke, Lennart -- AG011385/AG/NIA NIH HHS/ -- C06 RR018928/RR/NCRR NIH HHS/ -- NS041787/NS/NINDS NIH HHS/ -- NS057906/NS/NINDS NIH HHS/ -- R00 NS057906/NS/NINDS NIH HHS/ -- R00 NS057906-05/NS/NINDS NIH HHS/ -- R01 AG011385/AG/NIA NIH HHS/ -- R01 AG011385-07/AG/NIA NIH HHS/ -- R01 NS041787/NS/NINDS NIH HHS/ -- R01 NS041787-09/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 2010 Oct 8;330(6001):198. doi: 10.1126/science.1194653. Epub 2010 Sep 9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Gladstone Institute of Neurological Disease, San Francisco, CA 94158, USA. kvossel@gladstone.ucsf.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20829454" target="_blank"〉PubMed〈/a〉
    Keywords: Amyloid beta-Peptides/*metabolism/pharmacology ; Animals ; *Axonal Transport ; Cells, Cultured ; Hippocampus/cytology ; Mice ; Mitochondria/metabolism ; Neurons/*metabolism ; Peptide Fragments/*metabolism/pharmacology ; Receptor, trkA/metabolism ; tau Proteins/*metabolism
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    An essential developmental checkpoint for production of the T cell lineage (2010)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2010-07-03
    Description: In early T cell development, progenitors retaining the potential to generate myeloid and natural killer lineages are eventually determined to a specific T cell lineage. The molecular mechanisms that drive this determination step remain unclarified. We show that, when murine hematopoietic progenitors were cultured on immobilized Notch ligand DLL4 protein in the presence of a cocktail of cytokines including interleukin-7, progenitors developing toward T cells were arrested and the arrested cells entered a self-renewal cycle, maintaining non-T lineage potentials. Reduced concentrations of interleukin-7 promoted T cell lineage determination. A similar arrest and self-renewal of progenitors were observed in thymocytes of mice deficient in the transcription factor Bcl11b. Our study thus identifies the earliest checkpoint during T cell development and shows that it is Bcl11b-dependent.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ikawa, Tomokatsu -- Hirose, Satoshi -- Masuda, Kyoko -- Kakugawa, Kiyokazu -- Satoh, Rumi -- Shibano-Satoh, Asako -- Kominami, Ryo -- Katsura, Yoshimoto -- Kawamoto, Hiroshi -- New York, N.Y. -- Science. 2010 Jul 2;329(5987):93-6. doi: 10.1126/science.1188995.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory for Lymphocyte Development, RIKEN Research Center for Allergy and Immunology, Yokohama 230-0045, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20595615" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Cell Lineage ; Cells, Cultured ; Coculture Techniques ; Gene Expression Regulation, Developmental ; Gene Rearrangement, beta-Chain T-Cell Antigen Receptor ; Hematopoietic Stem Cells/cytology/*physiology ; Interleukin-7/metabolism ; Liver/embryology ; *Lymphopoiesis/genetics ; Mice ; Mice, Inbred C57BL ; Mice, Transgenic ; Precursor Cells, T-Lymphoid/cytology/*physiology ; Repressor Proteins/genetics/*metabolism ; Signal Transduction ; T-Lymphocytes/*cytology/*physiology ; Tumor Suppressor Proteins/genetics/*metabolism ; Up-Regulation
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    A septin diffusion barrier at the base of the primary cilium maintains ciliary membrane protein distribution (2010)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2010-06-19
    Description: In animal cells, the primary cilium transduces extracellular signals through signaling receptors localized in the ciliary membrane, but how these ciliary membrane proteins are retained in the cilium is unknown. We found that ciliary membrane proteins were highly mobile, but their diffusion was impeded at the base of the cilium by a diffusion barrier. Septin 2 (SEPT2), a member of the septin family of guanosine triphosphatases that form a diffusion barrier in budding yeast, localized at the base of the ciliary membrane. SEPT2 depletion resulted in loss of ciliary membrane protein localization and Sonic hedgehog signal transduction, and inhibited ciliogenesis. Thus, SEPT2 is part of a diffusion barrier at the base of the ciliary membrane and is essential for retaining receptor-signaling pathways in the primary cilium.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3092790/" 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/PMC3092790/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hu, Qicong -- Milenkovic, Ljiljana -- Jin, Hua -- Scott, Matthew P -- Nachury, Maxence V -- Spiliotis, Elias T -- Nelson, W James -- GM089933/GM/NIGMS NIH HHS/ -- GM35527/GM/NIGMS NIH HHS/ -- R01 GM089933/GM/NIGMS NIH HHS/ -- R37 GM035527/GM/NIGMS NIH HHS/ -- R37 GM035527-27/GM/NIGMS NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2010 Jul 23;329(5990):436-9. doi: 10.1126/science.1191054. Epub 2010 Jun 17.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biology, Stanford University, Stanford, CA 94305, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20558667" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Axoneme/metabolism ; Cell Line ; Cells, Cultured ; Cilia/*metabolism/ultrastructure ; Cytoskeletal Proteins/*metabolism ; Diffusion ; Fluorescence Recovery After Photobleaching ; GTP-Binding Proteins/*metabolism ; Hedgehog Proteins/metabolism ; Membrane Proteins/*metabolism ; Mice ; RNA, Small Interfering ; Receptors, Cell Surface/metabolism ; Receptors, G-Protein-Coupled/metabolism ; Receptors, Serotonin/metabolism ; Receptors, Somatostatin/metabolism ; Septins ; *Signal Transduction ; Transfection
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    ATP-binding cassette transporters and HDL suppress hematopoietic stem cell proliferation (2010)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2010-05-22
    Description: Elevated leukocyte cell numbers (leukocytosis), and monocytes in particular, promote atherosclerosis; however, how they become increased is poorly understood. Mice deficient in the adenosine triphosphate-binding cassette (ABC) transporters ABCA1 and ABCG1, which promote cholesterol efflux from macrophages and suppress atherosclerosis in hypercholesterolemic mice, displayed leukocytosis, a transplantable myeloproliferative disorder, and a dramatic expansion of the stem and progenitor cell population containing Lin(-)Sca-1(+)Kit+ (LSK) in the bone marrow. Transplantation of Abca1(-/-) Abcg1(-/-) bone marrow into apolipoprotein A-1 transgenic mice with elevated levels of high-density lipoprotein (HDL) suppressed the LSK population, reduced leukocytosis, reversed the myeloproliferative disorder, and accelerated atherosclerosis. The findings indicate that ABCA1, ABCG1, and HDL inhibit the proliferation of hematopoietic stem and multipotential progenitor cells and connect expansion of these populations with leukocytosis and accelerated atherosclerosis.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3032591/" 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/PMC3032591/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Yvan-Charvet, Laurent -- Pagler, Tamara -- Gautier, Emmanuel L -- Avagyan, Serine -- Siry, Read L -- Han, Seongah -- Welch, Carrie L -- Wang, Nan -- Randolph, Gwendalyn J -- Snoeck, Hans W -- Tall, Alan R -- HL54591/HL/NHLBI NIH HHS/ -- R01 AG029626/AG/NIA NIH HHS/ -- R01 AI049653/AI/NIAID NIH HHS/ -- R01 AI049653-09/AI/NIAID NIH HHS/ -- R01 AI049653-10/AI/NIAID NIH HHS/ -- R01 AI061741/AI/NIAID NIH HHS/ -- R01 AI061741-03/AI/NIAID NIH HHS/ -- R01 AI061741-04/AI/NIAID NIH HHS/ -- R01A1061741/PHS HHS/ -- R01AG016327/AG/NIA NIH HHS/ -- New York, N.Y. -- Science. 2010 Jun 25;328(5986):1689-93. doi: 10.1126/science.1189731. Epub 2010 May 20.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Molecular Medicine, Department of Medicine, Columbia University, New York, NY 10032, USA. ly2159@columbia.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20488992" target="_blank"〉PubMed〈/a〉
    Keywords: ATP Binding Cassette Transporter 1 ; ATP-Binding Cassette Transporters/genetics/*metabolism ; Animals ; Apolipoprotein A-I/genetics/metabolism ; Atherosclerosis/metabolism/*physiopathology/therapy ; Bone Marrow Transplantation ; Cell Proliferation ; Cells, Cultured ; Cholesterol/*metabolism ; Hematopoietic Stem Cells/*physiology ; Hypercholesterolemia/metabolism ; Leukocytosis/metabolism/*physiopathology/therapy ; Lipoproteins/genetics/*metabolism ; Lipoproteins, HDL/*metabolism ; Macrophages/metabolism ; Mice ; Mice, Inbred C57BL ; Mice, Inbred DBA ; Mice, Transgenic ; Multipotent Stem Cells/physiology ; Myeloid Progenitor Cells/*physiology ; Myeloproliferative Disorders/metabolism/physiopathology/therapy ; Phenotype ; Receptors, Granulocyte-Macrophage Colony-Stimulating Factor/metabolism ; Receptors, Interleukin-3/metabolism ; Signal Transduction
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    Homeostasis of the antibody response: immunoregulation by NK cells (1983)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1983-11-11
    Description: When injected into mice, the synthetic double-stranded polynucleotide poly(inosinic) X poly(cytidylic) acid induces high natural killer (NK) cell activity within 4 to 12 hours. Induction of NK activity in mice immunized 2 or 3 days previously, or the addition of NK cells to cultures immunized in vitro 2 or 3 days previously, promotes early termination of the ongoing primary immunoglobulin M antibody response. A target for NK cells is a population of accessory cells that has interacted with antigen and is necessary for sustaining the antibody response. The inference is strong that NK cells induced normally by immunization also terminate the usual antibody response in vivo by elimination of antigen-exposed accessory cells.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Abruzzo, L V -- Rowley, D A -- 5-T32-CA-09267/CA/NCI NIH HHS/ -- R01-10242/PHS HHS/ -- New York, N.Y. -- Science. 1983 Nov 11;222(4624):581-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6685343" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Antibody Formation ; Antibody-Producing Cells/immunology ; Cells, Cultured ; Homeostasis ; Killer Cells, Natural/*immunology/radiation effects ; Lymphocyte Cooperation ; Lymphocytes/*immunology ; Mice ; Poly I-C/immunology ; Spleen/immunology
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    Primary murine bone marrow cultures support continuous growth of infectious human trypanosomes (1983)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1983-04-22
    Description: The human parasite Trypanosoma brucei gambiense grew continuously at 37 degrees C in primary cultures of murine bone marrow. Cultured parasites remained virulent for mice. Rapid parasite growth coincided with the appearance of adherent adipocyte-epitheloid cell aggregates that also promoted hematopoiesis. This culture system should permit studies of host cell control of trypanosome proliferation, pathogenic effects of trypanosomes on blood cell development, and the relative trypanocidal and marrow suppressive activities of drugs.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Balber, A E -- CA 14049/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1983 Apr 22;220(4595):421-3.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6836284" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Bone Marrow ; Cells, Cultured ; Culture Media ; Humans ; Mice ; Mice, Inbred BALB C ; Trypanosoma brucei brucei/growth & development ; Trypanosoma brucei gambiense/*growth & development ; Trypanosomiasis, African/parasitology
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    Collagen formation by the hepatocyte in primary monolayer culture and in vivo (1983)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1983-03-18
    Description: Immunohistochemical techniques were used to confirm biochemical evidence that parenchymal cells isolated from adult rat liver and maintained in nonreplicating monolayer culture for 2 days synthesized type IV basement membrane collagen. On continued incubation in serum-free medium, the hepatocytes also synthesized the interstitial collagens, types I and III. Consistent with these results in culture, type IV collagen was localized to the hepatocytes in slices of pathologic rat liver. Hence collagen formation is a previously unrecognized function of the hepatocyte that may be important in the pathogenesis of liver fibrosis or cirrhosis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Diegelmann, R F -- Guzelian, P S -- Gay, R -- Gay, S -- AM18976/AM/NIADDK NIH HHS/ -- DE02570/DE/NIDCR NIH HHS/ -- HL11310/HL/NHLBI NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1983 Mar 18;219(4590):1343-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6828863" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Basement Membrane/metabolism ; Cells, Cultured ; Collagen/*biosynthesis/immunology ; Liver/cytology/*metabolism ; Molecular Weight ; Rats
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    Transformation of Bloom's syndrome fibroblasts by DNA transfection (1983)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1983-12-09
    Description: Nonmalignant diploid human fibroblast cells (GM3498B) derived from a skin biopsy of a patient with Bloom's syndrome have been transformed by transfection with DNA from a tumorigenic mouse cell line (Ha-8) carrying a single copy of the Harvey murine sarcoma virus (Ha-MuSV) genome. The transformed cell lines have an extended life-span, form colonies in agarose, and proliferate in nude mice--characteristics of neoplastic transformation. Like the parental cells, they also exhibit a high spontaneous level of sister chromatid exchanges. Finally, the transformed cells contain most, if not all, of the Ha-MuSV genome as well as the human rasH sequence. These experiments show that these diploid nonmalignant human cells can be used as recipients in transfection experiments for studying the genetic control of neoplastic transformation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Doniger, J -- Di Paolo, J A -- Popescu, N C -- New York, N.Y. -- Science. 1983 Dec 9;222(4628):1144-6.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6648529" target="_blank"〉PubMed〈/a〉
    Keywords: Bloom Syndrome/*genetics ; Cell Adhesion ; *Cell Transformation, Neoplastic ; Cells, Cultured ; DNA, Neoplasm/*genetics ; Humans ; Oncogenes ; Transfection
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    Formaldehyde damage to DNA and inhibition of DNA repair in human bronchial cells (1983)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1983-04-08
    Description: Cultured bronchial epithelial and fibroblastic cells from humans were used to study DNA damage and toxicity caused by formaldehyde. Formaldehyde caused the formation of cross-links between DNA and proteins, caused single-strand breaks in DNA, and inhibited the resealing of single-strand breaks produced by ionizing radiation. Formaldehyde also inhibited the unscheduled DNA synthesis that occurs after exposure of cells to ultraviolet irradiation or to benzo[a]pyrene diolexpoxide but at doses substantially higher than those required to inhibit the resealing of x-ray-induced single-strand breaks. Therefore, formaldehyde could exert its mutagenic and carcinogenic effects by both damaging DNA and inhibiting DNA repair.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Grafstrom, R C -- Fornace, A J Jr -- Autrup, H -- Lechner, J F -- Harris, C C -- New York, N.Y. -- Science. 1983 Apr 8;220(4593):216-8.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6828890" target="_blank"〉PubMed〈/a〉
    Keywords: Bronchi/*cytology/drug effects ; Cells, Cultured ; *DNA/biosynthesis ; DNA Repair/*drug effects ; Epithelium/drug effects ; Fibroblasts/drug effects ; Formaldehyde/*pharmacology ; Humans
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 39
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    Neuron-glia adhesion is inhibited by antibodies to neural determinants (1983)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1983-10-07
    Description: Suspensions of embryonic chick neuronal cells adhered to monolayers of glial cells, but few neurons bound to control monolayers of fibroblastic cells from meninges or skin. Neuronal cell-glial cell adhesion was inhibited by prior incubation of the neurons with Fab' fragments of antibodies to neuronal membranes. In contrast, antibodies to the neural cell adhesion molecule (N-CAM) did not inhibit the binding. These results suggest that a specific adhesive mechanism between neurons and glial cells exists and that it is mediated by CAM's that differ from those so far identified.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Grumet, M -- Rutishauser, U -- Edelman, G M -- AI-11378/AI/NIAID NIH HHS/ -- HD-09635/HD/NICHD NIH HHS/ -- HD-16550/HD/NICHD NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1983 Oct 7;222(4619):60-2.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6194561" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antibodies, Monoclonal ; Antigen-Antibody Complex ; *Cell Adhesion ; Cell Membrane/immunology ; Cells, Cultured ; Chick Embryo ; Epitopes ; Immunoglobulin Fab Fragments ; Neuroglia/*physiology ; Neurons/immunology/*physiology
    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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  • 40
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    Tumor-derived growth factor increases bone resorption in a tumor associated with humoral hypercalcemia of malignancy (1983)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1983-09-23
    Description: Evidence is presented that a tumor-derived transforming growth factor is responsible for stimulating bone resorption and causing hypercalcemia in an animal tumor model of the hypercalcemia of malignancy. Both conditioned medium harvested from cultured tumor cells and tumor extracts of the transplantable rat Leydig cell tumor associated with hypercalcemia contained a macromolecular bone resorbing factor with the chemical characteristics of a tumor-derived transforming growth factor.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ibbotson, K J -- D'Souza, S M -- Ng, K W -- Osborne, C K -- Niall, M -- Martin, T J -- Mundy, G R -- AM-28149/AM/NIADDK NIH HHS/ -- CA-29537/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1983 Sep 23;221(4617):1292-4.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6577602" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Bone Resorption ; Calcium ; Cells, Cultured ; Culture Media ; Growth Substances/*physiology ; Hypercalcemia/*etiology ; Leydig Cell Tumor/complications/*physiopathology ; Male ; Neoplasm Proteins/*physiology ; Neoplasms, Experimental/complications/physiopathology ; Peptides/*physiology ; Rats ; Transforming Growth Factors
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  • 41
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    Fragile sites in chromosomes: possible model for the study of spontaneous chromosome breakage (1983)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1983-04-01
    Description: The tissue culture condition that is required for the type of chromosome breakage seen at most fragile sites, namely, the absence of folic acid and thymidine in the medium, greatly enhanced micronucleus formation in proliferating lymphocyte cultures from normal individuals. This suggests that chromosome breakage at fragile sites and the apparently spontaneous damage that gives rise to micronuclei are controlled by the same mechanism.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Jacky, P B -- Beek, B -- Sutherland, G R -- New York, N.Y. -- Science. 1983 Apr 1;220(4592):69-70.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6828880" target="_blank"〉PubMed〈/a〉
    Keywords: Adolescent ; Adult ; Cell Nucleus/drug effects/ultrastructure ; Cells, Cultured ; Child ; *Chromosome Aberrations ; Chromosome Fragile Sites ; *Chromosome Fragility ; Culture Media ; Dose-Response Relationship, Drug ; Female ; Folic Acid/pharmacology ; Humans ; Lymphocytes/ultrastructure ; Male ; Middle Aged ; Thymidine/pharmacology
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    Oxygen tension regulates the expression of angiogenesis factor by macrophages (1983)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1983-09-23
    Description: When cultured in a hypoxic environment similar to that found in the center of a wound, macrophages secreted active angiogenesis factor into the medium. Under conditions similar to those of well-oxygenated tissue, macrophages did not secrete active angiogenesis factor. Macrophages that secreted the factor at hypoxic conditions stopped secreting it when returned to room air. Thus the control of angiogenesis in wound healing may be the result of macrophages responding to tissue oxygen tension without the necessity of interacting with other cell types or biochemical signals.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Knighton, D R -- Hunt, T K -- Scheuenstuhl, H -- Halliday, B J -- Werb, Z -- Banda, M J -- GM27345/GM/NIGMS NIH HHS/ -- HL26323/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1983 Sep 23;221(4617):1283-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6612342" target="_blank"〉PubMed〈/a〉
    Keywords: Angiogenesis Inducing Agents/*biosynthesis ; Animals ; Anoxia/physiopathology ; Cells, Cultured ; Cornea ; Growth Substances/*biosynthesis ; Macrophages/*physiology ; Models, Biological ; Oxygen/*physiology ; Rabbits ; *Wound Healing
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    Drug-induced alterations of cytokeratin organization in cultured epithelial cells (1983)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1983-02-04
    Description: The distribution of keratin intermediate filaments, previously considered static in organization and imperturbable by conventional drugs used to alter the structure and organization of the cytoskeleton, can be altered significantly by treatment with colchicine and cytochalasin D. The loss of microfilaments and microtubules converts the keratin cytoskeleton from a branching, even distribution to a series of starlike structures whose filaments are maintained by multiple membrane attachment sites. These findings provide a means for manipulating cytokeratin organization to investigate the role of keratins in cytoskeletal structure and function.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Knapp, L W -- O'Guin, W M -- Sawyer, R H -- New York, N.Y. -- Science. 1983 Feb 4;219(4584):501-3.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6186022" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cells, Cultured ; Colchicine/*pharmacology ; Cytochalasin D ; Cytochalasins/*pharmacology ; Cytoskeleton/*drug effects ; Epithelium ; *Keratins ; Mice ; Microtubules/drug effects
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    Human endothelial cells: use of heparin in cloning and long-term serial cultivation (1983)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1983-11-11
    Description: Endothelial cells from human blood vessels were cultured in vitro, with doubling times of 17 to 21 hours for 42 to 79 population doublings. Cloned human endothelial cell strains were established for the first time and had similar proliferative capacities. This vigorous cell growth was achieved by addition of heparin to culture medium containing reduced concentrations of endothelial cell growth factor. The routine cloning and long-term culture of human endothelial cells will facilitate studying the human endothelium in vitro.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Thornton, S C -- Mueller, S N -- Levine, E M -- AG-00839/AG/NIA NIH HHS/ -- T32-CA-09171/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1983 Nov 11;222(4624):623-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6635659" target="_blank"〉PubMed〈/a〉
    Keywords: Cell Division/drug effects ; Cells, Cultured ; Clone Cells/enzymology ; Endothelium/*cytology ; Growth Substances/pharmacology ; Heparin/*pharmacology ; Humans ; Time Factors
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  • 45
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    Interaction with membrane remnants of target myotubes maintains transmitter sensitivity of cultured neurons (1983)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1983-05-27
    Description: Parasympathetic neurons, when cultured alone, lose sensitivity to acetylcholine, but if striated muscle is included in the culture, neuronal chemosensitivity is maintained. The membrane remnants of myotubes ruptured by osmotic shock also supported the responsiveness of the cultured neurons to transmitter, whereas muscle-conditioned medium or membrane remnants of nonmuscle embryonic skin cells did not support this responsiveness. The regulation of chemosensitivity by contact of neurons with the target cell membrane may be important in the formation and maintenance of neuronal circuitry.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Tuttle, J B -- NS-10338/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1983 May 27;220(4600):977-9.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6133352" target="_blank"〉PubMed〈/a〉
    Keywords: Acetylcholine/physiology ; Animals ; Cell Membrane/physiology ; Cells, Cultured ; Chick Embryo ; Fibroblasts/physiology ; Muscles/*physiology ; Nervous System/growth & development ; Neurons/*physiology ; Neurotransmitter Agents/*physiology ; Synapses/physiology
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    High-frequency transfection and cytopathology of the hepatitis B virus core antigen gene in human cells (1983)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1983-10-28
    Description: A protoplast fusion method was developed to stably transfect human cells with pSV2-derived plasmids at frequencies greater than 10(-3). This procedure made it possible to test the biological effect of a hepatitis B virus (HBV) gene independent of the viral structures required for infection. A pSV2gpt+ plasmid constructed to carry a subgenomic fragment of HBV that contained the core antigen gene (HBc gene) was transfected into human cells. A human epithelial cell line was stably transfected with the HBc+ gene by selecting recipient cells for expression of guanine phosphoribosyl transferase expression. With this gpt+/HBc+ cell line it was shown that growth in serum-free medium or treatment with 5'-azacytidine stimulates the production of the HBV core antigen. A hepatocellular carcinoma carrying the entire HBV genome was stimulated to produce the HBc gene product in response to the same factors that stimulated HBcAg production in the gpt+/HBc+ cell line constructed by transfection. The temporal relation between the cytopathologic response and HBc gene expression was similar for both cell types, indicating a primary role for HBc gene expression in the cytopathology of HBV-infected human liver.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Yoakum, G H -- Korba, B E -- Lechner, J F -- Tokiwa, T -- Gazdar, A F -- Seeley, T -- Siegel, M -- Leeman, L -- Autrup, H -- Harris, C C -- New York, N.Y. -- Science. 1983 Oct 28;222(4622):385-9.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6194563" target="_blank"〉PubMed〈/a〉
    Keywords: Azacitidine/pharmacology ; Cell Fusion ; *Cell Transformation, Viral ; Cells, Cultured ; Cytopathogenic Effect, Viral ; Gene Expression Regulation/drug effects ; Genes, Viral ; Hepatitis B Core Antigens/*genetics ; Humans ; Transfection
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    Insulin receptor: evidence that it is a protein kinase (1983)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1983-01-21
    Description: Highly purified preparations of insulin receptor catalyzed the phosphorylation of the 95,000-dalton subunit of the insulin receptor. This subunit of the insulin receptor was also labeled with [alpha-32P]8-azidoadenosine 5'-triphosphate, a photoaffinity label for adenosine triphosphate binding sites. The identity of the 95,000-dalton band was confirmed in both cases by precipitation with a monoclonal antibody to the insulin receptor. These results suggest that the insulin receptor is itself a protein kinase.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Roth, R A -- Cassell, D J -- New York, N.Y. -- Science. 1983 Jan 21;219(4582):299-301.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6849137" target="_blank"〉PubMed〈/a〉
    Keywords: Adenosine Triphosphate/metabolism ; Cell Line ; Cells, Cultured ; Lymphocytes ; Molecular Weight ; Phosphoproteins/physiology ; Protein Kinases/*physiology ; Receptor, Insulin/*physiology
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  • 48
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    Heterogeneity of normal human diploid fibroblasts: isolation and characterization of one phenotype (1984)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1984-01-13
    Description: Cultures of human diploid fibroblasts contain cells that respond to exposure to the first component of complement (C1) by initiating DNA synthesis and growth. The plasma membranes of these cells have specific binding sites for the C1q subcomponent of C1. A fluorescence-activated cell sorter was used to isolate a subset of cells with a high affinity for C1q, and the growth and synthesis activities of these high-affinity cells were studied after numerous replications in vitro. These cells synthesize DNA and grow faster than the parent cultures and low-affinity cells, and they produce two to three times as much protein. About 40 percent of their total protein synthesis activity is directed to collagen production, unusually high proportions of collagen types III and V being produced. These properties and the high affinity of the cells for C1q are retained for at least six cell transfers. This phenotype has the properties expected of fibroblasts in healing wounds and inflamed tissues.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bordin, S -- Page, R C -- Narayanan, A S -- DE-02600/DE/NIDCR NIH HHS/ -- DE-03301/DE/NIDCR NIH HHS/ -- New York, N.Y. -- Science. 1984 Jan 13;223(4632):171-3.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6691142" target="_blank"〉PubMed〈/a〉
    Keywords: *Antigens, CD44 ; Carrier Proteins ; Cell Division ; Cell Separation ; Cells, Cultured ; Collagen/*biosynthesis/classification ; DNA/*biosynthesis ; Fibroblasts/analysis/cytology/*physiology ; Flow Cytometry ; Gingiva ; Humans ; *Membrane Glycoproteins ; Mitochondrial Proteins ; Phenotype ; *Protein Biosynthesis ; Receptors, Complement/*analysis
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    Recombination during gene transfer into mouse cells can restore the function of deleted genes (1983)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1983-01-14
    Description: Two plasmids containing nonoverlapping deletions of the herpes simplex virus thymidine kinase gene were introduced into thymidine kinase-deficient mouse L cells by DNA-mediated gene transfer. Thymidine kinase-producing transformants were generated by a mixture of the two plasmids at a frequency significantly greater than that generated by either plasmid alone. Southern blot analyses demonstrated that functional thymidine kinase genes were generated by homologous recombination between the two deletion mutants.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Small, J -- Scangos, G -- New York, N.Y. -- Science. 1983 Jan 14;219(4581):174-6.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6294829" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Base Sequence ; Cells, Cultured ; Chromosome Deletion ; *Genetic Engineering ; Mice ; Mutation ; *Plasmids ; *Recombination, Genetic ; Simplexvirus ; Thymidine Kinase/*genetics
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  • 50
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    Human macrophages armed with murine immunoglobulin G2a antibodies to tumors destroy human cancer cells (1983)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1983-08-26
    Description: Macrophages isolated from tumor-bearing patients as well as cultured human monocytes express Fc receptors that cross-react strongly with murine immunoglobulins of the G2a but only slightly or not at all with the G1, G2b, or G3 subclasses. Such macrophages in the presence of murine immunoglobulin G2a monoclonal antibodies to tumors mediated the killing of tumor cells in vitro. These data suggest that monoclonal antibodies of the G2a subclass may be useful in the immunotherapy of human cancer.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Steplewski, Z -- Lubeck, M D -- Koprowski, H -- CA-10815/CA/NCI NIH HHS/ -- CA-21124/CA/NCI NIH HHS/ -- CA-25874/CA/NCI NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1983 Aug 26;221(4613):865-7.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6879183" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antibodies, Monoclonal/*immunology ; Cells, Cultured ; Cytotoxicity, Immunologic ; Humans ; *Immunity, Cellular ; Immunoglobulin G/immunology ; Immunotherapy ; Macrophages/*immunology ; Mice ; Monocytes/immunology ; Neoplasms, Experimental/immunology/therapy ; Receptors, Fc/*immunology ; Species Specificity
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  • 51
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    A novel nuclear form of estradiol receptor in MCF-7 human breast cancer cells (1984)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1984-09-14
    Description: Nuclear estrogen receptor from MCF-7 cells undergoes a time-dependent, hormone-inducible transformation to a form that is less extractable from nuclei and less exchangeable with ligand. This receptor-modifying, intranuclear event is independent of receptor loss (processing) and appears associated with hormone responsiveness (progesterone-receptor induction) in these cells. The magnitude of receptor loss, however, is variable and apparently not a prerequisite for hormone action to induce progesterone receptor.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kasid, A -- Strobl, J S -- Huff, K -- Greene, G L -- Lippman, M E -- New York, N.Y. -- Science. 1984 Sep 14;225(4667):1162-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6474170" target="_blank"〉PubMed〈/a〉
    Keywords: Breast Neoplasms/*metabolism ; Cell Nucleus/metabolism ; Cells, Cultured ; Female ; Humans ; Receptors, Estradiol ; Receptors, Estrogen/*metabolism ; Receptors, Progesterone/biosynthesis ; Time Factors
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  • 52
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    Frequent detection and isolation of cytopathic retroviruses (HTLV-III) from patients with AIDS and at risk for AIDS (1984)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1984-05-04
    Description: Peripheral blood lymphocytes from patients with the acquired immunodeficiency syndrome (AIDS) or with signs or symptoms that frequently precede AIDS (pre-AIDS) were grown in vitro with added T-cell growth factor and assayed for the expression and release of human T-lymphotropic retroviruses (HTLV). Retroviruses belonging to the HTLV family and collectively designated HTLV-III were isolated from a total of 48 subjects including 18 of 21 patients wih pre-AIDS, three of four clinically normal mothers of juveniles with AIDS, 26 of 72 adult and juvenile patients with AIDS, and from one of 22 normal male homosexual subjects. No HTLV-III was detected in or isolated from 115 normal heterosexual subjects. The number of HTLV-III isolates reported here underestimates the true prevalence of the virus since many specimens were received in unsatisfactory condition. Other data show that serum samples from a high proportion of AIDS patients contain antibodies to HTLV-III. That these new isolates are members of the HTLV family but differ from the previous isolates known as HTLV-I and HTLV-II is indicated by their morphological, biological, and immunological characteristics. These results and those reported elsewhere in this issue suggest that HTLV-III may be the primary cause of AIDS.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gallo, R C -- Salahuddin, S Z -- Popovic, M -- Shearer, G M -- Kaplan, M -- Haynes, B F -- Palker, T J -- Redfield, R -- Oleske, J -- Safai, B -- New York, N.Y. -- Science. 1984 May 4;224(4648):500-3.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6200936" target="_blank"〉PubMed〈/a〉
    Keywords: Acquired Immunodeficiency Syndrome/blood/*microbiology ; Adult ; Antigens, Viral/analysis ; Cells, Cultured ; Cytopathogenic Effect, Viral ; Deltaretrovirus/*isolation & purification/physiology/ultrastructure ; Female ; Homosexuality ; Humans ; Immune Sera/pharmacology ; Interferon Type I/immunology ; Male ; RNA-Directed DNA Polymerase/metabolism ; Risk ; T-Lymphocytes/microbiology
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    Isolation and culture of a tetraploid subpopulation of smooth muscle cells from the normal rat aorta (1984)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1984-11-02
    Description: Smooth muscle cells with 4C (double diploid) DNA content have been found in major arteries. The proportion of 4C cells increases with normal aging and with hypertension. These cells may represent a state of arrest at the G2 phase of the cell cycle or may be examples of true tetraploidy. Flow cytometric cell sorting was used to isolate 4C smooth muscle cells from the rat aorta, and the cells were cultured. Flow cytometry, Feulgen microdensitometry, and karyotyping of the progeny of the 4C cells established the presence of true tetraploid cells. These findings demonstrate the presence of reproductively viable tetraploid cells in a normal mammalian tissue.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Goldberg, I D -- Rosen, E M -- Shapiro, H M -- Zoller, L C -- Myrick, K -- Levenson, S E -- Christenson, L -- 5-P01-CA-12662/CA/NCI NIH HHS/ -- AG00599/AG/NIA NIH HHS/ -- New York, N.Y. -- Science. 1984 Nov 2;226(4674):559-61.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6494901" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Aorta, Thoracic/analysis/*cytology ; Cells, Cultured ; DNA/analysis ; Flow Cytometry ; Humans ; Karyotyping ; Muscle, Smooth, Vascular/analysis/*cytology ; *Polyploidy ; Rats ; Rats, Inbred Strains
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    Reversal of knob formation on Plasmodium falciparum-infected erythrocytes (1984)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1984-10-05
    Description: The human malarial parasite Plasmodium falciparum can produce surface protrusions (knobs) on infected erythrocytes; however, long-term culturing of the parasite results in the appearance of knobless cells. In this study it was found that a knob-producing clone lost the ability to produce knobs in vitro. Furthermore, a clone not producing knobs derived from the knob-producing clone regained the capacity to produce knobby cells in vitro. Certain parasite proteins were associated with the knobby phenotype but not with the knobless type. These results indicate that the parasites change in vitro in a spontaneous and reversible manner independent of immunological selection.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gritzmacher, C A -- Reese, R T -- AI 18695/AI/NIAID NIH HHS/ -- DRR 00833/RR/NCRR NIH HHS/ -- New York, N.Y. -- Science. 1984 Oct 5;226(4670):65-7.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6382613" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cells, Cultured ; Clone Cells ; Erythrocytes/*parasitology/ultrastructure ; Humans ; Mutation ; Phenotype ; Plasmodium falciparum/analysis/genetics/growth & development/*physiology ; Proteins/analysis
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    Serotonin selectively inhibits growth cone motility and synaptogenesis of specific identified neurons (1984)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1984-11-02
    Description: The motile activity of growth cones of specific identified neurons is inhibited by the neurotransmitter serotonin, although other identified neurons are unaffected. As a consequence, affected neurons are unable to form electrical synapses, whereas other neurons whose growth is unaffected can still interconnect. This result demonstrates that neurotransmitters can play a prominent role in regulating neuronal architecture and connectivity in addition to their classical role in neurotransmission.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Haydon, P G -- McCobb, D P -- Kater, S B -- HD18577/HD/NICHD NIH HHS/ -- NS15350/NS/NINDS NIH HHS/ -- NS18819/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1984 Nov 2;226(4674):561-4.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6093252" target="_blank"〉PubMed〈/a〉
    Keywords: Animal Population Groups ; Animals ; Cells, Cultured ; Neurons/*drug effects/growth & development ; Serotonin/*pharmacology ; Snails ; Synapses/*drug effects ; Synaptic Transmission
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    Monoclonal antibody to Thy-1 enhances regeneration of processes by rat retinal ganglion cells in culture (1984)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1984-04-20
    Description: Ganglion cells were dissociated from postnatal rat retinas, identified by specific fluorescent labels, and maintained in culture on a variety of substrates. Regeneration of processes by retinal ganglion cells was enhanced when the cells were plated on glass coated with a monoclonal antibody against the Thy-1 determinant. Plain glass and glass coated with polylysine, collagen, fibronectin, or other monoclonal antibodies supported the growth of neural processes, but were less effective than antibody to Thy-1.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Leifer, D -- Lipton, S A -- Barnstable, C J -- Masland, R H -- EY01075/EY/NEI NIH HHS/ -- EY03735/EY/NEI NIH HHS/ -- EY04179/EY/NEI NIH HHS/ -- New York, N.Y. -- Science. 1984 Apr 20;224(4646):303-6.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6143400" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antibodies, Monoclonal/*physiology ; Antigens, Surface/*immunology ; Antigens, Thy-1 ; Cell Adhesion ; Cells, Cultured ; Isoantibodies/*physiology ; *Nerve Regeneration ; Polylysine/pharmacology ; Rats ; Retina/cytology/*physiology ; Retinal Ganglion Cells/*physiology
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    Isolation of lymphocytopathic retroviruses from San Francisco patients with AIDS (1984)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1984-08-24
    Description: Infectious retroviruses have been detected in 22 of 45 randomly selected patients with acquired immune deficiency syndrome (AIDS) and in other individuals from San Francisco. The AIDS-associated retroviruses (ARV) studied in detail had a type D morphology, Mg2+-dependent reverse transcriptase, and cytopathic effects on lymphocytes. The viruses can be propagated in an established adult human T cell line, HUT-78. They cross-react with antiserum to the lymphadenopathy-associated retrovirus isolated from AIDS patients in France. Antibodies to ARV were found in all 86 AIDS patients and in a high percentage of 88 other homosexual men in San Francisco. This observation indicates the widespread presence of these lymphocytopathic retroviruses and their close association with AIDS.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Levy, J A -- Hoffman, A D -- Kramer, S M -- Landis, J A -- Shimabukuro, J M -- Oshiro, L S -- CA-34980/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1984 Aug 24;225(4664):840-2.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6206563" target="_blank"〉PubMed〈/a〉
    Keywords: Acquired Immunodeficiency Syndrome/immunology/*microbiology ; Antibodies, Viral/analysis ; Bone Marrow/microbiology ; California ; Cell Line ; Cells, Cultured ; Cross Reactions ; Cytopathogenic Effect, Viral ; Deltaretrovirus/immunology/*isolation & purification/physiology/ultrastructure ; *Homosexuality ; Humans ; Leukocytes/microbiology ; Lymphatic Diseases/immunology ; Male ; RNA-Directed DNA Polymerase/metabolism ; Syndrome ; T-Lymphocytes ; Virus Cultivation
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    Time-varying magnetic fields: effect on DNA synthesis (1984)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1984-02-24
    Description: Human fibroblasts have exhibited enhanced DNA synthesis when exposed to sinusoidally varying magnetic fields for a wide range of frequencies (15 hertz to 4 kilohertz) and amplitudes (2.3 X 10(-6) to 5.6 X 10(-4) tesla). This effect, which is at maximum during the middle of the S phase of the cell cycle, appears to be independent of the time derivative of the magnetic field, suggesting an underlying mechanism other than Faraday's law. The threshold is estimated to be between 0.5 X 10(-5) and 2.5 X 10(-5) tesla per second. These results bring into question the allegedly specific magnetic wave shapes now used in therapeutic devices for bone nonunion. The range of magnetic field amplitudes tested encompass the geomagnetic field, suggesting the possibility of mutagenic interactions directly arising from short-term changes in the earth's field.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Liboff, A R -- Williams, T Jr -- Strong, D M -- Wistar, R Jr -- New York, N.Y. -- Science. 1984 Feb 24;223(4638):818-20.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6695183" target="_blank"〉PubMed〈/a〉
    Keywords: Cells, Cultured ; DNA/*biosynthesis ; Humans ; *Magnetics ; Mutation ; Periodicity
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    Sequential interaction of glia maturation factor with insulin (1984)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1984-03-30
    Description: Astroblasts in culture proliferated when exposed to glia maturation factor for at least 2 hours and then to insulin, but not when exposed in the reverse order. The sequential relation suggests that glia maturation factor is a competence factor.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lim, R -- Miller, J F -- CA-31796/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1984 Mar 30;223(4643):1419-20.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6367047" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Astrocytes/drug effects/physiology ; Cell Division/drug effects ; Cells, Cultured ; Drug Interactions ; Glia Maturation Factor ; Growth Substances/*pharmacology/physiology ; Insulin/*pharmacology/physiology ; Mice ; Mice, Inbred BALB C ; Nerve Tissue Proteins/*pharmacology/physiology ; Rats
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    Voltage-dependent calcium channels in glial cells (1984)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1984-12-14
    Description: The electrophysiological properties of glial cells were examined in primary culture in the presence of tetraethylammonium and Ba2+, a treatment that reduces K+ permeability of the membrane and enhances currents through voltage-dependent Ca2+ channels. Under these conditions, glial cells showed both spontaneous action potentials and action potentials evoked by the injections of current. These responses appear to represent entry of Ba2+ through Ca2+ channels because they were resistant to tetrodotoxin but were blocked by Mn2+ or Cd2+.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉MacVicar, B A -- New York, N.Y. -- Science. 1984 Dec 14;226(4680):1345-7.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6095454" target="_blank"〉PubMed〈/a〉
    Keywords: Action Potentials ; Barium/pharmacology ; Cadmium/pharmacology ; Calcium/*metabolism ; Cells, Cultured ; Evoked Potentials ; Ion Channels/*physiology ; Microelectrodes ; Neuroglia/*physiology ; Tetraethylammonium Compounds/pharmacology ; Tetrodotoxin/pharmacology
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    Beta-adrenergic mechanism of insulin-induced adrenocorticotropin release from the anterior pituitary (1984)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1984-11-30
    Description: Intraperitoneal administration of insulin to control rats and to rats with pituitary stalk transections or with lesions of the median eminence resulted in increased plasma adrenocorticotropin (ACTH) levels. The insulin-induced stimulation of ACTH release was blocked in both the control and lesioned animals by prior treatment with either the beta-adrenergic antagonist propranolol or the glucocorticoid analog dexamethasone. The direct application of insulin to primary cultures of the anterior pituitary did not evoke ACTH release or affect the maximal ability of corticotropin-releasing factor or epinephrine to stimulate ACTH secretion. The results suggest that insulin stimulates ACTH release by a mechanism in which catecholamines of peripheral origin act directly on the anterior pituitary.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Mezey, E -- Reisine, T D -- Brownstein, M J -- Palkovits, M -- Axelrod, J -- New York, N.Y. -- Science. 1984 Nov 30;226(4678):1085-7.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6093262" target="_blank"〉PubMed〈/a〉
    Keywords: Adrenocorticotropic Hormone/blood/*secretion ; Animals ; Cells, Cultured ; Corticotropin-Releasing Hormone/pharmacology ; Dexamethasone/pharmacology ; Epinephrine/pharmacology ; Insulin/*pharmacology ; Median Eminence/physiology ; Pituitary Gland/physiology ; Pituitary Gland, Anterior/drug effects/*secretion ; Propranolol/*pharmacology ; Rats ; Receptors, Adrenergic, beta/drug effects/*physiology
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    Human colon cells: culture and in vitro transformation (1984)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1984-06-29
    Description: Normal human colon mucosal epithelial cells were cultured in vitro and treated with the oncogenic simian DNA virus (SV40) and the chemical carcinogen azoxymethane. Both SV40 and azoxymethane altered a number of phenotypic characteristics of the normal human colon cells, including their morphology, culture longevity, growth in soft agar, substrate adherence, and peanut agglutinin binding. The SV40 transformants synthesized intranuclear T antigen. These data indicate that normal human colon mucosal cells were transformed toward the malignant phenotype.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Moyer, M P -- Aust, J B -- RRO5654/RR/NCRR NIH HHS/ -- New York, N.Y. -- Science. 1984 Jun 29;224(4656):1445-7.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6328655" target="_blank"〉PubMed〈/a〉
    Keywords: Antigens, Viral, Tumor/metabolism ; Azoxymethane/pharmacology ; Cell Transformation, Neoplastic/*physiopathology ; Cells, Cultured ; Colon/*cytology/drug effects ; Colonic Neoplasms/physiopathology ; Fibroblasts/drug effects ; Humans ; Lectins/pharmacology ; Simian virus 40/metabolism
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    Adaptive response of human lymphocytes to low concentrations of radioactive thymidine (1984)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1984-02-10
    Description: When human lymphocytes were cultured with [3H]thymidine, which acts as a source of low-level chronic radiation, and then exposed to 150 rad of x-rays at 5, 7, 9, or 11 hours before fixation, the yield of chromatid aberrations was less than the sum of the yields of aberrations induced by [3H]thymidine and x-rays separately. Often fewer aberrations were found after exposure to radiation from both sources than were found after exposure to x-rays alone. At the same fixation times, nonradioactive thymidine did not affect the yield of x-ray-induced aberrations. The same phenomenon occurred at earlier fixation times, after exposure to 30 or 40 rad of x-rays and [3H]thymidine. This response is analogous to the adaptive response to alkylating agents whereby prior treatment with small doses for a long period reduces the damage occurring from large doses of similar agents given for a short time.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Olivieri, G -- Bodycote, J -- Wolff, S -- New York, N.Y. -- Science. 1984 Feb 10;223(4636):594-7.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6695170" target="_blank"〉PubMed〈/a〉
    Keywords: Cells, Cultured ; *Chromosome Aberrations ; Chromosome Deletion ; Humans ; Lymphocytes/drug effects/physiology/*radiation effects ; Metaphase/drug effects/radiation effects ; Thymidine/*toxicity ; Tritium
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    Lymphokine production by cultured human T cells transformed by human T-cell leukemia-lymphoma virus-I (1984)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1984-02-17
    Description: Cell-free conditioned media from human T cells transformed by human T-cell leukemia-lymphoma virus (HTLV-I) were tested for the production of soluble biologically active factors, including several known lymphokines. The cell lines used were established from patients with T-cell leukemia-lymphoma and from human umbilical cord blood and bone marrow leukocytes transformed by HTLV-I in vitro. All of the cell lines liberated constitutively one or more of the 12 biological activities assayed. These included macrophage migration inhibitory factor (MIF), leukocyte migration inhibitory factor (LIF), leukocyte migration enhancing factor (MEF), macrophage activating factor (MAF), differentiation inducing factor (DIF), colony stimulating factor (CSF), eosinophil growth and maturation activity (eos. GMA), fibroblast activating factor (FAF), gamma-interferon and, in rare instances, T-cell growth factor (TCGF). Some cell lines produced interleukin 3 (IL-3), platelet-derived growth factor (PDGF), or B-cell growth factors (BCGF). Such cells should prove useful for the production of lymphokines and as sources of specific messenger RNA's for their genetic cloning.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Salahuddin, S Z -- Markham, P D -- Lindner, S G -- Gootenberg, J -- Popovic, M -- Hemmi, H -- Sarin, P S -- Gallo, R C -- New York, N.Y. -- Science. 1984 Feb 17;223(4637):703-7.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6320367" target="_blank"〉PubMed〈/a〉
    Keywords: Antibodies, Monoclonal ; Antigens, Neoplasm/analysis ; Bone Marrow ; Cell Line ; *Cell Transformation, Neoplastic ; Cells, Cultured ; Deltaretrovirus/*genetics ; Female ; Humans ; Leukemia/*microbiology ; Lymphokines/*biosynthesis ; Lymphoma/*microbiology ; Phenotype ; Pregnancy ; T-Lymphocytes/*immunology
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    Hepatitis B virus infection in cultured human lymphoblastoid cells (1983)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1983-08-12
    Description: Since it has been postulated that liver hepatocytes may become infected by hepatitis B virus (HBV) in vivo through direct contact with infected macrophages, the possibility that a circulating cell of hematopoietic origin might be susceptible to infection with HBV was investigated. Cells positive for HBV surface antigen were identified in aspirates of bone marrow cells from people infected with HBV. These cells were used to prepare a lymphoblastoid suspension culture that contains HBV-infected cells.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Romet-Lemonne, J L -- McLane, M F -- Elfassi, E -- Haseltine, W A -- Azocar, J -- Essex, M -- New York, N.Y. -- Science. 1983 Aug 12;221(4611):667-9.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6867736" target="_blank"〉PubMed〈/a〉
    Keywords: Cells, Cultured ; Hepatitis B/*microbiology/pathology ; Hepatitis B Surface Antigens/immunology ; Hepatitis B virus/growth & development ; Humans ; Liver/pathology ; Lymphocytes/*microbiology/pathology ; Male ; Middle Aged
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    Benzodiazepine receptor synthesis and degradation by neurons in culture (1984)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1984-11-16
    Description: The benzodiazepine-gamma-aminobutyric acid receptor complex was used to study functional receptor synthesis and degradation in primary cultures of neurons. Fifty percent of the receptors turned over with an unusually rapid half-life (4 hours); this was followed by a second, slower phase (32 hours). These results provide the basis for elucidating the mechanism by which neurons derived from the central nervous system control neurotransmitter receptor number, an important problem in cellular neurobiology. The findings may be of significance in the study of neurological and psychiatric disorders.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Borden, L A -- Czajkowski, C -- Chan, C Y -- Farb, D H -- New York, N.Y. -- Science. 1984 Nov 16;226(4676):857-60.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6093257" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cells, Cultured ; Chick Embryo ; Flunitrazepam/metabolism ; Half-Life ; Kinetics ; Neurons/*metabolism ; Receptors, GABA-A/biosynthesis/*metabolism ; Spinal Cord/cytology ; gamma-Aminobutyric Acid/physiology
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    Synaptic activity mediates death of hypoxic neurons (1983)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1983-04-29
    Description: Cultured hippocampal neurons, when exposed to cyanide or an anoxic atmosphere in the early stages of differentiation, were not visibly affected. However, neurons in the mature cultures died when exposed to cyanide or anoxia. Cell death could be prevented by treatment with magnesium, which eliminates synaptic activity. These observations suggest that damage in hypoxic neurons is mediated by synaptic activity.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rothman, S M -- 5 K07 N500568-02/PHS HHS/ -- New York, N.Y. -- Science. 1983 Apr 29;220(4596):536-7.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6836300" target="_blank"〉PubMed〈/a〉
    Keywords: Action Potentials/drug effects ; Animals ; Anoxia/*metabolism/physiopathology ; Cells, Cultured ; Hippocampus/cytology ; Magnesium/pharmacology ; Magnesium Chloride ; Membrane Potentials/drug effects ; Neurons/metabolism/*physiology ; Rats ; Sodium Cyanide/pharmacology ; Synapses/drug effects/*physiology
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Infection of normal human epithelial cells by Epstein-Barr virus (1983)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1983-03-11
    Description: Primary cultures of epithelial cells were grown from the tonsils and adenoids of patients with diseases not related to Epstein-Barr virus. The cells could not be infected by Epstein-Barr virus. Fluorescein-labeled Epstein-Barr virus and a cytofluorograph were then used to show that the epithelial cells do not have detectable receptors for the virus. However, implantation with Epstein-Barr virus receptors gave the cells the ability to bind the labeled virus. One to 5 percent of receptor-implanted cells exposed to the transforming B95-8 substrain of the virus expressed Epstein-Barr nuclear antigen. The early and viral capsid Epstein-Barr virus-determined antigens were not detected in the virus-infected cultures. The results show that normal human epithelial cells from the nasopharynx become susceptible to infection by Epstein-Barr virus when the membrane barrier resulting from the lack of viral receptors is overcome by receptor implantation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Shapiro, I M -- Volsky, D J -- 1R01 CA33386-01/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1983 Mar 11;219(4589):1225-8.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6298935" target="_blank"〉PubMed〈/a〉
    Keywords: Cells, Cultured ; Epithelium/*microbiology ; Herpesviridae Infections/*microbiology ; Herpesvirus 4, Human/growth & development ; Humans ; Receptors, Virus/metabolism ; Virus Replication
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    Expression of the c-fos gene and of an fos-related gene is stimulated by platelet-derived growth factor (1984)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1984-11-30
    Description: Complementary DNA clones of genes induced by platelet-derived growth factor (PDGF) in BALB/c-3T3 cells were isolated; one such clone contains a domain having nucleotide sequence homology with the third exon of c-fos. This nucleotide sequence homology is reflected in the predicted amino acid sequences of the gene products. Under low stringency conditions, the mouse v-fos gene cross-hybridizes with the PDGF-inducible complementary DNA clone. However, the messenger RNA transcripts of mouse c-fos and the new fos-related gene can be distinguished by gel electrophoresis and by S1 nuclease analysis. Expression of the authentic c-fos gene is induced by PDGF and superinduced by the combination of PDGF and cycloheximide.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cochran, B H -- Zullo, J -- Verma, I M -- Stiles, C D -- New York, N.Y. -- Science. 1984 Nov 30;226(4678):1080-2.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6093261" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Base Sequence ; Cells, Cultured ; *Cloning, Molecular ; DNA/analysis ; DNA Restriction Enzymes ; DNA Transposable Elements ; Endonucleases ; Genes/drug effects ; Mice ; Mice, Inbred BALB C ; Nucleic Acid Hybridization ; Oncogenes/*drug effects ; Platelet-Derived Growth Factor/*pharmacology ; Single-Strand Specific DNA and RNA Endonucleases ; Transcription, Genetic/drug effects
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Axonal proteins of presynaptic neurons during synaptogenesis (1983)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1983-09-23
    Description: Changes occur in the synthesis and axonal transport of neuronal proteins in dorsal-root ganglia axons as a result of contact with cells from the spinal cord during synapse formation. Dorsal-root ganglia cells were cultured in a compartmental cel culture system that allows separate access to neuronal cell bodies and their axons. When cells from the ventral spinal cord were cultured with the dorsal-root ganglia axons, synapses were established within a few days. Metabolic labeling and two-dimensional electrophoresis revealed that four of more than 300 axonal proteins had changed in their expression by the time synapses were established. The highly selective nature of these changes suggests that the proteins involved may be important in the processes of axon growth and synapse formation and their regulation by the regional environment.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sonderegger, P -- Fishman, M C -- Bokoum, M -- Bauer, H C -- Nelson, P G -- New York, N.Y. -- Science. 1983 Sep 23;221(4617):1294-7.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6612344" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Axons/*metabolism ; Cells, Cultured ; Chick Embryo ; Isoelectric Point ; Molecular Weight ; Nerve Tissue Proteins/*biosynthesis ; Synapses/*metabolism
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    Latrunculins: novel marine toxins that disrupt microfilament organization in cultured cells (1983)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1983-02-04
    Description: Two toxins, latrunculins A and B, which contain a new class of 16- and 14-membered marine macrolides attached to the rare 2-thiazolidinone moiety, were purified recently from the Red Sea sponge Latrunculia magnifica. The effects of these toxins on cultured mouse neuroblastoma and fibroblast cells have been evaluated. In both types of cells, submicromolar toxin concentrations rapidly induce striking changes in cell morphology that are reversible upon removal of the toxin. Immunofluorescence studies with antibodies specific for cytoskeletal proteins reveal that the toxins cause major alterations in the organization of microfilaments without obvious effects on the organization of the microtubular system.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Spector, I -- Shochet, N R -- Kashman, Y -- Groweiss, A -- New York, N.Y. -- Science. 1983 Feb 4;219(4584):493-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6681676" target="_blank"〉PubMed〈/a〉
    Keywords: Actins/metabolism ; Animals ; *Bicyclo Compounds, Heterocyclic ; Cells, Cultured ; Cytoskeleton/*drug effects ; Fibroblasts/ultrastructure ; Marine Toxins/*pharmacology ; Microscopy, Fluorescence ; Microtubules/drug effects ; Neuroblastoma/ultrastructure ; Thiazoles/*pharmacology ; Thiazolidines
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    Complete development of Cryptosporidium in cell culture (1984)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1984-05-11
    Description: Protozoan parasites of the genus Cryptosporidium cause a short-term, flu-like, gastrointestinal illness in immunocompetent persons and severe, persistent, life-threatening diarrhea in immunodeficient individuals. No effective therapy is available for the treatment of cryptosporidiosis in the immunodeficient host. Complete development (from sporozoite to sporulated oocyst) of a human isolate of Cryptosporidium was achieved in cultured human fetal lung cells and primary chicken kidney and porcine kidney cells. The growth of this newly recognized zoonotic agent in cell culture now provides a means of studying its behavior, development, and metabolism, and a mechanism for evaluation of potentially useful therapeutic agents.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Current, W L -- Haynes, T B -- New York, N.Y. -- Science. 1984 May 11;224(4649):603-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6710159" target="_blank"〉PubMed〈/a〉
    Keywords: Acquired Immunodeficiency Syndrome/complications ; Animals ; Cattle ; Cells, Cultured ; Coccidia/*growth & development ; Coccidiosis/etiology/parasitology ; Culture Media ; Humans ; Mice
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    Homologous recombination catalyzed by mammalian cell extracts in vitro (1984)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1984-12-07
    Description: An assay was developed to detect recombination events taking place in an in vitro reaction. Extracts of cultured mouse preB lymphocytes were found to catalyze homologous recombination between substrate DNA molecules but not site-specific recombination between cloned mouse immunoglobulin D and J genes. Addition of deoxyribonucleoside triphosphates increased the frequency of homologous recombination. This recombination activity was not observed in two differentiated lymphocyte cell lines.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Darby, V -- Blattner, F -- AI19325/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 1984 Dec 7;226(4679):1213-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6334360" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; B-Lymphocytes ; Cells, Cultured ; Crossing Over, Genetic ; DNA, Viral ; Immunoglobulin Variable Region/genetics ; Mice ; Mutation ; Nucleoproteins/genetics ; *Recombination, Genetic
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    Coexistence of acetylcholinesterase and somatostatin-immunoreactivity in neurons cultured from rat cerebrum (1984)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1984-01-06
    Description: Cultures derived from rat cerebral hemispheres were sequentially stained for acetylcholinesterase activity and for either somatostatin-like immunoreactivity or cholecystokinin-like immunoreactivity. Somatostatin-like immunoreactivity was found to coexist with acetylcholinesterase activity in individual neurons of several morphological subtypes, but cholecystokinin-like immunoreactivity and acetycholinesterase activity were never seen in the same neurons. These findings suggest a specific anatomical association, perhaps even an overlap, of the cholinergic and somatostatinergic systems in the mammalian cerebrum, and indicate that the combined deficiencies of somatostatin and cholinergic markers in Alzheimer's dementia and senile dementia of the Alzheimer type may be of pathophysiological importance.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Delfs, J R -- Zhu, C H -- Dichter, M A -- HD06276/HD/NICHD NIH HHS/ -- NS00608/NS/NINDS NIH HHS/ -- NS15362/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1984 Jan 6;223(4631):61-3.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6140757" target="_blank"〉PubMed〈/a〉
    Keywords: Acetylcholinesterase/*metabolism ; Animals ; Brain/*cytology/enzymology ; Brain Chemistry ; Cells, Cultured ; Fluorescent Antibody Technique ; Neurons/*analysis/enzymology ; Rats ; Sincalide/analysis ; Somatostatin/*analysis
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    Antigenic similarity between cells transformed by ultraviolet radiation in vitro and in vivo (1984)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1984-02-10
    Description: Cells of the 10T 1/2 mouse fibroblast line transformed in vitro by ultraviolet radiation are antigenically similar to those from skin cancers produced in mice by repeated exposure to ultraviolet radiation. Both types of tumor cells grew preferentially in ultraviolet-irradiated syngeneic mice relative to untreated animals, and both were recognized by ultraviolet radiation-induced tumor-specific suppressor lymphocytes. These properties were not shared by 10T 1/2 cells transformed in vitro by x-rays or 3-methylcholanthrene.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Fisher, M S -- Kripke, M L -- Chan, G L -- CA-09078/CA/NCI NIH HHS/ -- CA-11751/CA/NCI NIH HHS/ -- N01-CO-23909/CO/NCI NIH HHS/ -- New York, N.Y. -- Science. 1984 Feb 10;223(4636):593-4.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6695169" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, Neoplasm/*analysis ; Carcinogens ; Cell Line ; *Cell Transformation, Neoplastic ; Cells, Cultured ; Mice ; Mice, Inbred C3H ; Neoplasm Transplantation ; Transplantation, Isogeneic ; *Ultraviolet Rays
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    Activation of a c-K-ras oncogene by somatic mutation in mouse lymphomas induced by gamma radiation (1984)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1984-09-14
    Description: Mouse tumors induced by gamma radiation are a useful model system for oncogenesis. DNA from such tumors contains an activated K-ras oncogene that can transform NIH 3T3 cells. This report describes the cloning of a fragment of the mouse K-ras oncogene containing the first exon from both a transformant in rat-2 cells and the brain of the same mouse that developed the tumor. Hybrid constructs containing one of the two pieces were made and only the plasmid including the first exon from the transformant gave rise to foci in NIH 3T3 cells. There was only a single base difference (G----A) in the exonic sequence, which changed glycine to aspartic acid in the transformant. By use of a synthetic oligonucleotide the presence of the mutation was demonstrated in the original tumor, ruling out modifications during DNA-mediated gene transfer and indicating that the alteration was present in the thymic lymphoma but absent from other nonmalignant tissue. The results are compatible with gamma radiation being a source of point mutations.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Guerrero, I -- Villasante, A -- Corces, V -- Pellicer, A -- CA-36327/CA/NCI NIH HHS/ -- GM-32036/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1984 Sep 14;225(4667):1159-62.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6474169" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Base Sequence ; Cell Transformation, Neoplastic ; Cells, Cultured ; Cloning, Molecular ; Gamma Rays ; Lymphoma/*genetics ; Mice ; Mutation ; Neoplasms, Radiation-Induced/*genetics ; Nucleic Acid Hybridization ; *Oncogenes ; Rats
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    Differential development of two classes of acetylcholine receptors in Xenopus muscle in culture (1984)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1984-10-05
    Description: Physiological properties of acetylcholine receptors on muscle cells at very early stages of ontogeny were compared with those of cells at later stages. Two changes were observed that contributed to an overall shortening of the mean open time of single-channels. First, there was a shift in the relative proportions of two receptor types with different conductances and mean open times, such that the contribution of receptors with large conductance and short open time increased as development proceeded. Second, there was a sharp reduction in the mean open time of channels having small conductance, with no similar change in channels having large conductance.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Leonard, R J -- Nakajima, S -- Nakajima, Y -- Takahashi, T -- NS08601/NS/NINDS NIH HHS/ -- T32-GM-07211/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1984 Oct 5;226(4670):55-7.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6474189" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cells, Cultured ; Electric Conductivity ; Muscles/*embryology/physiology ; Receptors, Cholinergic/*physiology ; Xenopus
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    Endogenous regulation of macrophage proliferative expansion by colony-stimulating factor-induced interferon (1984)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1984-01-13
    Description: Stimulation of cultures of murine bone-marrow cells with specific macrophage growth factor (colony-stimulating factor I) resulted in the production of type I interferon. Neutralization of this endogenous interferon by antiserum directed against interferons alpha and beta resulted in a significant enhancement of mononuclear phagocyte proliferation from committed marrow precursors. The effect of the antiserum was lost in cultures depleted of adherent cells, an indication that an adherent regulatory cell (or cells) in the marrow limits mononuclear phagocyte proliferation by producing antiproliferative interferon in response to high levels of specific growth factor.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Moore, R N -- Larsen, H S -- Horohov, D W -- Rouse, B T -- AI-14981/AI/NIAID NIH HHS/ -- AI-18960/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 1984 Jan 13;223(4632):178-81.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6606850" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Bone Marrow ; Cell Division ; Cells, Cultured ; Clone Cells ; Colony-Stimulating Factors/*pharmacology ; Immune Sera ; Interferon Type I/biosynthesis/immunology/*physiology ; Macrophages/*cytology/physiology ; Mice ; Thymidine/metabolism
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    Sindbis virus mutants selected for rapid growth in cell culture display attenuated virulence in animals (1984)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1984-07-27
    Description: Mutants of Sindbis virus were selected for rapid growth in baby hamster kidney (BHK) cell cultures and screened for attenuation of virulence in suckling mice. Comparisons among independently isolated virulent and attenuated strains, as well as a classical reversion analysis, showed that accelerated penetration of BHK cells was correlated with attenuation in vivo. Both phenotypic changes resulted from a reorganization of virion structure as detected by monoclonal antibodies. These results suggest that mutants selected for rapid growth in cell culture may be useful as attenuated vaccines and for studies of the molecular basis of virus pathogenesis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Olmsted, R A -- Baric, R S -- Sawyer, B A -- Johnston, R E -- AI19433/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 1984 Jul 27;225(4660):424-7.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6204381" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antibodies, Monoclonal/immunology ; Antibodies, Viral/immunology ; Cells, Cultured ; Cricetinae ; Kidney/cytology ; Mice ; Mutation ; Neutralization Tests ; RNA/biosynthesis ; Sindbis Virus/genetics/growth & development/immunology/*pathogenicity ; Togaviridae Infections/microbiology
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    Vitamin D3--resistant fibroblasts have immunoassayable 1,25-dihydroxyvitamin D3 receptors (1984)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1984-05-25
    Description: Cultured fibroblasts obtained from patients with tissue resistance to 1,25-dihydroxyvitamin D3 (vitamin D3--dependent rickets, type II) contain normal, low, or undetectable concentrations of this hormone's receptor protein as measured by a ligand-binding assay. Extracts from these cells were evaluated for receptors by immunoassay with a recently developed monoclonal antibody to the chick receptor. The results show that a protein sedimenting at 3.7S and recognizable by the antibody exists in comparable concentrations in cells from both normal and resistant patients, irrespective of the hormone-binding abnormalities of the cells. This implies that deficiencies in hormone binding associated with inherited tissue resistance to 1,25-dihydroxyvitamin D3 probably arise from structural variations in the receptor molecule and not from defective receptor synthesis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pike, J W -- Dokoh, S -- Haussler, M R -- Liberman, U A -- Marx, S J -- Eil, C -- AM 15781/AM/NIADDK NIH HHS/ -- AM 32313/AM/NIADDK NIH HHS/ -- New York, N.Y. -- Science. 1984 May 25;224(4651):879-81.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6326262" target="_blank"〉PubMed〈/a〉
    Keywords: Antibodies, Monoclonal ; Cells, Cultured ; Fibroblasts/*analysis ; Humans ; Hypophosphatemia, Familial/*metabolism ; Radioimmunoassay ; Radioligand Assay ; Receptors, Calcitriol ; Receptors, Steroid/*analysis ; Skin/cytology
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    Insulin-mediated regulation of neuronal maturation (1984)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1984-09-14
    Description: Exposure to insulin increased stimulus-evoked transmission at synapses formed in culture by cholinergic retinal neurons derived from fetal rats. This effect occurred at physiological concentrations and was long lasting. The findings support the hypothesis that insulin may serve as a developmental signal to regulate the emergence of effective neurotransmission across nascent synapses.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Puro, D G -- Agardh, E -- New York, N.Y. -- Science. 1984 Sep 14;225(4667):1170-2.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6089343" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cells, Cultured ; Insulin/pharmacology/*physiology ; Muscles ; Neurons/*growth & development/physiology ; Parasympathetic Nervous System/physiology ; Rats ; Retina ; Synaptic Transmission ; Time Factors
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    Glucose stimulation of the antilipolytic effect of insulin in humans (1983)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1983-06-03
    Description: Dose-response studies of the inhibition of lipolysis by insulin in isolated human adipocytes were conducted with the use of a sensitive bioluminescent assay of glycerol release. The addition of glucose to the incubation medium was associated with an increase in insulin sensitivity and an increase in the maximum insulin effect. The results suggest that glucose plays an important role in regulating the antilipolytic action of insulin in humans.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Arner, P -- Bolinder, J -- Ostman, J -- New York, N.Y. -- Science. 1983 Jun 3;220(4601):1057-9.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6342138" target="_blank"〉PubMed〈/a〉
    Keywords: Adipose Tissue/cytology ; Cells, Cultured ; Dose-Response Relationship, Drug ; Drug Synergism ; Glucose/*pharmacology ; Humans ; Insulin/*pharmacology ; Isoproterenol/pharmacology ; Lipolysis/*drug effects
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  • 83
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    Fluoride directly stimulates proliferation and alkaline phosphatase activity of bone-forming cells (1983)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1983-10-21
    Description: Fluoride is one of the most potent but least well understood stimulators of bone formation in vivo. Bone formation was shown to arise from direct effects on bone cells. Treatment with sodium fluoride increased proliferation and alkaline phosphatase activity of bone cells in vitro and increased bone formation in embryonic calvaria at concentrations that stimulate bone formation in vivo.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Farley, J R -- Wergedal, J E -- Baylink, D J -- AM31061/AM/NIADDK NIH HHS/ -- AM31062/AM/NIADDK NIH HHS/ -- New York, N.Y. -- Science. 1983 Oct 21;222(4621):330-2.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6623079" target="_blank"〉PubMed〈/a〉
    Keywords: Alkaline Phosphatase/*metabolism ; Animals ; Bone Development/*drug effects ; Bone and Bones/*cytology/embryology/enzymology ; Cell Division/drug effects ; Cells, Cultured ; Chick Embryo ; Dose-Response Relationship, Drug ; Fluorides/*pharmacology ; Parathyroid Hormone/pharmacology
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 84
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    Cell growth on liquid microcarriers (1983)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1983-03-25
    Description: Anchorage-dependent cell growth is demonstrated on microcarriers of fluorocarbon fluid formed by emulsification and stabilized with polylysine.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Keese, C R -- Giaever, I -- New York, N.Y. -- Science. 1983 Mar 25;219(4591):1448-9.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6828872" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Adhesion ; Cell Division ; *Cell Physiological Phenomena ; Cells, Cultured ; Culture Media ; Emulsions ; Fluorocarbons ; Kinetics
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 85
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    Substance P and somatostatin regulate sympathetic noradrenergic function (1983)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1983-09-09
    Description: Peptidergic-noradrenergic interactions were examined in explants of rat sympathetic superior cervical ganglia and in cultures of dissociated cells. The putative peptide transmitters substance P and somatostatin each increased the activity of the catecholamine-synthesizing enzyme tyrosine hydroxylase after 1 week of exposure in culture. Maximal increases occurred at 10(-7) molar for each peptide, and either increasing or decreasing the concentration reduced the effects. Similar increases in tyrosine hydroxylase were produced by a metabolically stable agonist of substance P, while a substance P antagonist prevented the effects of the agonist. The data suggest that the increased tyrosine hydroxylase activity was mediated by peptide interaction with specific substance P receptors and that peptides may modulate sympathetic catecholaminergic function.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kessler, J A -- Adler, J E -- Black, I B -- New York, N.Y. -- Science. 1983 Sep 9;221(4615):1059-61.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6192502" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Bacitracin/pharmacology ; Captopril/pharmacology ; Cells, Cultured ; Culture Techniques ; Dose-Response Relationship, Drug ; Ganglia, Sympathetic/*enzymology ; Rats ; Somatostatin/*pharmacology ; Substance P/*pharmacology ; Tyrosine 3-Monooxygenase/*metabolism
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  • 86
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    Action potentials in macrophages derived from human monocytes (1983)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1983-02-25
    Description: The electrical activity of macrophages derived from human blood monocytes was recorded in vitro with intracellular microelectrodes and was analyzed with computer-assisted data acquisition and analysis techniques. In cells impaled 6 to 8 days after the cultures were prepared, the resting potentials reached a maximum value of -72 millivolts. The cells were electrically excitable; spikes exhibited a slow upstroke, a fast downstroke, a discrete threshold, a large overshoot, and a brief undershoot. Repetitive firing was induced by a maintained depolarizing current. A positive relation was observed between transmembrane currents and resting potential. Voltage-current relations were nonrectifying for subthreshold current injections. Since these cells had not been treated with any specific activation factors, the electrical activity recorded is evidence for the presence of voltage-dependent inward and outward currents in the membranes of mature macrophages. The electrical signals generated by these cells may be useful for the assay of sensor and effector functions of macrophages, such as chemotaxis, receptor-ligand interactions, and phagocytosis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉McCann, F V -- Cole, J J -- Guyre, P M -- Russell, J A -- AM0535/AM/NIADDK NIH HHS/ -- BRSG05392/RS/DRS NIH HHS/ -- CA17323/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1983 Feb 25;219(4587):991-3.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6823563" target="_blank"〉PubMed〈/a〉
    Keywords: Action Potentials ; Cell Differentiation ; Cells, Cultured ; Humans ; Macrophages/*physiology ; Monocytes/cytology
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 87
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    Cooperation between oncogenes. Investigators focus on cooperation between two or more oncogenes to help explain the multistep development of human cancers (1983)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1983-11-11
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Marx, J L -- New York, N.Y. -- Science. 1983 Nov 11;222(4624):602-3.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6635658" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Cycle ; Cells, Cultured ; Mice ; *Oncogenes ; Platelet-Derived Growth Factor/*genetics
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 88
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    RNA splice site selection: evidence for a 5' leads to 3' scanning model (1983)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1983-06-24
    Description: Human G gamma-globin genes containing tandem duplications of the donor (5') or acceptor (3') RNA splice sites of the second intervening sequence were constructed in order to ascertain the directionality of RNA splice site selection. These genes were introduced into cultured monkey cells, and their transcripts were analyzed. Transcripts of these duplication variants were spliced only at the proximal copy of the duplicated splice sites. These data are consistent with a 5' leads to 3' model of splice site selection.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lang, K M -- Spritz, R A -- AM28598/AM/NIADDK NIH HHS/ -- New York, N.Y. -- Science. 1983 Jun 24;220(4604):1351-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6304877" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Base Sequence ; Cells, Cultured ; Globins/genetics ; Haplorhini ; Humans ; Plasmids ; *RNA Splicing ; RNA, Messenger/genetics/physiology ; Simian virus 40/genetics ; Transcription, Genetic
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  • 89
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    Vasoactive intestinal peptide alters membrane potential and cyclic nucleotide levels in retinal horizontal cells (1983)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1983-09-09
    Description: Vasoactive intestinal peptide stimulated the synthesis of adenosine 3',5'-monophosphate in fractions of isolated carp horizontal cells. When applied extracellularly to isolated and cultured horizontal cells, the peptide also induced a slow depolarization (30 to 40 millivolts) accompanied by a decrease in membrane resistance. However, analogs of adenosine 3',5'-monophosphate applied extracellularly or intracellularly, and forscolin applied extracellularly, had no effect on the membrane potential of cultured horizontal cells, indicating that the induced depolarization was not related to the accumulation of adenosine 3',5'-monophosphate in these cells.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lasater, E M -- Watling, K J -- Dowling, J E -- EY-00811/EY/NEI NIH HHS/ -- EY-00824/EY/NEI NIH HHS/ -- EY-05476/EY/NEI NIH HHS/ -- New York, N.Y. -- Science. 1983 Sep 9;221(4615):1070-2.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6308770" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Carps ; Cells, Cultured ; Cyclic AMP/*metabolism ; Dopamine/pharmacology ; Gastrointestinal Hormones/*pharmacology ; Kainic Acid/pharmacology ; Membrane Potentials/*drug effects ; Retina/*drug effects/physiology ; Vasoactive Intestinal Peptide/*pharmacology
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  • 90
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    Evidence for the recessive nature of cellular immortality (1983)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1983-09-02
    Description: Fusion of immortal cell lines with normal human fibroblasts or certain other immortal cell lines yields hybrids having limited division potential. Cellular immortality was found to be a recessive phenotype in hybrids. It was also found that at least two separate events in the normal cell genome can result in immortality. In fusions involving certain immortal parent cells, these events can be complemented to result in hybrids with finite division capacity.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pereira-Smith, O M -- Smith, J R -- AG 03262/AG/NIA NIH HHS/ -- New York, N.Y. -- Science. 1983 Sep 2;221(4614):964-6.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6879195" target="_blank"〉PubMed〈/a〉
    Keywords: *Cell Division ; Cell Line ; *Cell Survival ; Cells, Cultured ; Genes, Recessive ; Humans ; Hybrid Cells/*physiology ; Phenotype
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  • 91
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    Activation of 2-aminofluorene by cultured plant cells (1983)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1983-03-25
    Description: Cultured tobacco plant cells activated 2-aminofluorene to an agent mutagenic to Salmonella typhimurium strain TA98. The plant activation of 2-aminofluorene is heat-inactivated and may not involve solely cytochrome P-450. The kinetics of activation demonstrated both time- and concentration-dependent responses.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Plewa, M J -- Weaver, D L -- Blair, L C -- Gentile, J M -- ES02384/ES/NIEHS NIH HHS/ -- New York, N.Y. -- Science. 1983 Mar 25;219(4591):1427-9.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6338591" target="_blank"〉PubMed〈/a〉
    Keywords: Biotransformation ; Cells, Cultured ; Fluorenes/*metabolism/pharmacology ; Kinetics ; Mutagenicity Tests ; Mutagens/*metabolism ; *Mutation ; *Plants, Toxic ; Salmonella typhimurium/drug effects ; Tobacco/*metabolism
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  • 92
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    Isolation and transmission of human retrovirus (human t-cell leukemia virus) (1983)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1983-02-18
    Description: Nine new isolates of human T-cell leukemia-lymphoma virus (HTLV) were obtained from cells of seven patients with malignancies of mature T cells and from two clinically normal relatives of a T-cell leukemia patient. These people were from the United States, Israel, the West Indies, and Japan. The virus was detected in the fresh T cells and was isolated from the established T-cell lines. Each isolate is closely related to the first HTLV isolate, and all the new HTLV isolates were transmitted into normal human T cells obtained from the umbilical cord blood of newborns.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Popovic, M -- Sarin, P S -- Robert-Gurroff, M -- Kalyanaraman, V S -- Mann, D -- Minowada, J -- Gallo, R C -- New York, N.Y. -- Science. 1983 Feb 18;219(4586):856-9.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6600519" target="_blank"〉PubMed〈/a〉
    Keywords: Cell Line ; Cells, Cultured ; Female ; Humans ; Leukemia/*microbiology ; Male ; Retroviridae/growth & development/*isolation & purification ; T-Lymphocytes/*microbiology
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  • 93
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    Mobilization of cellular calcium-45 and lead-210: effect of physiological stimuli (1983)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1983-04-15
    Description: Isolated rat hepatocytes in primary culture were used as a model system to evaluate the effects of selected hormones and culture conditions on the efflux of calcium-45 and lead-210 from cells labeled with these isotopes. Alpha-adrenergic stimuli, angiotensin, vasopressin, dibutyryl adenosine 3',5'-monophosphate, and reduced phosphate concentrations in the medium increased the efflux of calcium-45 and lead-210. Glucagon and insulin had no effect, but increased phosphate concentrations decreased the efflux of both isotopes. Experiments with hepatocytes cultured in a medium free of calcium and lead demonstrated that the increased efflux of calcium-45 and lead-210 induced by hormones was the result of mobilization of the ions from intracellular stores. The data indicate that the physiological stimuli that mobilized calcium ions also mobilized lead ions, and that the mobilized lead would be available to interact with calcium-mediated cell functions.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pounds, J G -- Mittelstaedt, R A -- New York, N.Y. -- Science. 1983 Apr 15;220(4594):308-10.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6301003" target="_blank"〉PubMed〈/a〉
    Keywords: Angiotensin II/pharmacology ; Animals ; Bucladesine/pharmacology ; Calcium Radioisotopes/*metabolism ; Cells, Cultured ; Epinephrine/pharmacology ; Insulin/pharmacology ; Lead/*metabolism ; Liver/cytology ; Phosphates/pharmacology ; Propranolol/pharmacology ; Radioisotopes ; Rats ; Vasopressins/pharmacology
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  • 94
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    Irreversible ligands with high selectivity toward delta and mu opiate receptors (1983)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1983-04-15
    Description: Alkylating agents that display strong selectivity for opiate receptor types delta or mu were prepared by appropriate modification of the structures of the strong analgesics fentanyl, etonitazene, and endoethenotetrahydrooripavine. The availability of these substances should facilitate studies of the structural basis of receptor specificity and of the physiologic roles of these receptors.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rice, K C -- Jacobson, A E -- Burke, T R Jr -- Bajwa, B S -- Streaty, R A -- Klee, W A -- New York, N.Y. -- Science. 1983 Apr 15;220(4594):314-6.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6132444" target="_blank"〉PubMed〈/a〉
    Keywords: Alkylation ; Animals ; Benzimidazoles/analogs & derivatives/metabolism ; Brain/physiology ; Cells, Cultured ; Chemical Phenomena ; Chemistry ; Enkephalin, Methionine/analogs & derivatives/metabolism ; Fentanyl/analogs & derivatives/metabolism ; *Isothiocyanates ; Ligands ; Rats ; Receptors, Opioid/*metabolism/physiology ; Thebaine/analogs & derivatives/pharmacology
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  • 95
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    Modulation of the metastatic capability in B16 melanoma by cell shape (1983)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1983-09-23
    Description: The lung colonization of B16-F1 cells grown in flat and spherical configurations was studied. Cells cultivated in vitro as spheroids on a nonadhesive substrate expressed in a reversible fashion a marked increase in their propensity to establish metastases. The altered metastatic capability was accompanied by a reversible reduction in the accessibility of cell surface proteins to external iodination and by a dramatic decrease in the synthesis of vimentin.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Raz, A -- Ben-Ze'ev, A -- New York, N.Y. -- Science. 1983 Sep 23;221(4617):1307-10.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6612347" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Adhesion ; Cell Division ; Cells, Cultured ; Intermediate Filament Proteins/biosynthesis ; Lung Neoplasms/secondary ; Melanoma/*pathology ; Membrane Proteins/physiology ; Mice ; *Neoplasm Metastasis ; Neoplasm Proteins/physiology ; Neoplasms, Experimental/pathology ; Vimentin
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  • 96
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    Isolation of a T-lymphotropic retrovirus from a patient at risk for acquired immune deficiency syndrome (AIDS) (1983)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1983-05-20
    Description: A retrovirus belonging to the family of recently discovered human T-cell leukemia viruses (HTLV), but clearly distinct from each previous isolate, has been isolated from a Caucasian patient with signs and symptoms that often precede the acquired immune deficiency syndrome (AIDS). This virus is a typical type-C RNA tumor virus, buds from the cell membrane, prefers magnesium for reverse transcriptase activity, and has an internal antigen (p25) similar to HTLV p24. Antibodies from serum of this patient react with proteins from viruses of the HTLV-I subgroup, but type-specific antisera to HTLV-I do not precipitate proteins of the new isolate. The virus from this patient has been transmitted into cord blood lymphocytes, and the virus produced by these cells is similar to the original isolate. From these studies it is concluded that this virus as well as the previous HTLV isolates belong to a general family of T-lymphotropic retroviruses that are horizontally transmitted in humans and may be involved in several pathological syndromes, including AIDS.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Barre-Sinoussi, F -- Chermann, J C -- Rey, F -- Nugeyre, M T -- Chamaret, S -- Gruest, J -- Dauguet, C -- Axler-Blin, C -- Vezinet-Brun, F -- Rouzioux, C -- Rozenbaum, W -- Montagnier, L -- New York, N.Y. -- Science. 1983 May 20;220(4599):868-71.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6189183" target="_blank"〉PubMed〈/a〉
    Keywords: Acquired Immunodeficiency Syndrome/*microbiology ; Adult ; Animals ; Antibodies, Viral/immunology ; Cells, Cultured ; Humans ; Male ; Microscopy, Electron ; RNA-Directed DNA Polymerase/metabolism ; Retroviridae/*isolation & purification ; T-Lymphocytes/microbiology ; Tumor Virus Infections/*microbiology
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  • 97
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    Myasthenic globulin enhances the loss of acetylcholine receptor clusters (1983)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1983-01-14
    Description: Acetylcholine receptors are present in the sarcolemma of cultured skeletal muscle myotubes either as large clusters or in a diffuse distribution. Both the clustered and diffuse acetylcholine receptors are potentially removable from the membrane. Treatment of myotubes with globulin from patients with myasthenia gravis causes the loss of acetylcholine receptor clusters and the concomitant appearance of acetylcholine receptor microaggregates. The rate of acetylcholine receptor cluster loss is greater than the rate of acetylcholine receptor degradation, indicating that acetylcholine receptors are disrupted from clusters to form microaggregates before being removed from the plasma membrane.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bursztajn, S -- McManaman, J L -- Elias, S B -- Appel, S H -- New York, N.Y. -- Science. 1983 Jan 14;219(4581):195-7.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6849132" target="_blank"〉PubMed〈/a〉
    Keywords: *Autoantibodies ; Cells, Cultured ; Humans ; Immunologic Capping ; Macromolecular Substances ; Membrane Proteins/metabolism ; Myasthenia Gravis/*immunology ; Pinocytosis ; Receptors, Cholinergic/immunology/*metabolism
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  • 98
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    Sodium currents in segments of human heart cells (1983)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1983-04-15
    Description: Isolated human heart cells were partially drawn into the lumen of a plastic tube and cleaved at the partitioning tube wall by intraluminal suction pulses. The extraluminal segment (10 to 20 percent of the cell length) was suitable for intracellular perfusion and voltage clamp. The time and voltage dependence of the sodium current, and the responses to changes in driving force and channel blockers, illustrate the potential of these preparations as models for the study of membrane channels.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bustamante, J O -- McDonald, T F -- New York, N.Y. -- Science. 1983 Apr 15;220(4594):320-1.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6301004" target="_blank"〉PubMed〈/a〉
    Keywords: Cells, Cultured ; Humans ; Ion Channels/drug effects ; Lidocaine/pharmacology ; Membrane Potentials/drug effects ; Myocardium/*cytology/metabolism ; Sodium/*metabolism/physiology ; Tetrodotoxin/pharmacology
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  • 99
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    Human brain tumor--derived cell lines: growth rate reduced by human fibroblast interferon (1983)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1983-02-18
    Description: The biological response modifier human beta-interferon had pronounced antigrowth effects on various histologic types of human brain tumor cells but no effects on a nontransformed cell line, MRC-5. The cultures of brain tumor cells showed severe alterations indicative of cell injury and death after exposure to beta-interferon for 2 to 6 days. Similar results were obtained with cells freshly explanted from human brain tumors. The results indicate that it may be possible to use fresh, explanted tumor tissue to identify patients who might benefit from therapy with beta-interferon.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cook, A W -- Carter, W A -- Nidzgorski, F -- Akhtar, L -- New York, N.Y. -- Science. 1983 Feb 18;219(4586):881-3.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6401866" target="_blank"〉PubMed〈/a〉
    Keywords: Brain Neoplasms/pathology/*therapy ; Cell Division ; Cells, Cultured ; Humans ; Interferon-gamma/pharmacology/*therapeutic use
    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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    Cell-to-cell transfer of interferon-induced antiproliferative activity (1983)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1983-09-02
    Description: Interferon-treated cells rapidly and efficiently transferred the antiproliferative activity of interferon to untreated cells. This phenomenon was not due to the carry-over of interferon by the interferon-treated cells. Thus, to evoke an antiproliferative state, interferon did not directly contact each cell in a population. The results suggest a novel mechanism by which interferon may indirectly regulate cell growth, and suggests that cells other than those of the immune system may play a role in controlling tumor growth in tissue where cell-to-cell contact occurs.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lloyd, R E -- Blalock, J E -- Stanton, G J -- 03348/PHS HHS/ -- AM 30046/AM/NIADDK NIH HHS/ -- New York, N.Y. -- Science. 1983 Sep 2;221(4614):953-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6192500" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Cell Communication ; Cell Division/*drug effects ; Cells, Cultured ; Humans ; Interferons/*pharmacology ; Leukemia L1210 ; Mice ; Species Specificity
    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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