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  • 11
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    Unknown
    American Association for the Advancement of Science (AAAS)
    Publication Date: 1995-03-10
    Description: Fas ligand (FasL), a cell surface molecule belonging to the tumor necrosis factor family, binds to its receptor Fas, thus inducing apoptosis of Fas-bearing cells. Various cells express Fas, whereas FasL is expressed predominantly in activated T cells. In the immune system, Fas and FasL are involved in down-regulation of immune reactions as well as in T cell-mediated cytotoxicity. Malfunction of the Fas system causes lymphoproliferative disorders and accelerates autoimmune diseases, whereas its exacerbation may cause tissue destruction.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Nagata, S -- Golstein, P -- New York, N.Y. -- Science. 1995 Mar 10;267(5203):1449-56.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Osaka Bioscience Institute, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7533326" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Antigens, CD95 ; Antigens, Surface/chemistry/genetics/*physiology ; *Apoptosis ; Autoimmune Diseases/genetics/immunology ; Base Sequence ; Cytotoxicity, Immunologic ; Down-Regulation ; Fas Ligand Protein ; Humans ; Lymphocyte Activation ; Lymphocytes/cytology/*immunology ; Lymphoproliferative Disorders/genetics/immunology ; Membrane Glycoproteins/chemistry/genetics/*physiology ; Molecular Sequence Data ; T-Lymphocytes, Cytotoxic/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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  • 12
    Publication Date: 1994-07-22
    Description: Two molecular mechanisms of T cell-mediated cytotoxicity, one perforin-based, the other Fas-based, have been demonstrated. To determine the extent of their contribution to T cell-mediated cytotoxicity, a range of effector cells from normal control or perforin-deficient mice were tested against a panel of target cells with various levels of Fas expression. All cytotoxicity observed was due to either of these mechanisms, and no third mechanism was detected. Thus, the perforin- and Fas-based mechanisms may account for all T cell-mediated cytotoxicity in short-term in vitro assays.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kagi, D -- Vignaux, F -- Ledermann, B -- Burki, K -- Depraetere, V -- Nagata, S -- Hengartner, H -- Golstein, P -- New York, N.Y. -- Science. 1994 Jul 22;265(5171):528-30.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology, University of Zurich, Switzerland.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7518614" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Antigens, CD95 ; Antigens, Surface/*immunology ; Cells, Cultured ; Concanavalin A/pharmacology ; *Cytotoxicity, Immunologic ; Ionomycin/pharmacology ; Leukemia L1210 ; Lymphocyte Culture Test, Mixed ; Lymphocytic choriomeningitis virus/immunology ; Membrane Glycoproteins/*immunology ; Mice ; Mice, Inbred BALB C ; Mice, Inbred C3H ; Mice, Inbred C57BL ; Mice, Mutant Strains ; Molecular Sequence Data ; Perforin ; Pore Forming Cytotoxic Proteins ; T-Lymphocytes, Cytotoxic/*immunology ; Tetradecanoylphorbol Acetate/pharmacology ; Tumor Cells, Cultured
    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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  • 13
    Publication Date: 2007-12-08
    Description: The penumbra of a sunspot is composed of numerous thin, radially extended, bright and dark filaments carrying outward gas flows (the Evershed flow). Using high-resolution images obtained by the Solar Optical Telescope aboard the solar physics satellite Hinode, we discovered a number of penumbral bright filaments revealing twisting motions about their axes. These twisting motions are observed only in penumbrae located in the direction perpendicular to the symmetry line connecting the sunspot center and the solar disk center, and the direction of the twist (that is, lateral motions of intensity fluctuation across filaments) is always from limb side to disk-center side. Thus, the twisting feature is not an actual twist or turn of filaments but a manifestation of dynamics of penumbral filaments with three-dimensional radiative transfer effects.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ichimoto, K -- Suematsu, Y -- Tsuneta, S -- Katsukawa, Y -- Shimizu, T -- Shine, R A -- Tarbell, T D -- Title, A M -- Lites, B W -- Kubo, M -- Nagata, S -- New York, N.Y. -- Science. 2007 Dec 7;318(5856):1597-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉National Astronomical Observatory of Japan, 2-21-1, Osawa, Mitaka, Toyko 181-8588, Japan. ichimoto@solar.mtk.nao.ac.jp〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18063792" target="_blank"〉PubMed〈/a〉
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
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  • 14
    Publication Date: 2007-12-08
    Description: The heating of the solar chromosphere and corona is a long-standing puzzle in solar physics. Hinode observations show the ubiquitous presence of chromospheric anemone jets outside sunspots in active regions. They are typically 3 to 7 arc seconds = 2000 to 5000 kilometers long and 0.2 to 0.4 arc second = 150 to 300 kilometers wide, and their velocity is 10 to 20 kilometers per second. These small jets have an inverted Y-shape, similar to the shape of x-ray anemone jets in the corona. These features imply that magnetic reconnection similar to that in the corona is occurring at a much smaller spatial scale throughout the chromosphere and suggest that the heating of the solar chromosphere and corona may be related to small-scale ubiquitous reconnection.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Shibata, Kazunari -- Nakamura, Tahei -- Matsumoto, Takuma -- Otsuji, Kenichi -- Okamoto, Takenori J -- Nishizuka, Naoto -- Kawate, Tomoko -- Watanabe, Hiroko -- Nagata, Shin'ichi -- Ueno, Satoru -- Kitai, Reizaburo -- Nozawa, Satoshi -- Tsuneta, Saku -- Suematsu, Yoshinori -- Ichimoto, Kiyoshi -- Shimizu, Toshifumi -- Katsukawa, Yukio -- Tarbell, Theodore D -- Berger, Thomas E -- Lites, Bruce W -- Shine, Richard A -- Title, Alan M -- New York, N.Y. -- Science. 2007 Dec 7;318(5856):1591-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Kwasan and Hida Observatories, Kyoto University, Yamashina, Kyoto 607-8471, Japan. shibata@kwasan.kyoto-u.ac.jp〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18063790" target="_blank"〉PubMed〈/a〉
    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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  • 15
    Publication Date: 2007-12-08
    Description: We observed fine-scale jetlike features, referred to as penumbral microjets, in chromospheres of sunspot penumbrae. The microjets were identified in image sequences of a sunspot taken through a Ca II H-line filter on the Solar Optical Telescope on board the Japanese solar physics satellite Hinode. The microjets' small width of 400 kilometers and short duration of less than 1 minute make them difficult to identify in existing observations. The microjets are possibly caused by magnetic reconnection in the complex magnetic configuration in penumbrae and have the potential to heat the corona above a sunspot.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Katsukawa, Y -- Berger, T E -- Ichimoto, K -- Lites, B W -- Nagata, S -- Shimizu, T -- Shine, R A -- Suematsu, Y -- Tarbell, T D -- Title, A M -- Tsuneta, S -- New York, N.Y. -- Science. 2007 Dec 7;318(5856):1594-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉National Astronomical Observatory of Japan, 2-21-1 Osawa, Mitaka, Tokyo 181-8588, Japan. yukio.katsukawa@nao.ac.jp〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18063791" target="_blank"〉PubMed〈/a〉
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    Electronic ISSN: 1095-9203
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  • 16
    Publication Date: 2007-12-08
    Description: Solar prominences are cool 10(4) kelvin plasma clouds supported in the surrounding 10(6) kelvin coronal plasma by as-yet-undetermined mechanisms. Observations from Hinode show fine-scale threadlike structures oscillating in the plane of the sky with periods of several minutes. We suggest that these represent Alfven waves propagating on coronal magnetic field lines and that these may play a role in heating the corona.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Okamoto, T J -- Tsuneta, S -- Berger, T E -- Ichimoto, K -- Katsukawa, Y -- Lites, B W -- Nagata, S -- Shibata, K -- Shimizu, T -- Shine, R A -- Suematsu, Y -- Tarbell, T D -- Title, A M -- New York, N.Y. -- Science. 2007 Dec 7;318(5856):1577-80.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉National Astronomical Observatory (NAOJ), Mitaka, Tokyo 181-8588, Japan. joten.okamoto@nao.ac.jp〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18063785" target="_blank"〉PubMed〈/a〉
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
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  • 17
    Publication Date: 2013-07-13
    Description: A classic feature of apoptotic cells is the cell-surface exposure of phosphatidylserine (PtdSer) as an "eat me" signal for engulfment. We show that the Xk-family protein Xkr8 mediates PtdSer exposure in response to apoptotic stimuli. Mouse Xkr8(-/-) cells or human cancer cells in which Xkr8 expression was repressed by hypermethylation failed to expose PtdSer during apoptosis and were inefficiently engulfed by phagocytes. Xkr8 was activated directly by caspases and required a caspase-3 cleavage site for its function. CED-8, the only Caenorhabditis elegans Xk-family homolog, also promoted apoptotic PtdSer exposure and cell-corpse engulfment. Thus, Xk-family proteins have evolutionarily conserved roles in promoting the phagocytosis of dying cells by altering the phospholipid distribution in the plasma membrane.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Suzuki, Jun -- Denning, Daniel P -- Imanishi, Eiichi -- Horvitz, H Robert -- Nagata, Shigekazu -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2013 Jul 26;341(6144):403-6. doi: 10.1126/science.1236758. Epub 2013 Jul 11.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medical Chemistry, Graduate School of Medicine, Kyoto University, Yoshida-Konoe, Sakyo-ku, Kyoto, Kyoto 606-8501, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23845944" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; *Apoptosis ; Apoptosis Regulatory Proteins/chemistry/genetics/*metabolism ; Caenorhabditis elegans Proteins/*metabolism ; Calcium/metabolism ; Caspases/metabolism ; Cell Line ; Cell Line, Tumor ; Cell Membrane/*metabolism ; CpG Islands ; Humans ; Macrophages/physiology ; Membrane Proteins/chemistry/genetics/*metabolism ; Mice ; Mice, Knockout ; Molecular Sequence Data ; *Phagocytosis ; Phosphatidylserines/*metabolism ; Recombinant Fusion Proteins/metabolism
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    Electronic ISSN: 1095-9203
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  • 18
    Publication Date: 2014-06-07
    Description: Phospholipids are asymmetrically distributed in the plasma membrane. This asymmetrical distribution is disrupted during apoptosis, exposing phosphatidylserine (PtdSer) on the cell surface. Using a haploid genetic screen in human cells, we found that ATP11C (adenosine triphosphatase type 11C) and CDC50A (cell division cycle protein 50A) are required for aminophospholipid translocation from the outer to the inner plasma membrane leaflet; that is, they display flippase activity. ATP11C contained caspase recognition sites, and mutations at these sites generated caspase-resistant ATP11C without affecting its flippase activity. Cells expressing caspase-resistant ATP11C did not expose PtdSer during apoptosis and were not engulfed by macrophages, which suggests that inactivation of the flippase activity is required for apoptotic PtdSer exposure. CDC50A-deficient cells displayed PtdSer on their surface and were engulfed by macrophages, indicating that PtdSer is sufficient as an "eat me" signal.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Segawa, Katsumori -- Kurata, Sachiko -- Yanagihashi, Yuichi -- Brummelkamp, Thijn R -- Matsuda, Fumihiko -- Nagata, Shigekazu -- New York, N.Y. -- Science. 2014 Jun 6;344(6188):1164-8. doi: 10.1126/science.1252809.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medical Chemistry, Graduate School of Medicine, Kyoto University, Yoshida-Konoe, Kyoto 606-8501, Japan. ; Netherlands Cancer Institute, Plesmanlaan 121, 1066 CX Amsterdam, Netherlands. ; Center for Genomic Medicine, Graduate School of Medicine, Kyoto University, Yoshida-Konoe, Kyoto 606-8501, Japan. ; Department of Medical Chemistry, Graduate School of Medicine, Kyoto University, Yoshida-Konoe, Kyoto 606-8501, Japan. Core Research for Evolutional Science and Technology, Japan Science and Technology Corporation, Kyoto 606-8501, Japan. snagata@mfour.med.kyoto-u.ac.jp.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24904167" target="_blank"〉PubMed〈/a〉
    Keywords: Adenosine Triphosphatases/genetics/*metabolism ; *Apoptosis ; Caspases/*metabolism ; Cell Line ; Cell Membrane/*enzymology ; Genetic Testing ; Humans ; Membrane Proteins/*metabolism ; Membrane Transport Proteins ; Phosphatidylserines/*metabolism ; Phospholipid Transfer Proteins/genetics/*metabolism ; Protein Transport
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  • 19
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    Unknown
    Nature Publishing Group (NPG)
    Publication Date: 2016-05-27
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Nagata, Shigekazu -- England -- Nature. 2016 May 18;533(7604):474-6. doi: 10.1038/nature18439.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Biochemistry and Immunology, WPI Immunology Frontier Research Center, Osaka University, Osaka 565-0871, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/27225115" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Caspases/*metabolism ; *Cell Differentiation ; Cytochrome c Group/*metabolism ; Drosophila melanogaster/*cytology ; Male ; Spermatozoa/*cytology/*metabolism
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 20
    Publication Date: 1980-09-19
    Description: Interferon-alpha 1 from Escherichia coli transformed with a hybrid plasmid containing a human leukocyte complementary DNA insert, induces resistance to virus in appropriate target cells. It also shares the following properties with natural leukocyte interferon (IFN). (i) It enhances natural killing activity of human lymphocytes, (ii) it enhances antibody-dependent cell-mediated cytotoxicity, (iii) it suppresses antigen- and mitogen-induced leukocyte migration inhibition, (iv) it inhibits growth of IFN-sensitive Burkitt lymphoma cells. Since these activities are exhibited by a cloned protein species, they are due to IFN itself and not to other human proteins.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Masucci, M G -- Szigeti, R -- Klein, E -- Klein, G -- Gruest, J -- Montagnier, L -- Taira, H -- Hall, A -- Nagata, S -- Weissmann, C -- New York, N.Y. -- Science. 1980 Sep 19;209(4463):1431-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6158096" target="_blank"〉PubMed〈/a〉
    Keywords: Antibody-Dependent Cell Cytotoxicity/drug effects ; Cell Division/drug effects ; Cell Migration Inhibition ; Cloning, Molecular ; *DNA, Recombinant ; Escherichia coli ; Humans ; Hypersensitivity, Delayed/immunology ; Immunity, Cellular/drug effects ; Interferons/genetics/*pharmacology ; Structure-Activity Relationship
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