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  • 1
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    Requirement of DNase II for definitive erythropoiesis in the mouse fetal liver (2001)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2001-05-26
    Description: Mature erythrocytes in mammals have no nuclei, although they differentiate from nucleated precursor cells. The mechanism by which enucleation occurs is not well understood. Here we show that deoxyribonuclease II (DNase II) is indispensable for definitive erythropoiesis in mouse fetal liver. No live DNase II-null mice were born, owing to severe anemia. When mutant fetal liver cells were transferred into lethally irradiated wild-type mice, mature red blood cells were generated from the mutant cells, suggesting that DNase II functions in a non-cell-autonomous manner. Histochemical analyses indicated that the critical cellular sources of DNase II are macrophages present at the site of definitive erythropoiesis in the fetal liver. Thus, DNase II in macrophages appears to be responsible for destroying the nuclear DNA expelled from erythroid precursor cells.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kawane, K -- Fukuyama, H -- Kondoh, G -- Takeda, J -- Ohsawa, Y -- Uchiyama, Y -- Nagata, S -- New York, N.Y. -- Science. 2001 May 25;292(5521):1546-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Genetics, Osaka University Medical School, and Core Research for Evolutional Science and Technology, Japan Science and Technology Corporation, Suita, Osaka 565-0871, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11375492" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Apoptosis ; Cell Differentiation ; Cell Transplantation ; DNA/analysis/metabolism ; DNA-Binding Proteins/genetics/metabolism ; Endodeoxyribonucleases/genetics/*metabolism ; Erythroblasts/cytology/metabolism ; Erythroid Precursor Cells/cytology/metabolism ; *Erythropoiesis ; Fetus/enzymology ; Gene Targeting ; Globins/genetics/metabolism ; *Hematopoiesis, Extramedullary ; Kruppel-Like Transcription Factors ; Liver/cytology/*embryology/enzymology/*physiology ; Lysosomes/enzymology ; Macrophages/chemistry/*enzymology/ultrastructure ; Mice ; Mice, Knockout ; Mutation ; RNA, Messenger/genetics/metabolism ; Transcription Factors/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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  • 2
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    Chromospheric alfvenic waves strong enough to power the solar wind (2007)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2007-12-08
    Description: Alfven waves have been invoked as a possible mechanism for the heating of the Sun's outer atmosphere, or corona, to millions of degrees and for the acceleration of the solar wind to hundreds of kilometers per second. However, Alfven waves of sufficient strength have not been unambiguously observed in the solar atmosphere. We used images of high temporal and spatial resolution obtained with the Solar Optical Telescope onboard the Japanese Hinode satellite to reveal that the chromosphere, the region sandwiched between the solar surface and the corona, is permeated by Alfven waves with strong amplitudes on the order of 10 to 25 kilometers per second and periods of 100 to 500 seconds. Estimates of the energy flux carried by these waves and comparisons with advanced radiative magnetohydrodynamic simulations indicate that such Alfven waves are energetic enough to accelerate the solar wind and possibly to heat the quiet corona.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉De Pontieu, B -- McIntosh, S W -- Carlsson, M -- Hansteen, V H -- Tarbell, T D -- Schrijver, C J -- Title, A M -- Shine, R A -- Tsuneta, S -- Katsukawa, Y -- Ichimoto, K -- Suematsu, Y -- Shimizu, T -- Nagata, S -- New York, N.Y. -- Science. 2007 Dec 7;318(5856):1574-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Lockheed Martin Solar and Astrophysics Laboratory, 3251 Hanover Street, Organization ADBS, Building 252, Palo Alto, CA 94304, USA. bdp@lmsal.com〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18063784" 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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  • 3
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    Requirement for the CD95 receptor-ligand pathway in c-Myc-induced apoptosis (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-11-21
    Description: Induction of apoptosis by oncogenes like c-myc may be important in restraining the emergence of neoplasia. However, the mechanism by which c-myc induces apoptosis is unknown. CD95 (also termed Fas or APO-1) is a cell surface transmembrane receptor of the tumor necrosis factor receptor family that activates an intrinsic apoptotic suicide program in cells upon binding either its ligand CD95L or antibody. c-myc-induced apoptosis was shown to require interaction on the cell surface between CD95 and its ligand. c-Myc acts downstream of the CD95 receptor by sensitizing cells to the CD95 death signal. Moreover, IGF-I signaling and Bcl-2 suppress c-myc-induced apoptosis by also acting downstream of CD95. These findings link two apoptotic pathways previously thought to be independent and establish the dependency of Myc on CD95 signaling for its killing activity.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hueber, A O -- Zornig, M -- Lyon, D -- Suda, T -- Nagata, S -- Evan, G I -- New York, N.Y. -- Science. 1997 Nov 14;278(5341):1305-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Imperial Cancer Research Fund (ICRF) Laboratories, 44 Lincoln's Inn Fields, London WC2A 3PX, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9360929" target="_blank"〉PubMed〈/a〉
    Keywords: 3T3 Cells ; *Adaptor Proteins, Signal Transducing ; Animals ; Antigens, CD95/*metabolism ; *Apoptosis ; Autocrine Communication ; Carrier Proteins/metabolism ; Cell Line ; Cell Membrane/metabolism ; Cells, Cultured ; Fas Ligand Protein ; Fas-Associated Death Domain Protein ; Gene Expression Regulation ; Genes, myc ; Insulin-Like Growth Factor I/pharmacology/physiology ; Membrane Glycoproteins/*metabolism ; Mice ; Proto-Oncogene Proteins c-bcl-2/pharmacology/physiology ; Proto-Oncogene Proteins c-myc/*metabolism ; Rats
    Print ISSN: 0036-8075
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  • 4
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    Autoimmune disease and impaired uptake of apoptotic cells in MFG-E8-deficient mice (2004)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2004-05-25
    Description: Apoptotic cells expose phosphatidylserine and are swiftly engulfed by macrophages. Milk fat globule epidermal growth factor (EGF) factor 8 (MFG-E8) is a protein that binds to apoptotic cells by recognizing phosphatidylserine and that enhances the engulfment of apoptotic cells by macrophages. We report that tingible body macrophages in the germinal centers of the spleen and lymph nodes strongly express MFG-E8. Many apoptotic lymphocytes were found on the MFG-E8-/- tingible body macrophages, but they were not efficiently engulfed. The MFG-E8-/- mice developed splenomegaly, with the formation of numerous germinal centers, and suffered from glomerulonephritis as a result of autoantibody production. These data demonstrate that MFG-E8 has a critical role in removing apoptotic B cells in the germinal centers and that its failure can lead to autoimmune diseases.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hanayama, Rikinari -- Tanaka, Masato -- Miyasaka, Kay -- Aozasa, Katsuyuki -- Koike, Masato -- Uchiyama, Yasuo -- Nagata, Shigekazu -- New York, N.Y. -- Science. 2004 May 21;304(5674):1147-50.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Genetics, Osaka University Medical School, 2-2 Yamada-oka, Suita, Osaka 565-0871, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15155946" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antibodies, Antinuclear/blood ; Antigens, CD/analysis ; Antigens, Differentiation, Myelomonocytic/analysis ; *Antigens, Surface ; *Apoptosis ; Autoantibodies/biosynthesis/blood ; Autoimmune Diseases/*immunology ; B-Lymphocytes/immunology ; Blotting, Northern ; Female ; Gene Targeting ; Germinal Center/cytology/immunology/metabolism ; Glomerulonephritis/*immunology ; In Situ Nick-End Labeling ; Macrophage Activation ; Macrophages/immunology/*metabolism/ultrastructure ; Macrophages, Peritoneal/immunology/metabolism ; Membrane Glycoproteins/genetics/*metabolism ; Mice ; *Milk Proteins ; *Phagocytosis ; Phosphatidylserines/metabolism ; Protein Binding ; Spleen/cytology/metabolism/pathology ; Splenomegaly/pathology ; T-Lymphocytes/immunology
    Print ISSN: 0036-8075
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  • 5
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    Rational design of potent antagonists to the human growth hormone receptor (1992)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1992-06-19
    Description: A hybrid receptor was constructed that contained the extracellular binding domain of the human growth hormone (hGH) receptor linked to the transmembrane and intracellular domains of the murine granulocyte colony-stimulating factor receptor. Addition of hGH to a myeloid leukemia cell line (FDC-P1) that expressed the hybrid receptor caused proliferation of these cells. The mechanism for signal transduction of the hybrid receptor required dimerization because monoclonal antibodies to the hGH receptor were agonists whereas their monovalent fragments were not. Receptor dimerization occurs sequentially--a receptor binds to site 1 on hGH, and then a second receptor molecule binds to site 2 on hGH. On the basis of this sequential mechanism, which may occur in many other cytokine receptors, inactive hGH analogs were designed that were potent antagonists to hGH-induced cell proliferation. Such antagonists could be useful for treating clinical conditions of hGH excess, such as acromegaly.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Fuh, G -- Cunningham, B C -- Fukunaga, R -- Nagata, S -- Goeddel, D V -- Wells, J A -- New York, N.Y. -- Science. 1992 Jun 19;256(5064):1677-80.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Protein Engineering, Genentech, Inc., South San Francisco, CA 94080.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1535167" target="_blank"〉PubMed〈/a〉
    Keywords: Antibodies, Monoclonal ; Cell Division/drug effects ; Cell Line ; DNA Replication/drug effects ; Dose-Response Relationship, Drug ; Growth Hormone/analysis/physiology ; Humans ; Models, Molecular ; Receptors, Granulocyte Colony-Stimulating Factor/physiology ; Receptors, Somatotropin/*physiology ; Signal Transduction/physiology ; Transfection
    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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  • 6
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    The Fas death factor (1995)
    American Association for the Advancement of Science (AAAS)
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    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
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  • 7
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    Fas and perforin pathways as major mechanisms of T cell-mediated cytotoxicity (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    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
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  • 8
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    Twisting motions of sunspot penumbral filaments (2007)
    American Association for the Advancement of Science (AAAS)
    Details
    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〉
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  • 9
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    Chromospheric anemone jets as evidence of ubiquitous reconnection (2007)
    American Association for the Advancement of Science (AAAS)
    Details
    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〉
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  • 10
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    Small-scale jetlike features in penumbral chromospheres (2007)
    American Association for the Advancement of Science (AAAS)
    Details
    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〉
    Print ISSN: 0036-8075
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