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  • 1
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    Prion-induced amyloid heart disease with high blood infectivity in transgenic mice (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-07-11
    Description: We investigated extraneural manifestations in scrapie-infected transgenic mice expressing prion protein lacking the glycophosphatydylinositol membrane anchor. In the brain, blood, and heart, both abnormal protease-resistant prion protein (PrPres) and prion infectivity were readily detected by immunoblot and by inoculation into nontransgenic recipients. The titer of infectious scrapie in blood plasma exceeded 10(7) 50% infectious doses per milliliter. The hearts of these transgenic mice contained PrPres-positive amyloid deposits that led to myocardial stiffness and cardiac disease.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1820586/" 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/PMC1820586/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Trifilo, Matthew J -- Yajima, Toshitaka -- Gu, Yusu -- Dalton, Nancy -- Peterson, Kirk L -- Race, Richard E -- Meade-White, Kimberly -- Portis, John L -- Masliah, Eliezer -- Knowlton, Kirk U -- Chesebro, Bruce -- Oldstone, Michael B A -- 5R01HL66424-04/HL/NHLBI NIH HHS/ -- AGO4342/PHS HHS/ -- NS041219-05/NS/NINDS NIH HHS/ -- P01 AG004342/AG/NIA NIH HHS/ -- New York, N.Y. -- Science. 2006 Jul 7;313(5783):94-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Viral-Immunobiology Laboratory, Departments of Molecular and Integrative Neurosciences and Infectology, Scripps Research Institute, La Jolla, CA 92037, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16825571" target="_blank"〉PubMed〈/a〉
    Keywords: Amyloid/*analysis ; Amyloidosis/blood/etiology/*pathology/physiopathology ; Animals ; Blotting, Western ; Cardiac Catheterization ; Coronary Vessels/chemistry/pathology ; Disease Models, Animal ; Glycosylphosphatidylinositols ; Heart Diseases/blood/etiology/*pathology/physiopathology ; Heart Function Tests ; Immunohistochemistry ; Mice ; Mice, Inbred C57BL ; Mice, Transgenic ; Microcirculation/chemistry/pathology ; Myocardial Contraction ; Myocardium/*chemistry/*pathology ; PrPC Proteins/chemistry ; PrPSc Proteins/*analysis/blood ; Scrapie/blood/*pathology/physiopathology ; Staining and Labeling ; Time Factors
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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  • 2
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    Activation of interferon-gamma inducing factor mediated by interleukin-1beta converting enzyme (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-01-10
    Description: The interleukin-1beta (IL-1beta) converting enzyme (ICE) processes the inactive IL-1beta precursor to the proinflammatory cytokine. ICE was also shown to cleave the precursor of interferon-gamma inducing factor (IGIF) at the authentic processing site with high efficiency, thereby activating IGIF and facilitating its export. Lipopolysaccharide-activated ICE-deficient (ICE-/-) Kupffer cells synthesized the IGIF precursor but failed to process it into the active form. Interferon-gamma and IGIF were diminished in the sera of ICE-/- mice exposed to Propionibacterium acnes and lipopolysaccharide. The lack of multiple proinflammatory cytokines in ICE-/- mice may account for their protection from septic shock.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gu, Y -- Kuida, K -- Tsutsui, H -- Ku, G -- Hsiao, K -- Fleming, M A -- Hayashi, N -- Higashino, K -- Okamura, H -- Nakanishi, K -- Kurimoto, M -- Tanimoto, T -- Flavell, R A -- Sato, V -- Harding, M W -- Livingston, D J -- Su, M S -- New York, N.Y. -- Science. 1997 Jan 10;275(5297):206-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Vertex Pharmaceuticals, Inc., 130 Waverly Street, Cambridge, MA 02139, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8999548" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; COS Cells ; Caspase 1 ; Caspase 3 ; *Caspases ; Caspases, Initiator ; Culture Media, Conditioned ; Cysteine Endopeptidases/*metabolism ; Cytokines/blood/*metabolism/pharmacology ; Humans ; Interferon-gamma/biosynthesis/blood ; Interleukin-18 ; Kupffer Cells/*metabolism ; Lipopolysaccharides/pharmacology ; Mice ; Protein Precursors/metabolism ; Protein Processing, Post-Translational ; Recombinant Proteins/metabolism/pharmacology ; Spleen/cytology/metabolism ; Transfection
    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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  • 3
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    Hematopoietic cell regulation by Rac1 and Rac2 guanosine triphosphatases (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-10-18
    Description: The Rho guanosine triphosphatases (GTPases) Rac1 and Rac2 are critical signaling regulators in mammalian cells. The deletion of both Rac1 and Rac2 murine alleles leads to a massive egress of hematopoietic stem/progenitor cells (HSC/Ps) into the blood from the marrow, whereas Rac1-/- but not Rac2-/- HSC/Ps fail to engraft in the bone marrow of irradiated recipient mice. In contrast, Rac2, but not Rac1, regulates superoxide production and directed migration in neutrophils, and in each cell type, the two GTPases play distinct roles in actin organization, cell survival, and proliferation. Thus, Rac1 and Rac2 regulate unique aspects of hematopoietic development and function.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gu, Yi -- Filippi, Marie-Dominique -- Cancelas, Jose A -- Siefring, Jamie E -- Williams, Emily P -- Jasti, Aparna C -- Harris, Chad E -- Lee, Andrew W -- Prabhakar, Rethinasamy -- Atkinson, Simon J -- Kwiatkowski, David J -- Williams, David A -- DK62757/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 2003 Oct 17;302(5644):445-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Experimental Hematology, Cincinnati Children's Hospital Medical Center, Cincinnati, OH 45229, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/14564009" target="_blank"〉PubMed〈/a〉
    Keywords: Actins/metabolism ; Animals ; Apoptosis ; Bone Marrow Transplantation ; Cell Adhesion ; Cell Cycle ; Cell Movement ; Cell Size ; Colony-Forming Units Assay ; Cyclin D1/metabolism ; Fibronectins/metabolism ; Hematopoiesis ; Hematopoietic Stem Cell Mobilization ; Hematopoietic Stem Cell Transplantation ; Hematopoietic Stem Cells/*physiology ; Mice ; Mice, Inbred NOD ; Mice, SCID ; Mitogen-Activated Protein Kinases/metabolism ; Neutrophils/*physiology ; *Protein-Serine-Threonine Kinases ; Proto-Oncogene Proteins/metabolism ; Proto-Oncogene Proteins c-akt ; Recombination, Genetic ; Signal Transduction ; Stem Cell Factor/pharmacology ; Superoxides/metabolism ; rac GTP-Binding Proteins/genetics/*metabolism ; rac1 GTP-Binding Protein/genetics/*metabolism
    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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