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  • Lunar and Planetary Science and Exploration  (147)
  • Mice, Inbred C57BL  (98)
  • ASTROPHYSICS
  • Life and Medical Sciences
  • 2010-2014  (245)
  • 1950-1954
  • 2011  (131)
  • 2010  (114)
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  • 2010-2014  (245)
  • 1950-1954
Year
  • 1
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    Equilibrative nucleoside transporter 3 deficiency perturbs lysosome function and macrophage homeostasis (2011)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2011-12-17
    Description: Lysosomal storage diseases (LSDs) are a group of heterogeneous disorders caused by defects in lysosomal enzymes or transporters, resulting in accumulation of undegraded macromolecules or metabolites. Macrophage numbers are expanded in several LSDs, leading to histiocytosis of unknown pathophysiology. Here, we found that mice lacking the equilibrative nucleoside transporter 3 (ENT3) developed a spontaneous and progressive macrophage-dominated histiocytosis. In the absence of ENT3, defective apoptotic cell clearance led to lysosomal nucleoside buildup, elevated intralysosomal pH, and altered macrophage function. The macrophage accumulation was partly due to increased macrophage colony-stimulating factor and receptor expression and signaling secondary to the lysosomal defects. These studies suggest a cellular and molecular basis for the development of histiocytosis in several human syndromes associated with ENT3 mutations and potentially other LSDs.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hsu, Chia-Lin -- Lin, Weiyu -- Seshasayee, Dhaya -- Chen, Yung-Hsiang -- Ding, Xiao -- Lin, Zhonghua -- Suto, Eric -- Huang, Zhiyu -- Lee, Wyne P -- Park, Hyunjoo -- Xu, Min -- Sun, Mei -- Rangell, Linda -- Lutman, Jeff L -- Ulufatu, Sheila -- Stefanich, Eric -- Chalouni, Cecile -- Sagolla, Meredith -- Diehl, Lauri -- Fielder, Paul -- Dean, Brian -- Balazs, Mercedesz -- Martin, Flavius -- New York, N.Y. -- Science. 2012 Jan 6;335(6064):89-92. doi: 10.1126/science.1213682. Epub 2011 Dec 15.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Immunology, Genentech Inc., 1 DNA Way, South San Francisco, CA 94080, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22174130" target="_blank"〉PubMed〈/a〉
    Keywords: Adenosine/metabolism ; Animals ; Apoptosis ; Cell Count ; Cell Proliferation ; Cells, Cultured ; Histiocytosis/*physiopathology ; *Homeostasis ; Humans ; Hydrogen-Ion Concentration ; Listeriosis/immunology/microbiology ; Lysosomal Storage Diseases/physiopathology ; Lysosomes/*physiology/ultrastructure ; Macrophage Colony-Stimulating Factor/metabolism ; Macrophages/immunology/*physiology/ultrastructure ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Myelopoiesis ; Nucleoside Transport Proteins/genetics/*physiology ; Phagocytosis ; Receptor, Macrophage Colony-Stimulating Factor/metabolism ; Signal Transduction ; Thymocytes/immunology/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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  • 2
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    ATP-binding cassette transporters and HDL suppress hematopoietic stem cell proliferation (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    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
    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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    TAp63 suppresses metastasis through coordinate regulation of Dicer and miRNAs (2010)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2010-10-22
    Description: Aberrant expression of microRNAs (miRNAs) and the enzymes that control their processing have been reported in multiple biological processes including primary and metastatic tumours, but the mechanisms governing this are not clearly understood. Here we show that TAp63, a p53 family member, suppresses tumorigenesis and metastasis, and coordinately regulates Dicer and miR-130b to suppress metastasis. Metastatic mouse and human tumours deficient in TAp63 express Dicer at very low levels, and we found that modulation of expression of Dicer and miR-130b markedly affected the metastatic potential of cells lacking TAp63. TAp63 binds to and transactivates the Dicer promoter, demonstrating direct transcriptional regulation of Dicer by TAp63. These data provide a novel understanding of the roles of TAp63 in tumour and metastasis suppression through the coordinate transcriptional regulation of Dicer and miR-130b and may have implications for the many processes regulated by miRNAs.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3055799/" 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/PMC3055799/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Su, Xiaohua -- Chakravarti, Deepavali -- Cho, Min Soon -- Liu, Lingzhi -- Gi, Young Jin -- Lin, Yu-Li -- Leung, Marco L -- El-Naggar, Adel -- Creighton, Chad J -- Suraokar, Milind B -- Wistuba, Ignacio -- Flores, Elsa R -- 01DE019765/DE/NIDCR NIH HHS/ -- CA16672/CA/NCI NIH HHS/ -- P30 CA016672-27/CA/NCI NIH HHS/ -- P50 CA070907/CA/NCI NIH HHS/ -- P50 CA070907-10/CA/NCI NIH HHS/ -- P50 CA091846/CA/NCI NIH HHS/ -- P50 CA091846-10/CA/NCI NIH HHS/ -- P50CA070907/CA/NCI NIH HHS/ -- P50CA091846/CA/NCI NIH HHS/ -- U01 DE019765/DE/NIDCR NIH HHS/ -- U01 DE019765-03/DE/NIDCR NIH HHS/ -- England -- Nature. 2010 Oct 21;467(7318):986-90. doi: 10.1038/nature09459.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular and Cellular Oncology, The University of Texas M. D. Anderson Cancer Center, 1515 Holcombe Boulevard, Houston, Texas 77030, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20962848" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Aging ; Cell Line ; Cell Line, Tumor ; DEAD-box RNA Helicases/biosynthesis/deficiency/genetics/*metabolism ; Endoribonucleases/genetics/*metabolism ; Female ; *Gene Expression Regulation, Neoplastic ; Genes, Tumor Suppressor/physiology ; Genomic Instability ; Humans ; Male ; Mice ; Mice, Inbred C57BL ; MicroRNAs/*biosynthesis/genetics/metabolism ; Neoplasm Metastasis/*genetics ; Neoplasms/genetics/pathology/secretion ; Phosphoproteins/deficiency/genetics/*metabolism ; Promoter Regions, Genetic/genetics ; Ribonuclease III/biosynthesis/deficiency/genetics/*metabolism ; Trans-Activators/deficiency/genetics/*metabolism ; Transcription Factors ; Transcriptional Activation ; Tumor Suppressor Proteins/deficiency/genetics/*metabolism
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Published by Nature Publishing Group (NPG)
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  • 4
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    Vascular endothelial growth factor B controls endothelial fatty acid uptake (2010)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2010-03-17
    Description: The vascular endothelial growth factors (VEGFs) are major angiogenic regulators and are involved in several aspects of endothelial cell physiology. However, the detailed role of VEGF-B in blood vessel function has remained unclear. Here we show that VEGF-B has an unexpected role in endothelial targeting of lipids to peripheral tissues. Dietary lipids present in circulation have to be transported through the vascular endothelium to be metabolized by tissue cells, a mechanism that is poorly understood. Bioinformatic analysis showed that Vegfb was tightly co-expressed with nuclear-encoded mitochondrial genes across a large variety of physiological conditions in mice, pointing to a role for VEGF-B in metabolism. VEGF-B specifically controlled endothelial uptake of fatty acids via transcriptional regulation of vascular fatty acid transport proteins. As a consequence, Vegfb(-/-) mice showed less uptake and accumulation of lipids in muscle, heart and brown adipose tissue, and instead shunted lipids to white adipose tissue. This regulation was mediated by VEGF receptor 1 and neuropilin 1 expressed by the endothelium. The co-expression of VEGF-B and mitochondrial proteins introduces a novel regulatory mechanism, whereby endothelial lipid uptake and mitochondrial lipid use are tightly coordinated. The involvement of VEGF-B in lipid uptake may open up the possibility for novel strategies to modulate pathological lipid accumulation in diabetes, obesity and cardiovascular diseases.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hagberg, Carolina E -- Falkevall, Annelie -- Wang, Xun -- Larsson, Erik -- Huusko, Jenni -- Nilsson, Ingrid -- van Meeteren, Laurens A -- Samen, Erik -- Lu, Li -- Vanwildemeersch, Maarten -- Klar, Joakim -- Genove, Guillem -- Pietras, Kristian -- Stone-Elander, Sharon -- Claesson-Welsh, Lena -- Yla-Herttuala, Seppo -- Lindahl, Per -- Eriksson, Ulf -- England -- Nature. 2010 Apr 8;464(7290):917-21. doi: 10.1038/nature08945. Epub 2010 Mar 14.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Tissue Biology Group, Division of Matrix Biology, Department of Medical Biochemistry and Biophysics, Karolinska Institutet, SE-171 77 Stockholm, Sweden.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20228789" target="_blank"〉PubMed〈/a〉
    Keywords: Adipose Tissue, Brown/metabolism ; Adipose Tissue, White/metabolism ; Animals ; Biological Transport ; Cell Line ; Cell Nucleus/genetics ; Cells, Cultured ; Endothelium/cytology/*metabolism ; Fatty Acid Transport Proteins/genetics ; Fatty Acids/*metabolism ; Gene Expression Regulation ; Humans ; Male ; Mice ; Mice, Inbred C57BL ; Mitochondria/genetics/metabolism ; Mitochondrial Proteins/genetics/metabolism ; Muscles/metabolism ; Myocardium/metabolism ; Neuropilin-1/genetics/metabolism ; Oligonucleotide Array Sequence Analysis ; Organ Specificity ; Signal Transduction ; Transcription, Genetic ; Vascular Endothelial Growth Factor B/deficiency/genetics/*metabolism ; Vascular Endothelial Growth Factor Receptor-1/metabolism
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 5
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    Gut inflammation provides a respiratory electron acceptor for Salmonella (2010)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2010-09-25
    Description: Salmonella enterica serotype Typhimurium (S. Typhimurium) causes acute gut inflammation by using its virulence factors to invade the intestinal epithelium and survive in mucosal macrophages. The inflammatory response enhances the transmission success of S. Typhimurium by promoting its outgrowth in the gut lumen through unknown mechanisms. Here we show that reactive oxygen species generated during inflammation react with endogenous, luminal sulphur compounds (thiosulphate) to form a new respiratory electron acceptor, tetrathionate. The genes conferring the ability to use tetrathionate as an electron acceptor produce a growth advantage for S. Typhimurium over the competing microbiota in the lumen of the inflamed gut. We conclude that S. Typhimurium virulence factors induce host-driven production of a new electron acceptor that allows the pathogen to use respiration to compete with fermenting gut microbes. Thus the ability to trigger intestinal inflammation is crucial for the biology of this diarrhoeal pathogen.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2946174/" 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/PMC2946174/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Winter, Sebastian E -- Thiennimitr, Parameth -- Winter, Maria G -- Butler, Brian P -- Huseby, Douglas L -- Crawford, Robert W -- Russell, Joseph M -- Bevins, Charles L -- Adams, L Garry -- Tsolis, Renee M -- Roth, John R -- Baumler, Andreas J -- AI040124/AI/NIAID NIH HHS/ -- AI044170/AI/NIAID NIH HHS/ -- AI073120/AI/NIAID NIH HHS/ -- AI076246/AI/NIAID NIH HHS/ -- AI088122/AI/NIAID NIH HHS/ -- R21 AI088122/AI/NIAID NIH HHS/ -- R21 AI088122-01/AI/NIAID NIH HHS/ -- R21 AI088122-02/AI/NIAID NIH HHS/ -- England -- Nature. 2010 Sep 23;467(7314):426-9. doi: 10.1038/nature09415.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medical Microbiology and Immunology, School of Medicine, University of California, Davis, One Shields Avenue, Davis, California 95616, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20864996" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Cell Respiration ; Colitis/metabolism/microbiology ; Electron Transport ; *Electrons ; Female ; Gastrointestinal Tract/metabolism/*microbiology/*pathology ; Inflammation/metabolism/microbiology/pathology ; Intestinal Mucosa/metabolism/microbiology/pathology ; Mice ; Mice, Inbred C57BL ; Reactive Oxygen Species/metabolism ; Salmonella typhimurium/growth & development/*metabolism ; Tetrathionic Acid/metabolism ; Thiosulfates/metabolism
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 6
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    Altered histone acetylation is associated with age-dependent memory impairment in mice (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-05-08
    Description: As the human life span increases, the number of people suffering from cognitive decline is rising dramatically. The mechanisms underlying age-associated memory impairment are, however, not understood. Here we show that memory disturbances in the aging brain of the mouse are associated with altered hippocampal chromatin plasticity. During learning, aged mice display a specific deregulation of histone H4 lysine 12 (H4K12) acetylation and fail to initiate a hippocampal gene expression program associated with memory consolidation. Restoration of physiological H4K12 acetylation reinstates the expression of learning-induced genes and leads to the recovery of cognitive abilities. Our data suggest that deregulated H4K12 acetylation may represent an early biomarker of an impaired genome-environment interaction in the aging mouse brain.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Peleg, Shahaf -- Sananbenesi, Farahnaz -- Zovoilis, Athanasios -- Burkhardt, Susanne -- Bahari-Javan, Sanaz -- Agis-Balboa, Roberto Carlos -- Cota, Perla -- Wittnam, Jessica Lee -- Gogol-Doering, Andreas -- Opitz, Lennart -- Salinas-Riester, Gabriella -- Dettenhofer, Markus -- Kang, Hui -- Farinelli, Laurent -- Chen, Wei -- Fischer, Andre -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2010 May 7;328(5979):753-6. doi: 10.1126/science.1186088.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory for Aging and Cognitive Diseases, European Neuroscience Institute, Grisebach Str. 5, D-37077 Goettingen, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20448184" target="_blank"〉PubMed〈/a〉
    Keywords: Acetylation ; Aging/*genetics ; Animals ; Chromatin/metabolism ; *Chromatin Assembly and Disassembly ; Conditioning (Psychology) ; Epigenesis, Genetic ; Fear ; Gene Expression Profiling ; *Gene Expression Regulation ; Hippocampus/*metabolism ; Histone Deacetylase Inhibitors/metabolism/pharmacology ; Histones/*metabolism ; Hydroxamic Acids/pharmacology ; Learning/drug effects ; Lysine/metabolism ; Memory/drug effects ; Memory Disorders/*genetics/metabolism ; Mice ; Mice, Inbred C57BL ; Microfilament Proteins/genetics/metabolism ; Nuclear Proteins/genetics/metabolism ; Signal Transduction ; Transcription Initiation Site ; Transcription, Genetic ; Up-Regulation
    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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    Autophagy-dependent anticancer immune responses induced by chemotherapeutic agents in mice (2011)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2011-12-17
    Description: Antineoplastic chemotherapies are particularly efficient when they elicit immunogenic cell death, thus provoking an anticancer immune response. Here we demonstrate that autophagy, which is often disabled in cancer, is dispensable for chemotherapy-induced cell death but required for its immunogenicity. In response to chemotherapy, autophagy-competent, but not autophagy-deficient, cancers attracted dendritic cells and T lymphocytes into the tumor bed. Suppression of autophagy inhibited the release of adenosine triphosphate (ATP) from dying tumor cells. Conversely, inhibition of extracellular ATP-degrading enzymes increased pericellular ATP in autophagy-deficient tumors, reestablished the recruitment of immune cells, and restored chemotherapeutic responses but only in immunocompetent hosts. Thus, autophagy is essential for the immunogenic release of ATP from dying cells, and increased extracellular ATP concentrations improve the efficacy of antineoplastic chemotherapies when autophagy is disabled.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Michaud, Mickael -- Martins, Isabelle -- Sukkurwala, Abdul Qader -- Adjemian, Sandy -- Ma, Yuting -- Pellegatti, Patrizia -- Shen, Shensi -- Kepp, Oliver -- Scoazec, Marie -- Mignot, Gregoire -- Rello-Varona, Santiago -- Tailler, Maximilien -- Menger, Laurie -- Vacchelli, Erika -- Galluzzi, Lorenzo -- Ghiringhelli, Francois -- di Virgilio, Francesco -- Zitvogel, Laurence -- Kroemer, Guido -- New York, N.Y. -- Science. 2011 Dec 16;334(6062):1573-7. doi: 10.1126/science.1208347.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉INSERM, U848, Villejuif, France.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22174255" target="_blank"〉PubMed〈/a〉
    Keywords: Adenosine Triphosphate/metabolism ; Animals ; Antineoplastic Agents/*pharmacology/therapeutic use ; Autophagy/drug effects/*physiology ; Calreticulin/pharmacology ; Cell Death/immunology ; Cell Line, Tumor ; Dendritic Cells/immunology ; Humans ; Mice ; Mice, Inbred BALB C ; Mice, Inbred C57BL ; Mitoxantrone/pharmacology ; Neoplasms/drug therapy/*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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  • 8
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    Asymmetric B cell division in the germinal center reaction (2011)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2011-12-17
    Description: Lifelong antibody responses to vaccination require reorganization of lymphoid tissue and dynamic intercellular communication called the germinal center reaction. B lymphocytes undergo cellular polarization during antigen stimulation, acquisition, and presentation, which are critical steps for initiating humoral immunity. Here, we show that germinal center B lymphocytes asymmetrically segregate the transcriptional regulator Bcl6, the receptor for interleukin-21, and the ancestral polarity protein atypical protein kinase C to one side of the plane of division, generating unequal inheritance of fate-altering molecules by daughter cells. Germinal center B lymphocytes from mice with a defect in leukocyte adhesion fail to divide asymmetrically. These results suggest that motile cells lacking constitutive attachment can receive provisional polarity cues from the microenvironment to generate daughter cell diversity and self-renewal.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3282111/" 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/PMC3282111/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Barnett, Burton E -- Ciocca, Maria L -- Goenka, Radhika -- Barnett, Lisa G -- Wu, Junmin -- Laufer, Terri M -- Burkhardt, Janis K -- Cancro, Michael P -- Reiner, Steven L -- 3T32GM007170-36S1/GM/NIGMS NIH HHS/ -- AI042370/AI/NIAID NIH HHS/ -- AI065644/AI/NIAID NIH HHS/ -- AI076458/AI/NIAID NIH HHS/ -- R01 AI042370/AI/NIAID NIH HHS/ -- R01 AI042370-14/AI/NIAID NIH HHS/ -- R01 AI042370-15/AI/NIAID NIH HHS/ -- R01 AI061699/AI/NIAID NIH HHS/ -- R01 AI076458/AI/NIAID NIH HHS/ -- R01 AI076458-04/AI/NIAID NIH HHS/ -- R01 AI076458-05/AI/NIAID NIH HHS/ -- T32 AI007532/AI/NIAID NIH HHS/ -- T32 AI055428/AI/NIAID NIH HHS/ -- T32AI055428/AI/NIAID NIH HHS/ -- T32GM07229/GM/NIGMS NIH HHS/ -- T32HD007516/HD/NICHD NIH HHS/ -- New York, N.Y. -- Science. 2012 Jan 20;335(6066):342-4. doi: 10.1126/science.1213495. Epub 2011 Dec 15.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Abramson Family Cancer Research Institute, University of Pennsylvania, Philadelphia, PA 19104, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22174128" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, CD40/metabolism ; *Asymmetric Cell Division ; B-Lymphocytes/*cytology/*immunology/metabolism ; Cell Adhesion ; Cell Communication ; Cell Polarity ; Cellular Microenvironment ; Cues ; DNA-Binding Proteins/metabolism ; Germinal Center/*cytology/*immunology ; Immunization ; Mice ; Mice, Inbred C57BL ; Mitosis ; Protein Kinase C/metabolism ; Receptors, Interleukin-21/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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  • 9
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    Temporal and Spatial Aspects of Gas Release During the 2010 Apparition of Comet 103P/Hartley-2 (2011)
    In:  CASI
    Details
    Publication Date: 2019-07-13
    Description: We report measurements of eight primary volatiles (H2O, HCN, CH4, C2H6, CH3OH, C2H2, H2CO, and NH3) and two product species (OH and NH2) in comet 103P/Hartley-2 using high dispersion infrared spectroscopy. We present production rates for individual volatiles species, their mixing ratios relative to water, and their spatial distributions in the coma on multiple dates that span the interval Sept. - Dec. 2010. The production rates vary strongly with nucleus rotation, but the mixing ratios remain constant throughout the campaign. The released primary volatiles exhibit diverse spatial properties which favor the presence of separate polar and apolar ice phases in the nucleus, establish dust and gas release from icy clumps (and also, directly from the nucleus), and provide insights into the driver for the cyanogen (CN) polar jet.
    Keywords: Lunar and Planetary Science and Exploration
    Type: GSFC.OVPR.4972.2011 , 43rd Annual DPS Meeting; Oct 02, 2011 - Oct 07, 2011; Nantes; France
    Format: application/pdf
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  • 10
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    Evidence for Hesperian Impact-Induced Hydrothermalism on Mars (2010)
    In:  Other Sources
    Details
    Publication Date: 2019-07-13
    Description: Several hydrated silicate deposits on Mars are observed within craters and are interpreted as excavated Noachian material. Toro crater (71.8 deg E, 17.0 deg N), located on the northern edge of the Syrtis Major Volcanic Plains, shows spectral and morphologic evidence of impact-induced hydrothermal activity. Spectroscopic observations were used to identify extensive hydrated silicate deposits, including prehnite, chlorites, smectites, and opaline material, a suite of phases that frequently results from hydrothermal alteration in terrestrial craters and also expected on Mars from geochemical modeling of hydrothermal environments. When combined with altimetry and high-resolution imaging data, these deposits appear associated predominantly with the central uplift and with portions of the northern part of the crater floor. Detailed geologic mapping of these deposits reveals geomorphic features that are consistent with hydrothermal activity that followed the impact event, including vent-like and conical mound structures, and a complex network of tectonic structures caused by fluid interactions such as fractures and joints. The crater age has been calculated from the cumulative crater size-frequency distributions and is found to be Early Hesperian. The evidence presented here provides support for impact-induced hydrothermal activity in Toro crater, that extends phyllosilicate formation processes beyond the Noachian era.
    Keywords: Lunar and Planetary Science and Exploration
    Type: Icarus; 208; 667-683
    Format: text
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