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  • 1
    Keywords: Medicine ; Immunology ; Virology ; Infectious Diseases ; Biomedicine ; Virology ; Infectious Diseases ; Immunology ; Springer eBooks
    Description / Table of Contents: Preface -- Part I Alphaherpesviruses -- Chapter1The Role of Herpes Simplex Virus Glycoproteins in Mediating Cell Entry -- Chapter2 Virus assembly and egress of HSV -- Chapter3 Us3 protein kinase encoded by HSV: the precise function and mechanism on viral life cycle -- Chapter4 Oncolytic virotherapy by HSV -- Chapter5 Neurological disorders by human alphaherpesviruses -- Chapter6 Antiviral drugs against alphaherpesvirus -- Chapter7 Vaccine development for VZV -- Part II℗ Betaherpesviruses -- Chapter8 Glycoproteins of HHV-6A and HHV-6B -- Chapter9 Betaherpesvirus virion assembly and egress -- Chapter10 Chromosomal Integration by Human Herpesviruses 6A and 6B -- Chapter11 Structural aspects of betaherpesvirus-encoded proteins -- Chapter12 Betaherpesvirus complications and management during stem cell transplantation -- Chapter13 Vaccine development for Cytomegalovirus -- Part III℗ Gammaherpesviruses -- Chapter14 KSHV genome replication and maintenance in latency -- Chapter15 Signal transduction pathways associated with Kapos퀙s sarcoma-associated herpesvirus-related tumors -- Chapter16 Pathological features of Kapos퀙s sarcoma-associated herpesvirus infection -- Chapter17 EBV-encoded latent genes -- Chapter18 Encyclopedia of EBV-encoded lytic genes: an update -- Chapter19 Animal models of human gammaherpesvirus infections -- Chapter20 Gastritis-infection-cancer sequence of Epstein Barr virus-associated gastric cancer -- Chapter21 EBV in T/NK-cell tumorigenesis -- Chapter22 Vaccine development for Epstein-Barr Virus
    Abstract: This book introduces and reviews several topics for each human herpesvirus. One of the most important features of the book is that it covers aspects of both basic research and clinical medicine. Herpesviridae, a family of double-strand DNA viruses, has unique biological features by which these viruses establish latency after primary infection and reactivate in later life. Nine human herpesviruses are known so far, and each of them causes a variety of diseases in both primary infection and reactivation. Since the discovery of each human herpesvirus, an abundance of findings related to them has accumulated in basic research and clinical medicine. However, the vast majority of biological features is still masked in mystery. Furthermore, a strategy of treatment and prevention has not yet been established for most human herpesviruses. A wide range of readers will be interested in this volume with its treatment of problematic points and latest findings in the field
    Pages: VIII, 501 p. 69 illus., 41 illus. in color. : online resource.
    ISBN: 9789811072307
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  • 2
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    Cham : Springer International Publishing
    Keywords: Medicine ; Human Physiology ; Pharmacology ; Diabetes ; Medical Biochemistry ; Systems Biology ; Biomedicine ; Pharmacology/Toxicology ; Human Physiology ; Diabetes ; Systems Biology ; Medical Biochemistry ; Springer eBooks
    Description / Table of Contents: Ligands at Free Fatty Acid Receptor 1 (GPR40) -- Ligands at Free Fatty Acid Receptor 2/3 (GPR43)/GPR41 -- Ligands at GPR84 -- Ligands at Free Fatty Acid Receptor 4 (GPR120) -- Homology modelling of FFA receptors -- Sensors for FFA receptors -- Key questions for translation of FFA receptors from pharmacology to medicines -- Polymorphic variation in FFA receptors. Functions and consequences -- The role and future of FFA1 as a therapeutic target -- Gut hormone regulation and secretion via FFA1 and FFA4 -- The role of FFA2 and FFA3 in metabolic regulation -- Anti-inflammatory and insulin sensitizing effects of free fatty acid receptors -- Free Fatty Acid receptors and cancer
    Abstract: This book highlights the important role free fatty acids (FFA) play as potential drug targets. While FFA have long been considered byproducts of cell metabolism, they are now recognized as ligands that regulate cell and tissue function via G-protein-coupled receptors. At least three receptors have been identified for which FFA appear to be the endogenous ligands
    Pages: VIII, 256 p. 70 illus. : online resource.
    ISBN: 9783319506937
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  • 3
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    New York : Harper & Row
    Call number: 09-MA:286
    Keywords: Population genetics
    Pages: xiv, 591 p. : illus.
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    09-MA:286 departmental collection or stack – please contact the library
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  • 4
    Keywords: Life sciences ; Neurosciences ; Toxicology ; Biochemistry ; Life sciences ; Biochemistry, general ; Medical Biochemistry ; Pharmacology/Toxicology ; Neurosciences ; Springer eBooks
    Description / Table of Contents: Biogenesis and Catabolism of Hydrogen Sulfide -- Multiple roles of H2S in inflammation – a new class of therapeutics? -- Hydrogen Sulfide and Oxygen Sensing -- The signal transduction of H2S: identification of the ‘receptor’ for H2S -- Hydrogen sulfide: Physiological and pathophysiological functions -- Therapeutic Applications of Hydrogen Sulfide -- Biological effects of H2S inhalation and its therapeutic potential -- H2S-mediated defense against antibiotics in bacteria -- Modulation of cellular signaling and induction of cytoprotection by hydrogen sulfide
    Pages: IX, 207 p. 39 illus., 23 illus. in color. : online resource.
    ISBN: 9783709115503
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  • 5
    ISSN: 0040-4039
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Chemistry and Pharmacology
    Type of Medium: Electronic Resource
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  • 6
    Publication Date: 2018-06-29
    Description: MicroRNA 33 (miR-33) targets ATP-binding cassette transporter A1 (ABCA1), and its deficiency increases serum high-density lipoprotein (HDL)-cholesterol (HDL-C) and ameliorates atherosclerosis. Although we previously reported that miR-33 deficiency increased peripheral Ly6C high monocytes on an ApoE-deficient background, the effect of miR-33 on the monocyte population has not been fully elucidated, especially in a wild-type (WT) background. We found that Ly6C high monocytes in miR-33 –/– mice were decreased in peripheral blood and increased in bone marrow (BM). Expansion of myeloid progenitors and decreased apoptosis in Lin – Sca1 + c-Kit + (LSK) cells were observed in miR-33 –/– mice. A BM transplantation study and competitive repopulation assay revealed that hematopoietic miR-33 deficiency caused myeloid expansion and increased peripheral Ly6C high monocytes and that nonhematopoietic miR-33 deficiency caused reduced peripheral Ly6C high monocytes. Expression of high-mobility group AT-hook 2 (HMGA2) targeted by miR-33 increased in miR-33-deficient LSK cells, and its knockdown abolished the reduction of apoptosis. Transduction of human apolipoprotein A1 and ABCA1 in WT mouse liver increased HDL-C and reduced peripheral Ly6C high monocytes. These data indicate that miR-33 deficiency affects distribution of inflammatory monocytes through dual pathways. One pathway involves the enhancement of Hmga2 expression in hematopoietic stem cells to increase Ly6C high monocytes, and the other involves the elevation of HDL-C to decrease peripheral Ly6C high monocytes.
    Print ISSN: 0270-7306
    Electronic ISSN: 1098-5549
    Topics: Biology , Medicine
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  • 7
    Publication Date: 2018-03-31
    Description: Biochemistry DOI: 10.1021/acs.biochem.8b00042
    Print ISSN: 0006-2960
    Electronic ISSN: 1520-4995
    Topics: Biology , Chemistry and Pharmacology
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  • 8
    Publication Date: 2014-05-03
    Description: PINK1 (PTEN induced putative kinase 1) and PARKIN (also known as PARK2) have been identified as the causal genes responsible for hereditary recessive early-onset Parkinsonism. PINK1 is a Ser/Thr kinase that specifically accumulates on depolarized mitochondria, whereas parkin is an E3 ubiquitin ligase that catalyses ubiquitin transfer to mitochondrial substrates. PINK1 acts as an upstream factor for parkin and is essential both for the activation of latent E3 parkin activity and for recruiting parkin onto depolarized mitochondria. Recently, mechanistic insights into mitochondrial quality control mediated by PINK1 and parkin have been revealed, and PINK1-dependent phosphorylation of parkin has been reported. However, the requirement of PINK1 for parkin activation was not bypassed by phosphomimetic parkin mutation, and how PINK1 accelerates the E3 activity of parkin on damaged mitochondria is still obscure. Here we report that ubiquitin is the genuine substrate of PINK1. PINK1 phosphorylated ubiquitin at Ser 65 both in vitro and in cells, and a Ser 65 phosphopeptide derived from endogenous ubiquitin was only detected in cells in the presence of PINK1 and following a decrease in mitochondrial membrane potential. Unexpectedly, phosphomimetic ubiquitin bypassed PINK1-dependent activation of a phosphomimetic parkin mutant in cells. Furthermore, phosphomimetic ubiquitin accelerates discharge of the thioester conjugate formed by UBCH7 (also known as UBE2L3) and ubiquitin (UBCH7 approximately ubiquitin) in the presence of parkin in vitro, indicating that it acts allosterically. The phosphorylation-dependent interaction between ubiquitin and parkin suggests that phosphorylated ubiquitin unlocks autoinhibition of the catalytic cysteine. Our results show that PINK1-dependent phosphorylation of both parkin and ubiquitin is sufficient for full activation of parkin E3 activity. These findings demonstrate that phosphorylated ubiquitin is a parkin activator.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Koyano, Fumika -- Okatsu, Kei -- Kosako, Hidetaka -- Tamura, Yasushi -- Go, Etsu -- Kimura, Mayumi -- Kimura, Yoko -- Tsuchiya, Hikaru -- Yoshihara, Hidehito -- Hirokawa, Takatsugu -- Endo, Toshiya -- Fon, Edward A -- Trempe, Jean-Francois -- Saeki, Yasushi -- Tanaka, Keiji -- Matsuda, Noriyuki -- Canadian Institutes of Health Research/Canada -- England -- Nature. 2014 Jun 5;510(7503):162-6. doi: 10.1038/nature13392. Epub 2014 Jun 4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉1] Laboratory of Protein Metabolism, Tokyo Metropolitan Institute of Medical Science, Setagaya-ku, Tokyo 156-8506, Japan [2] Graduate School of Frontier Sciences, The University of Tokyo, Kashiwa, Chiba 277-8561, Japan. ; Division of Cell Signaling, Fujii Memorial Institute of Medical Sciences, The University of Tokushima, Tokushima 770-8503, Japan. ; Research Center for Materials Science, Nagoya University, Nagoya, Aichi 464-8602, Japan. ; Laboratory of Protein Metabolism, Tokyo Metropolitan Institute of Medical Science, Setagaya-ku, Tokyo 156-8506, Japan. ; 1] Laboratory of Protein Metabolism, Tokyo Metropolitan Institute of Medical Science, Setagaya-ku, Tokyo 156-8506, Japan [2] Graduate School of Agriculture, Shizuoka University, 836 Ohya, Shizuoka 422-8529, Japan. ; Molecular Profiling Research Center for Drug Discovery, National Institute of Advanced Industrial Science and Technology, 2-4-7 Aomi, Koto-ku, Tokyo 135-0064, Japan. ; 1] JST-CREST/Department of Chemistry, Graduate School of Science, Nagoya University, Chikusa-ku, Nagoya 464-8602, Japan [2] JST-CREST/Faculty of Life Sciences, Kyoto Sangyo University, Kamigamo-motoyama, Kita-ku, Kyoto 603-8555, Japan. ; McGill Parkinson Program, Department of Neurology and Neurosurgery, Montreal Neurological Institute and Hospital, McGill University, Montreal, Quebec H3A 2B4, Canada. ; Department of Pharmacology & Therapeutics, McGill University, Montreal, Quebec H3G 1Y6, Canada. ; 1] Laboratory of Protein Metabolism, Tokyo Metropolitan Institute of Medical Science, Setagaya-ku, Tokyo 156-8506, Japan [2] Protein Metabolism Project, Tokyo Metropolitan Institute of Medical Science, Setagaya-ku, Tokyo 156-8506, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24784582" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Enzyme Activation ; Fibroblasts ; HeLa Cells ; Humans ; Membrane Potential, Mitochondrial ; Mice ; Mitochondria/metabolism ; Mutation/genetics ; Parkinson Disease ; Phosphorylation ; Phosphoserine/metabolism ; Protein Kinases/*metabolism ; Ubiquitin/chemistry/*metabolism ; Ubiquitin-Protein Ligases/genetics/*metabolism ; Ubiquitination
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 9
    Publication Date: 2018-09-20
    Description: Sounding-rocket microgravity experiments on alumina dust Sounding-rocket microgravity experiments on alumina dust, Published online: 19 September 2018; doi:10.1038/s41467-018-06359-y Alumina is thought to be the main condensate to form in the gas outflow from oxygen-rich evolved stars. Here, the authors perform a condensation experiment with alumina in a low-gravity environment, and find spectroscopic evidence for a sharp feature at a wavelength of 13.55 μm.
    Electronic ISSN: 2041-1723
    Topics: Biology , Chemistry and Pharmacology , Natural Sciences in General , Physics
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  • 10
    Publication Date: 2018-03-23
    Description: CD8 + T cells are the major effector cells that protect against malaria liver-stage infection, forming clusters around Plasmodium -infected hepatocytes and eliminating parasites after a prolonged interaction with these hepatocytes. We aimed to investigate the roles of specific and nonspecific CD8 + T cells in cluster formation and protective immunity. To this end, we used Plasmodium berghei ANKA expressing ovalbumin as well as CD8 + T cells from transgenic mice expressing a T cell receptor specific for ovalbumin (OT-I) and CD8 + T cells specific for an unrelated antigen, respectively. While antigen-specific CD8 + T cells were essential for cluster formation, both antigen-specific and nonspecific CD8 + T cells joined the clusters. However, nonspecific CD8 + T cells did not significantly contribute to protective immunity. In the livers of infected mice, specific CD8 + T cells expressed high levels of CD25, compatible with a local, activated effector phenotype. In vivo imaging of the liver revealed that specific CD8 + T cells interact with CD11c + cells around infected hepatocytes. The depletion of CD11c + cells virtually eliminated the clusters in the liver, leading to a significant decrease in protection. These experiments reveal an essential role of hepatic CD11c + dendritic cells and presumably macrophages in the formation of CD8 + T cell clusters around Plasmodium -infected hepatocytes. Once cluster formation is triggered by parasite-specific CD8 + T cells, specific and unrelated activated CD8 + T cells join the clusters in a chemokine- and dendritic cell-dependent manner. Nonspecific CD8 + T cells seem to play a limited role in protective immunity against Plasmodium parasites.
    Print ISSN: 0019-9567
    Electronic ISSN: 1098-5522
    Topics: Medicine
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