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  • Animals  (51)
  • American Association for the Advancement of Science (AAAS)  (36)
  • Nature Publishing Group (NPG)  (15)
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  • American Association for the Advancement of Science (AAAS)  (36)
  • Nature Publishing Group (NPG)  (15)
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  • 1
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    Low potential for climatic stress adaptation in a rainforest Drosophila species (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-07-05
    Description: The ability of sensitive rainforest species to evolve in response to climate change is largely unknown. We show that the Australian tropical rainforest fly Drosophila birchii exhibits clinal variation in desiccation resistance, but the most resistant population lacks the ability to evolve further resistance even after intense selection for over 30 generations. Parent-offspring comparisons indicate low heritable variation for this trait but high levels of genetic variation for morphology. D. birchii also exhibits abundant genetic variation at microsatellite loci. The low potential for resistance evolution highlights the importance of assessing evolutionary potential in targeted ecological traits and species from threatened habitats.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hoffmann, A A -- Hallas, R J -- Dean, J A -- Schiffer, M -- New York, N.Y. -- Science. 2003 Jul 4;301(5629):100-2.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Centre for Environmental Stress and Adaptation Research, La Trobe University, Bundoora, Victoria 3086, Australia. A.Hoffmann@latrobe.edu.au〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12843394" target="_blank"〉PubMed〈/a〉
    Keywords: *Adaptation, Physiological ; Animals ; Australia ; *Biological Evolution ; *Climate ; Crosses, Genetic ; Dehydration ; Drosophila/*genetics/*physiology ; Ecosystem ; Environment ; Female ; *Genetic Variation ; Geography ; Inbreeding ; Male ; Microsatellite Repeats ; Selection, Genetic ; Trees
    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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    Constitutive activation of toll-mediated antifungal defense in serpin-deficient Drosophila (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-09-18
    Description: The antifungal defense of Drosophila is controlled by the spaetzle/Toll/cactus gene cassette. Here, a loss-of-function mutation in the gene encoding a blood serine protease inhibitor, Spn43Ac, was shown to lead to constitutive expression of the antifungal peptide drosomycin, and this effect was mediated by the spaetzle and Toll gene products. Spaetzle was cleaved by proteolytic enzymes to its active ligand form shortly after immune challenge, and cleaved Spaetzle was constitutively present in Spn43Ac-deficient flies. Hence, Spn43Ac negatively regulates the Toll signaling pathway, and Toll does not function as a pattern recognition receptor in the Drosophila host defense.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Levashina, E A -- Langley, E -- Green, C -- Gubb, D -- Ashburner, M -- Hoffmann, J A -- Reichhart, J M -- New York, N.Y. -- Science. 1999 Sep 17;285(5435):1917-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉UPR 9022 CNRS, Institut de Biologie Moleculaire et Cellulaire, 15 Rue Rene Descartes, Strasbourg 67084, France.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10489372" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antifungal Agents/*metabolism ; *Antimicrobial Cationic Peptides ; Body Patterning ; Drosophila/embryology/genetics/*immunology ; *Drosophila Proteins ; Escherichia coli/genetics/immunology ; Genes, Insect ; Hemolymph/metabolism ; Insect Proteins/*biosynthesis/genetics/metabolism/*physiology ; Membrane Glycoproteins/genetics/*physiology ; Micrococcus luteus/immunology ; Molecular Sequence Data ; Mutagenesis ; Peptides/genetics/metabolism ; *Receptors, Cell Surface ; Recombinant Fusion Proteins/genetics/metabolism ; Serine Proteinase Inhibitors/genetics/*metabolism ; Serpins/genetics/*metabolism ; Signal Transduction ; Toll-Like Receptors ; 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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  • 3
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    Phylogenetic perspectives in innate immunity (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-05-21
    Description: The concept of innate immunity refers to the first-line host defense that serves to limit infection in the early hours after exposure to microorganisms. Recent data have highlighted similarities between pathogen recognition, signaling pathways, and effector mechanisms of innate immunity in Drosophila and mammals, pointing to a common ancestry of these defenses. In addition to its role in the early phase of defense, innate immunity in mammals appears to play a key role in stimulating the subsequent, clonal response of adaptive immunity.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hoffmann, J A -- Kafatos, F C -- Janeway, C A -- Ezekowitz, R A -- New York, N.Y. -- Science. 1999 May 21;284(5418):1313-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute of Molecular and Cellular Biology, CNRS, Strasbourg, 67084, France. jhoff@ibmc.u-strasbg.fr〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10334979" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Culicidae/immunology/microbiology ; Drosophila/immunology/microbiology ; Humans ; Immunity, Active ; *Immunity, Innate ; Infection/*immunology ; Insect Vectors/immunology/microbiology ; Mammals/immunology ; Models, Immunological ; Phagocytosis ; Phylogeny ; Proteins/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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  • 4
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    Neural mechanisms of saccadic suppression (2002)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2002-03-30
    Description: In normal vision our gaze leaps from detail to detail, resulting in rapid image motion across the retina. Yet we are unaware of such motion, a phenomenon known as saccadic suppression. We recorded neural activity in the middle temporal and middle superior temporal cortical areas during saccades and identical image motion under passive viewing conditions. Some neurons were selectively silenced during saccadic image motion, but responded well to identical external image motion. In addition, a subpopulation of neurons reversed their preferred direction of motion during saccades. Consequently, oppositely directed motion signals annul one another, and motion percepts are suppressed.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Thiele, A -- Henning, P -- Kubischik, M -- Hoffmann, K-P -- New York, N.Y. -- Science. 2002 Mar 29;295(5564):2460-2.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Allgemeine Zoologie und Neurobiologie, Ruhr-University Bochum, Bochum, 44780, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11923539" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Macaca mulatta ; Motion Perception ; Neurons/*physiology ; *Perceptual Masking ; Retina/physiology ; Saccades/*physiology ; Temporal Lobe/*physiology ; Visual Pathways ; *Visual Perception
    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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  • 5
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    Activation of Drosophila Toll during fungal infection by a blood serine protease (2002)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2002-07-06
    Description: Drosophila host defense to fungal and Gram-positive bacterial infection is mediated by the Spaetzle/Toll/cactus gene cassette. It has been proposed that Toll does not function as a pattern recognition receptor per se but is activated through a cleaved form of the cytokine Spaetzle. The upstream events linking infection to the cleavage of Spaetzle have long remained elusive. Here we report the identification of a central component of the fungal activation of Toll. We show that ethylmethane sulfonate-induced mutations in the persephone gene, which encodes a previously unknown serine protease, block induction of the Toll pathway by fungi and resistance to this type of infection.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ligoxygakis, Petros -- Pelte, Nadege -- Hoffmann, Jules A -- Reichhart, Jean-Marc -- New York, N.Y. -- Science. 2002 Jul 5;297(5578):114-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institut de Biologie Moleculaire et Cellulaire, UPR 9022 du CNRS, 15 rue R. Descartes, F67084 Strasbourg Cedex, France.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12098703" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Chromosome Mapping ; Drosophila/genetics/immunology/*metabolism/*microbiology ; Drosophila Proteins/*blood/chemistry/*genetics/*metabolism ; Escherichia coli/physiology ; Female ; Gene Expression Regulation ; Genes, Insect ; Gram-Positive Cocci/physiology ; Hemolymph/immunology/metabolism ; Hypocreales/*physiology ; Insect Proteins/genetics/metabolism ; Male ; Molecular Sequence Data ; Mutation ; Protein Sorting Signals ; Protein Structure, Tertiary ; Receptors, Cell Surface/genetics/*metabolism ; Serine Endopeptidases/*blood/chemistry/*genetics ; Toll-Like Receptors
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
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  • 6
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    A kinetic framework for a mammalian RNA polymerase in vivo (2002)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2002-11-26
    Description: We have analyzed the kinetics of assembly and elongation of the mammalian RNA polymerase I complex on endogenous ribosomal genes in the nuclei of living cells with the use of in vivo microscopy. We show that components of the RNA polymerase I machinery are brought to ribosomal genes as distinct subunits and that assembly occurs via metastable intermediates. With the use of computational modeling of imaging data, we have determined the in vivo elongation time of the polymerase, and measurements of recruitment and incorporation frequencies show that incorporation of components into the assembling polymerase is inefficient. Our data provide a kinetic and mechanistic framework for the function of a mammalian RNA polymerase in living cells.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Dundr, Miroslav -- Hoffmann-Rohrer, Urs -- Hu, Qiyue -- Grummt, Ingrid -- Rothblum, Lawrence I -- Phair, Robert D -- Misteli, Tom -- New York, N.Y. -- Science. 2002 Nov 22;298(5598):1623-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉National Cancer Institute (NCI), National Institutes of Health, Bethesda, MD 20892, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12446911" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Catalytic Domain ; Cell Line ; Cell Nucleolus/metabolism ; Cell Nucleus/*metabolism ; Computer Simulation ; DNA, Ribosomal/genetics ; Fluorescence ; Fluorescence Recovery After Photobleaching ; Fluorescent Dyes ; Green Fluorescent Proteins ; Haplorhini ; Humans ; In Situ Hybridization, Fluorescence ; Kinetics ; Least-Squares Analysis ; Luminescent Proteins ; Microscopy ; Pol1 Transcription Initiation Complex Proteins/metabolism ; Probability ; Promoter Regions, Genetic ; Protein Subunits ; RNA Polymerase I/genetics/*metabolism ; Recombinant Fusion Proteins/metabolism ; *Transcription, Genetic ; Transfection
    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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    Immune response and myoblasts that express Fas ligand (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-12-31
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kang, S M -- Hoffmann, A -- Le, D -- Springer, M L -- Stock, P G -- Blau, H M -- F32 HL08991/HL/NHLBI NIH HHS/ -- R01-CA59717/CA/NCI NIH HHS/ -- R01-HD18179/HD/NICHD NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1997 Nov 14;278(5341):1322-4.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9411754" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, CD95/biosynthesis ; Apoptosis ; Cell Differentiation ; Cell Transplantation ; Fas Ligand Protein ; *Graft Rejection ; Immune Tolerance ; Islets of Langerhans/cytology ; *Islets of Langerhans Transplantation ; Membrane Glycoproteins/genetics/*physiology ; Mice ; Mice, Inbred C3H ; Mice, Inbred C57BL ; Muscle Fibers, Skeletal/*cytology/metabolism ; Muscle, Skeletal/*cytology/metabolism ; Neutrophils/*immunology ; Transfection
    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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    Action needed to prevent extinctions caused by disease (2008)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2008-07-11
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hoffmann, Michael -- Hawkins, Clare E -- Walsh, Peter D -- England -- Nature. 2008 Jul 10;454(7201):159. doi: 10.1038/454159a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18615062" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Communicable Diseases, Emerging/immunology/prevention & control/*veterinary ; Conservation of Natural Resources/*trends ; Ebolavirus/immunology ; *Extinction, Biological ; Gorilla gorilla ; *Marsupialia ; Vaccines
    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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  • 9
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    Human host factors required for influenza virus replication (2009)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2009-12-23
    Description: Influenza A virus is an RNA virus that encodes up to 11 proteins and this small coding capacity demands that the virus use the host cellular machinery for many aspects of its life cycle. Knowledge of these host cell requirements not only informs us of the molecular pathways exploited by the virus but also provides further targets that could be pursued for antiviral drug development. Here we use an integrative systems approach, based on genome-wide RNA interference screening, to identify 295 cellular cofactors required for early-stage influenza virus replication. Within this group, those involved in kinase-regulated signalling, ubiquitination and phosphatase activity are the most highly enriched, and 181 factors assemble into a highly significant host-pathogen interaction network. Moreover, 219 of the 295 factors were confirmed to be required for efficient wild-type influenza virus growth, and further analysis of a subset of genes showed 23 factors necessary for viral entry, including members of the vacuolar ATPase (vATPase) and COPI-protein families, fibroblast growth factor receptor (FGFR) proteins, and glycogen synthase kinase 3 (GSK3)-beta. Furthermore, 10 proteins were confirmed to be involved in post-entry steps of influenza virus replication. These include nuclear import components, proteases, and the calcium/calmodulin-dependent protein kinase (CaM kinase) IIbeta (CAMK2B). Notably, growth of swine-origin H1N1 influenza virus is also dependent on the identified host factors, and we show that small molecule inhibitors of several factors, including vATPase and CAMK2B, antagonize influenza virus replication.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2862546/" 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/PMC2862546/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Konig, Renate -- Stertz, Silke -- Zhou, Yingyao -- Inoue, Atsushi -- Hoffmann, H-Heinrich -- Bhattacharyya, Suchita -- Alamares, Judith G -- Tscherne, Donna M -- Ortigoza, Mila B -- Liang, Yuhong -- Gao, Qinshan -- Andrews, Shane E -- Bandyopadhyay, Sourav -- De Jesus, Paul -- Tu, Buu P -- Pache, Lars -- Shih, Crystal -- Orth, Anthony -- Bonamy, Ghislain -- Miraglia, Loren -- Ideker, Trey -- Garcia-Sastre, Adolfo -- Young, John A T -- Palese, Peter -- Shaw, Megan L -- Chanda, Sumit K -- 1 P01 AI058113/AI/NIAID NIH HHS/ -- 1 S10 RR0 9145-01/RR/NCRR NIH HHS/ -- 1 T32 AI07647/AI/NIAID NIH HHS/ -- 1F32AI081428/AI/NIAID NIH HHS/ -- 1R21AI083673/AI/NIAID NIH HHS/ -- 5R24 CA095823-04/CA/NCI NIH HHS/ -- HHSN266200700010C/PHS HHS/ -- HHSN272200900032C/PHS HHS/ -- P01 AI058113/AI/NIAID NIH HHS/ -- P01 AI058113-010004/AI/NIAID NIH HHS/ -- P01 AI058113-020004/AI/NIAID NIH HHS/ -- P01 AI058113-030004/AI/NIAID NIH HHS/ -- P01 AI058113-040004/AI/NIAID NIH HHS/ -- P01 AI058113-050004/AI/NIAID NIH HHS/ -- T32 AI007647/AI/NIAID NIH HHS/ -- T32 AI007647-01/AI/NIAID NIH HHS/ -- T32 AI007647-02/AI/NIAID NIH HHS/ -- T32 AI007647-03/AI/NIAID NIH HHS/ -- T32 AI007647-04/AI/NIAID NIH HHS/ -- T32 AI007647-05/AI/NIAID NIH HHS/ -- T32 AI007647-06/AI/NIAID NIH HHS/ -- T32 AI007647-07/AI/NIAID NIH HHS/ -- T32 AI007647-08/AI/NIAID NIH HHS/ -- T32 AI007647-09/AI/NIAID NIH HHS/ -- T32 AI007647-10/AI/NIAID NIH HHS/ -- T32 GM007280/GM/NIGMS NIH HHS/ -- U01 AI074539/AI/NIAID NIH HHS/ -- U01 AI074539-01/AI/NIAID NIH HHS/ -- U01 AI074539-02/AI/NIAID NIH HHS/ -- U01 AI074539-03/AI/NIAID NIH HHS/ -- U01 AI1074539/AI/NIAID NIH HHS/ -- U54 AI057158/AI/NIAID NIH HHS/ -- U54 AI057158-065713/AI/NIAID NIH HHS/ -- U54 AI057159/AI/NIAID NIH HHS/ -- England -- Nature. 2010 Feb 11;463(7282):813-7. doi: 10.1038/nature08699.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Infectious and Inflammatory Disease Center, Burnham Institute for Medical Research.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20027183" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Biological Factors/*genetics/*physiology ; Cell Line ; Cercopithecus aethiops ; Gene Library ; Genome, Human/genetics ; Host-Pathogen Interactions/genetics/*physiology ; Humans ; Influenza A Virus, H1N1 Subtype/classification/growth & development ; Influenza A virus/classification/*growth & development ; Influenza, Human/*genetics/*virology ; RNA Interference ; Vero Cells ; Virus Internalization ; Virus Replication/*physiology
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 10
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    Genetic suppression of mutations in the Drosophila abl proto-oncogene homolog (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-05-18
    Description: The Drosophila abelson (abl) gene encodes the homolog of the mammalian c-abl cytoplasmic tyrosine kinase and is an essential gene for the development of viable adult flies. Three second-site mutations that suppress the lethality caused by the absence of abl function have been isolated, and all three map to the gene enabled (ena). The mutations are recessive embryonic lethal mutations but act as dominant mutations to compensate for the neural defects of abl mutants. Thus, mutations in a specific gene can compensate for the absence of a tyrosine kinase.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gertler, F B -- Doctor, J S -- Hoffmann, F M -- CA-07175/CA/NCI NIH HHS/ -- CA-09135/CA/NCI NIH HHS/ -- CA-49582/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1990 May 18;248(4957):857-60.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉McArdle Laboratory for Cancer Research, University of Wisconsin, Madison 53706.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2188361" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Drosophila/embryology/*genetics ; Enhancer Elements, Genetic/genetics ; Eye/growth & development/ultrastructure ; Genes, Lethal ; Heterozygote ; Homozygote ; Larva/growth & development ; Microscopy, Electron ; *Mutation ; Nervous System/embryology/growth & development ; Phenotype ; Protein-Tyrosine Kinases/*genetics ; Proto-Oncogene Proteins/*genetics ; Proto-Oncogene Proteins c-abl ; *Suppression, Genetic
    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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