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  • Animals  (187)
  • 2005-2009  (96)
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  • 1
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    The genome sequence of taurine cattle: a window to ruminant biology and evolution (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-04-25
    Description: To understand the biology and evolution of ruminants, the cattle genome was sequenced to about sevenfold coverage. The cattle genome contains a minimum of 22,000 genes, with a core set of 14,345 orthologs shared among seven mammalian species of which 1217 are absent or undetected in noneutherian (marsupial or monotreme) genomes. Cattle-specific evolutionary breakpoint regions in chromosomes have a higher density of segmental duplications, enrichment of repetitive elements, and species-specific variations in genes associated with lactation and immune responsiveness. Genes involved in metabolism are generally highly conserved, although five metabolic genes are deleted or extensively diverged from their human orthologs. The cattle genome sequence thus provides a resource for understanding mammalian evolution and accelerating livestock genetic improvement for milk and meat production.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2943200/" 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/PMC2943200/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bovine Genome Sequencing and Analysis Consortium -- Elsik, Christine G -- Tellam, Ross L -- Worley, Kim C -- Gibbs, Richard A -- Muzny, Donna M -- Weinstock, George M -- Adelson, David L -- Eichler, Evan E -- Elnitski, Laura -- Guigo, Roderic -- Hamernik, Debora L -- Kappes, Steve M -- Lewin, Harris A -- Lynn, David J -- Nicholas, Frank W -- Reymond, Alexandre -- Rijnkels, Monique -- Skow, Loren C -- Zdobnov, Evgeny M -- Schook, Lawrence -- Womack, James -- Alioto, Tyler -- Antonarakis, Stylianos E -- Astashyn, Alex -- Chapple, Charles E -- Chen, Hsiu-Chuan -- Chrast, Jacqueline -- Camara, Francisco -- Ermolaeva, Olga -- Henrichsen, Charlotte N -- Hlavina, Wratko -- Kapustin, Yuri -- Kiryutin, Boris -- Kitts, Paul -- Kokocinski, Felix -- Landrum, Melissa -- Maglott, Donna -- Pruitt, Kim -- Sapojnikov, Victor -- Searle, Stephen M -- Solovyev, Victor -- Souvorov, Alexandre -- Ucla, Catherine -- Wyss, Carine -- Anzola, Juan M -- Gerlach, Daniel -- Elhaik, Eran -- Graur, Dan -- Reese, Justin T -- Edgar, Robert C -- McEwan, John C -- Payne, Gemma M -- Raison, Joy M -- Junier, Thomas -- Kriventseva, Evgenia V -- Eyras, Eduardo -- Plass, Mireya -- Donthu, Ravikiran -- Larkin, Denis M -- Reecy, James -- Yang, Mary Q -- Chen, Lin -- Cheng, Ze -- Chitko-McKown, Carol G -- Liu, George E -- Matukumalli, Lakshmi K -- Song, Jiuzhou -- Zhu, Bin -- Bradley, Daniel G -- Brinkman, Fiona S L -- Lau, Lilian P L -- Whiteside, Matthew D -- Walker, Angela -- Wheeler, Thomas T -- Casey, Theresa -- German, J Bruce -- Lemay, Danielle G -- Maqbool, Nauman J -- Molenaar, Adrian J -- Seo, Seongwon -- Stothard, Paul -- Baldwin, Cynthia L -- Baxter, Rebecca -- Brinkmeyer-Langford, Candice L -- Brown, Wendy C -- Childers, Christopher P -- Connelley, Timothy -- Ellis, Shirley A -- Fritz, Krista -- Glass, Elizabeth J -- Herzig, Carolyn T A -- Iivanainen, Antti -- Lahmers, Kevin K -- Bennett, Anna K -- Dickens, C Michael -- Gilbert, James G R -- Hagen, Darren E -- Salih, Hanni -- Aerts, Jan -- Caetano, Alexandre R -- Dalrymple, Brian -- Garcia, Jose Fernando -- Gill, Clare A -- Hiendleder, Stefan G -- Memili, Erdogan -- Spurlock, Diane -- Williams, John L -- Alexander, Lee -- Brownstein, Michael J -- Guan, Leluo -- Holt, Robert A -- Jones, Steven J M -- Marra, Marco A -- Moore, Richard -- Moore, Stephen S -- Roberts, Andy -- Taniguchi, Masaaki -- Waterman, Richard C -- Chacko, Joseph -- Chandrabose, Mimi M -- Cree, Andy -- Dao, Marvin Diep -- Dinh, Huyen H -- Gabisi, Ramatu Ayiesha -- Hines, Sandra -- Hume, Jennifer -- Jhangiani, Shalini N -- Joshi, Vandita -- Kovar, Christie L -- Lewis, Lora R -- Liu, Yih-Shin -- Lopez, John -- Morgan, Margaret B -- Nguyen, Ngoc Bich -- Okwuonu, Geoffrey O -- Ruiz, San Juana -- Santibanez, Jireh -- Wright, Rita A -- Buhay, Christian -- Ding, Yan -- Dugan-Rocha, Shannon -- Herdandez, Judith -- Holder, Michael -- Sabo, Aniko -- Egan, Amy -- Goodell, Jason -- Wilczek-Boney, Katarzyna -- Fowler, Gerald R -- Hitchens, Matthew Edward -- Lozado, Ryan J -- Moen, Charles -- Steffen, David -- Warren, James T -- Zhang, Jingkun -- Chiu, Readman -- Schein, Jacqueline E -- Durbin, K James -- Havlak, Paul -- Jiang, Huaiyang -- Liu, Yue -- Qin, Xiang -- Ren, Yanru -- Shen, Yufeng -- Song, Henry -- Bell, Stephanie Nicole -- Davis, Clay -- Johnson, Angela Jolivet -- Lee, Sandra -- Nazareth, Lynne V -- Patel, Bella Mayurkumar -- Pu, Ling-Ling -- Vattathil, Selina -- Williams, Rex Lee Jr -- Curry, Stacey -- Hamilton, Cerissa -- Sodergren, Erica -- Wheeler, David A -- Barris, Wes -- Bennett, Gary L -- Eggen, Andre -- Green, Ronnie D -- Harhay, Gregory P -- Hobbs, Matthew -- Jann, Oliver -- Keele, John W -- Kent, Matthew P -- Lien, Sigbjorn -- McKay, Stephanie D -- McWilliam, Sean -- Ratnakumar, Abhirami -- Schnabel, Robert D -- Smith, Timothy -- Snelling, Warren M -- Sonstegard, Tad S -- Stone, Roger T -- Sugimoto, Yoshikazu -- Takasuga, Akiko -- Taylor, Jeremy F -- Van Tassell, Curtis P -- Macneil, Michael D -- Abatepaulo, Antonio R R -- Abbey, Colette A -- Ahola, Virpi -- Almeida, Iassudara G -- Amadio, Ariel F -- Anatriello, Elen -- Bahadue, Suria M -- Biase, Fernando H -- Boldt, Clayton R -- Carroll, Jeffery A -- Carvalho, Wanessa A -- Cervelatti, Eliane P -- Chacko, Elsa -- Chapin, Jennifer E -- Cheng, Ye -- Choi, Jungwoo -- Colley, Adam J -- de Campos, Tatiana A -- De Donato, Marcos -- Santos, Isabel K F de Miranda -- de Oliveira, Carlo J F -- Deobald, Heather -- Devinoy, Eve -- Donohue, Kaitlin E -- Dovc, Peter -- Eberlein, Annett -- Fitzsimmons, Carolyn J -- Franzin, Alessandra M -- Garcia, Gustavo R -- Genini, Sem -- Gladney, Cody J -- Grant, Jason R -- Greaser, Marion L -- Green, Jonathan A -- Hadsell, Darryl L -- Hakimov, Hatam A -- Halgren, Rob -- Harrow, Jennifer L -- Hart, Elizabeth A -- Hastings, Nicola -- Hernandez, Marta -- Hu, Zhi-Liang -- Ingham, Aaron -- Iso-Touru, Terhi -- Jamis, Catherine -- Jensen, Kirsty -- Kapetis, Dimos -- Kerr, Tovah -- Khalil, Sari S -- Khatib, Hasan -- Kolbehdari, Davood -- Kumar, Charu G -- Kumar, Dinesh -- Leach, Richard -- Lee, Justin C-M -- Li, Changxi -- Logan, Krystin M -- Malinverni, Roberto -- Marques, Elisa -- Martin, William F -- Martins, Natalia F -- Maruyama, Sandra R -- Mazza, Raffaele -- McLean, Kim L -- Medrano, Juan F -- Moreno, Barbara T -- More, Daniela D -- Muntean, Carl T -- Nandakumar, Hari P -- Nogueira, Marcelo F G -- Olsaker, Ingrid -- Pant, Sameer D -- Panzitta, Francesca -- Pastor, Rosemeire C P -- Poli, Mario A -- Poslusny, Nathan -- Rachagani, Satyanarayana -- Ranganathan, Shoba -- Razpet, Andrej -- Riggs, Penny K -- Rincon, Gonzalo -- Rodriguez-Osorio, Nelida -- Rodriguez-Zas, Sandra L -- Romero, Natasha E -- Rosenwald, Anne -- Sando, Lillian -- Schmutz, Sheila M -- Shen, Libing -- Sherman, Laura -- Southey, Bruce R -- Lutzow, Ylva Strandberg -- Sweedler, Jonathan V -- Tammen, Imke -- Telugu, Bhanu Prakash V L -- Urbanski, Jennifer M -- Utsunomiya, Yuri T -- Verschoor, Chris P -- Waardenberg, Ashley J -- Wang, Zhiquan -- Ward, Robert -- Weikard, Rosemarie -- Welsh, Thomas H Jr -- White, Stephen N -- Wilming, Laurens G -- Wunderlich, Kris R -- Yang, Jianqi -- Zhao, Feng-Qi -- 062023/Wellcome Trust/United Kingdom -- 077198/Wellcome Trust/United Kingdom -- BBS/B/13438/Biotechnology and Biological Sciences Research Council/United Kingdom -- BBS/B/13446/Biotechnology and Biological Sciences Research Council/United Kingdom -- P30 DA018310/DA/NIDA NIH HHS/ -- U54 HG003273/HG/NHGRI NIH HHS/ -- U54 HG003273-04/HG/NHGRI NIH HHS/ -- U54 HG003273-04S1/HG/NHGRI NIH HHS/ -- U54 HG003273-05/HG/NHGRI NIH HHS/ -- U54 HG003273-05S1/HG/NHGRI NIH HHS/ -- U54 HG003273-05S2/HG/NHGRI NIH HHS/ -- U54 HG003273-06/HG/NHGRI NIH HHS/ -- U54 HG003273-06S1/HG/NHGRI NIH HHS/ -- U54 HG003273-06S2/HG/NHGRI NIH HHS/ -- U54 HG003273-07/HG/NHGRI NIH HHS/ -- U54 HG003273-08/HG/NHGRI NIH HHS/ -- New York, N.Y. -- Science. 2009 Apr 24;324(5926):522-8. doi: 10.1126/science.1169588.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19390049" target="_blank"〉PubMed〈/a〉
    Keywords: Alternative Splicing ; Animals ; Animals, Domestic ; *Biological Evolution ; Cattle ; Evolution, Molecular ; Female ; Genetic Variation ; *Genome ; Humans ; Male ; MicroRNAs/genetics ; Molecular Sequence Data ; Proteins/genetics ; Sequence Analysis, DNA ; Species Specificity ; Synteny
    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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    Premature aging in mice deficient in DNA repair and transcription (2002)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2002-04-16
    Description: One of the factors postulated to drive the aging process is the accumulation of DNA damage. Here, we provide strong support for this hypothesis by describing studies of mice with a mutation in XPD, a gene encoding a DNA helicase that functions in both repair and transcription and that is mutated in the human disorder trichothiodystrophy (TTD). TTD mice were found to exhibit many symptoms of premature aging, including osteoporosis and kyphosis, osteosclerosis, early greying, cachexia, infertility, and reduced life-span. TTD mice carrying an additional mutation in XPA, which enhances the DNA repair defect, showed a greatly accelerated aging phenotype, which correlated with an increased cellular sensitivity to oxidative DNA damage. We hypothesize that aging in TTD mice is caused by unrepaired DNA damage that compromises transcription, leading to functional inactivation of critical genes and enhanced apoptosis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉de Boer, Jan -- Andressoo, Jaan Olle -- de Wit, Jan -- Huijmans, Jan -- Beems, Rudolph B -- van Steeg, Harry -- Weeda, Geert -- van der Horst, Gijsbertus T J -- van Leeuwen, Wibeke -- Themmen, Axel P N -- Meradji, Morteza -- Hoeijmakers, Jan H J -- AG 17242-02/AG/NIA NIH HHS/ -- New York, N.Y. -- Science. 2002 May 17;296(5571):1276-9. Epub 2002 Apr 11.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Medical Genetics Center, Department of Cell Biology and Genetics, Center for Biomedical Genetics, Erasmus University, 3000 DR Rotterdam, Netherlands.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11950998" target="_blank"〉PubMed〈/a〉
    Keywords: *Aging ; Aging, Premature/*etiology ; Animals ; Apoptosis ; Bone Density ; Cachexia/etiology ; Crosses, Genetic ; *DNA Damage ; DNA Helicases/genetics/*physiology ; *DNA Repair ; DNA-Binding Proteins/genetics/physiology ; Female ; Fertility ; Gene Targeting ; Growth Disorders/etiology/genetics ; Hair Diseases/genetics ; Kyphosis/etiology/genetics/pathology ; Male ; Mice ; Mutation ; Oxidative Stress ; Phenotype ; Point Mutation ; Proteins/genetics/*physiology ; RNA-Binding Proteins/genetics/physiology ; *Transcription Factors ; Transcription, Genetic ; Xeroderma Pigmentosum Group A Protein ; Xeroderma Pigmentosum Group D Protein
    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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    Draft genome sequence of the sexually transmitted pathogen Trichomonas vaginalis (2007)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2007-01-16
    Description: We describe the genome sequence of the protist Trichomonas vaginalis, a sexually transmitted human pathogen. Repeats and transposable elements comprise about two-thirds of the approximately 160-megabase genome, reflecting a recent massive expansion of genetic material. This expansion, in conjunction with the shaping of metabolic pathways that likely transpired through lateral gene transfer from bacteria, and amplification of specific gene families implicated in pathogenesis and phagocytosis of host proteins may exemplify adaptations of the parasite during its transition to a urogenital environment. The genome sequence predicts previously unknown functions for the hydrogenosome, which support a common evolutionary origin of this unusual organelle with mitochondria.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2080659/" 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/PMC2080659/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Carlton, Jane M -- Hirt, Robert P -- Silva, Joana C -- Delcher, Arthur L -- Schatz, Michael -- Zhao, Qi -- Wortman, Jennifer R -- Bidwell, Shelby L -- Alsmark, U Cecilia M -- Besteiro, Sebastien -- Sicheritz-Ponten, Thomas -- Noel, Christophe J -- Dacks, Joel B -- Foster, Peter G -- Simillion, Cedric -- Van de Peer, Yves -- Miranda-Saavedra, Diego -- Barton, Geoffrey J -- Westrop, Gareth D -- Muller, Sylke -- Dessi, Daniele -- Fiori, Pier Luigi -- Ren, Qinghu -- Paulsen, Ian -- Zhang, Hanbang -- Bastida-Corcuera, Felix D -- Simoes-Barbosa, Augusto -- Brown, Mark T -- Hayes, Richard D -- Mukherjee, Mandira -- Okumura, Cheryl Y -- Schneider, Rachel -- Smith, Alias J -- Vanacova, Stepanka -- Villalvazo, Maria -- Haas, Brian J -- Pertea, Mihaela -- Feldblyum, Tamara V -- Utterback, Terry R -- Shu, Chung-Li -- Osoegawa, Kazutoyo -- de Jong, Pieter J -- Hrdy, Ivan -- Horvathova, Lenka -- Zubacova, Zuzana -- Dolezal, Pavel -- Malik, Shehre-Banoo -- Logsdon, John M Jr -- Henze, Katrin -- Gupta, Arti -- Wang, Ching C -- Dunne, Rebecca L -- Upcroft, Jacqueline A -- Upcroft, Peter -- White, Owen -- Salzberg, Steven L -- Tang, Petrus -- Chiu, Cheng-Hsun -- Lee, Ying-Shiung -- Embley, T Martin -- Coombs, Graham H -- Mottram, Jeremy C -- Tachezy, Jan -- Fraser-Liggett, Claire M -- Johnson, Patricia J -- 072031/Wellcome Trust/United Kingdom -- G0000508/Medical Research Council/United Kingdom -- G0000508(56841)/Medical Research Council/United Kingdom -- G9722968/Medical Research Council/United Kingdom -- G9722968(65078)/Medical Research Council/United Kingdom -- R01 LM006845/LM/NLM NIH HHS/ -- R01 LM006845-08/LM/NLM NIH HHS/ -- R01 LM007938/LM/NLM NIH HHS/ -- R01 LM007938-04/LM/NLM NIH HHS/ -- U01 AI050913/AI/NIAID NIH HHS/ -- U01 AI050913-01A1/AI/NIAID NIH HHS/ -- U01 AI050913-02/AI/NIAID NIH HHS/ -- UO1 AI50913-01/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 2007 Jan 12;315(5809):207-12.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute for Genomic Research, 9712 Medical Research Drive, Rockville, MD 20850, USA. jane.carlton@med.nyu.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17218520" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Biological Transport/genetics ; DNA Transposable Elements ; DNA, Protozoan/genetics ; Gene Transfer, Horizontal ; Genes, Protozoan ; *Genome, Protozoan ; Humans ; Hydrogen/metabolism ; Metabolic Networks and Pathways/genetics ; Molecular Sequence Data ; Multigene Family ; Organelles/metabolism ; Oxidative Stress/genetics ; Peptide Hydrolases/genetics/metabolism ; Protozoan Proteins/genetics/physiology ; RNA Processing, Post-Transcriptional ; Repetitive Sequences, Nucleic Acid ; *Sequence Analysis, DNA ; Sexually Transmitted Diseases/parasitology ; Trichomonas Infections/parasitology/transmission ; Trichomonas vaginalis/cytology/*genetics/metabolism/pathogenicity
    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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    Early forebrain wiring: genetic dissection using conditional Celsr3 mutant mice (2008)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2008-05-20
    Description: Development of axonal tracts requires interactions between growth cones and the environment. Tracts such as the anterior commissure and internal capsule are defective in mice with null mutation of Celsr3. We generated a conditional Celsr3 allele, allowing regional inactivation. Inactivation in telencephalon, ventral forebrain, or cortex demonstrated essential roles for Celsr3 in neurons that project axons to the anterior commissure and subcerebral targets, as well as in cells that guide axons through the internal capsule. When Celsr3 was inactivated in cortex, subcerebral projections failed to grow, yet corticothalamic axons developed normally, indicating that besides guidepost cells, additional Celsr3-independent cues can assist their progression. These observations provide in vivo evidence that Celsr3-mediated interactions between axons and guidepost cells govern axonal tract formation in mammals.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2746700/" 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/PMC2746700/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zhou, Libing -- Bar, Isabelle -- Achouri, Younes -- Campbell, Kenneth -- De Backer, Olivier -- Hebert, Jean M -- Jones, Kevin -- Kessaris, Nicoletta -- de Rouvroit, Catherine Lambert -- O'Leary, Dennis -- Richardson, William D -- Goffinet, Andre M -- Tissir, Fadel -- G0501173/Medical Research Council/United Kingdom -- G0800575/Medical Research Council/United Kingdom -- G9708005/Medical Research Council/United Kingdom -- R01 MH086147/MH/NIMH NIH HHS/ -- R01 MH086147-05/MH/NIMH NIH HHS/ -- R37 NS031558/NS/NINDS NIH HHS/ -- R37 NS031558-15/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 2008 May 16;320(5878):946-9. doi: 10.1126/science.1155244.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Developmental Neurobiology, Universite Catholique de Louvain, 1200 Bruxelles, Belgique.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18487195" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Axons/*physiology ; Cadherins/*genetics/*physiology ; Cerebral Cortex/cytology/embryology ; Female ; Gene Silencing ; Internal Capsule/cytology/embryology/physiology ; Male ; Mice ; Neural Pathways/*embryology/physiology ; Neurons/*physiology ; Prosencephalon/cytology/*embryology/physiology ; Receptors, Cell Surface/*genetics/*physiology ; Septal Nuclei/embryology/physiology ; Thalamus/cytology/embryology ; Tissue Culture Techniques
    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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    Anti-inflammatory activity of human IgG4 antibodies by dynamic Fab arm exchange (2007)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2007-09-18
    Description: Antibodies play a central role in immunity by forming an interface with the innate immune system and, typically, mediate proinflammatory activity. We describe a novel posttranslational modification that leads to anti-inflammatory activity of antibodies of immunoglobulin G, isotype 4 (IgG4). IgG4 antibodies are dynamic molecules that exchange Fab arms by swapping a heavy chain and attached light chain (half-molecule) with a heavy-light chain pair from another molecule, which results in bispecific antibodies. Mutagenesis studies revealed that the third constant domain is critical for this activity. The impact of IgG4 Fab arm exchange was confirmed in vivo in a rhesus monkey model with experimental autoimmune myasthenia gravis. IgG4 Fab arm exchange is suggested to be an important biological mechanism that provides the basis for the anti-inflammatory activity attributed to IgG4 antibodies.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉van der Neut Kolfschoten, Marijn -- Schuurman, Janine -- Losen, Mario -- Bleeker, Wim K -- Martinez-Martinez, Pilar -- Vermeulen, Ellen -- den Bleker, Tamara H -- Wiegman, Luus -- Vink, Tom -- Aarden, Lucien A -- De Baets, Marc H -- van de Winkel, Jan G J -- Aalberse, Rob C -- Parren, Paul W H I -- New York, N.Y. -- Science. 2007 Sep 14;317(5844):1554-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Sanquin Research-AMC Landsteiner Laboratory, Department of Immunopathology, Plesmanlaan 125, 1066 CX Amsterdam, the Netherlands.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17872445" target="_blank"〉PubMed〈/a〉
    Keywords: Allergens/immunology ; Animals ; Antibodies, Bispecific/immunology ; Antibodies, Monoclonal/immunology ; Antigens, CD20/immunology ; Antigens, Plant ; Autoantibodies/immunology ; Glycoproteins/immunology ; Humans ; Immunoglobulin Constant Regions/chemistry ; Immunoglobulin Fab Fragments/*chemistry/*immunology/metabolism ; Immunoglobulin G/*chemistry/*immunology/metabolism ; Immunoglobulin Heavy Chains ; Macaca mulatta ; Mice ; Mutation ; Myasthenia Gravis, Autoimmune, Experimental/immunology/prevention & control ; Protein Processing, Post-Translational ; Receptor, Epidermal Growth Factor/immunology ; Receptors, Cholinergic/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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  • 6
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    Pathogenesis and transmission of swine-origin 2009 A(H1N1) influenza virus in ferrets (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-07-04
    Description: The swine-origin A(H1N1) influenza virus that has emerged in humans in early 2009 has raised concerns about pandemic developments. In a ferret pathogenesis and transmission model, the 2009 A(H1N1) influenza virus was found to be more pathogenic than a seasonal A(H1N1) virus, with more extensive virus replication occurring in the respiratory tract. Replication of seasonal A(H1N1) virus was confined to the nasal cavity of ferrets, but the 2009 A(H1N1) influenza virus also replicated in the trachea, bronchi, and bronchioles. Virus shedding was more abundant from the upper respiratory tract for 2009 A(H1N1) influenza virus as compared with seasonal virus, and transmission via aerosol or respiratory droplets was equally efficient. These data suggest that the 2009 A(H1N1) influenza virus has the ability to persist in the human population, potentially with more severe clinical consequences.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Munster, Vincent J -- de Wit, Emmie -- van den Brand, Judith M A -- Herfst, Sander -- Schrauwen, Eefje J A -- Bestebroer, Theo M -- van de Vijver, David -- Boucher, Charles A -- Koopmans, Marion -- Rimmelzwaan, Guus F -- Kuiken, Thijs -- Osterhaus, Albert D M E -- Fouchier, Ron A M -- HHSN266200700010C/PHS HHS/ -- New York, N.Y. -- Science. 2009 Jul 24;325(5939):481-3. doi: 10.1126/science.1177127. Epub 2009 Jul 2.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉National Influenza Center and Department of Virology, Erasmus Medical Center, 3015GE Rotterdam, The Netherlands.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19574348" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Bronchi/virology ; Child, Preschool ; Disease Models, Animal ; Female ; Ferrets ; Humans ; Influenza A Virus, H1N1 Subtype/*pathogenicity ; Influenza, Human/pathology/transmission/*virology ; Orthomyxoviridae Infections/pathology/transmission/virology ; Respiratory System/virology ; Seasons ; Swine/virology ; Trachea/virology ; Virus Replication ; Virus Shedding
    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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    Mutations in FUS, an RNA processing protein, cause familial amyotrophic lateral sclerosis type 6 (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-03-03
    Description: Amyotrophic lateral sclerosis (ALS) is a fatal neurodegenerative disease that is familial in 10% of cases. We have identified a missense mutation in the gene encoding fused in sarcoma (FUS) in a British kindred, linked to ALS6. In a survey of 197 familial ALS index cases, we identified two further missense mutations in eight families. Postmortem analysis of three cases with FUS mutations showed FUS-immunoreactive cytoplasmic inclusions and predominantly lower motor neuron degeneration. Cellular expression studies revealed aberrant localization of mutant FUS protein. FUS is involved in the regulation of transcription and RNA splicing and transport, and it has functional homology to another ALS gene, TARDBP, which suggests that a common mechanism may underlie motor neuron degeneration.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4516382/" 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/PMC4516382/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Vance, Caroline -- Rogelj, Boris -- Hortobagyi, Tibor -- De Vos, Kurt J -- Nishimura, Agnes Lumi -- Sreedharan, Jemeen -- Hu, Xun -- Smith, Bradley -- Ruddy, Deborah -- Wright, Paul -- Ganesalingam, Jeban -- Williams, Kelly L -- Tripathi, Vineeta -- Al-Saraj, Safa -- Al-Chalabi, Ammar -- Leigh, P Nigel -- Blair, Ian P -- Nicholson, Garth -- de Belleroche, Jackie -- Gallo, Jean-Marc -- Miller, Christopher C -- Shaw, Christopher E -- 078662/Wellcome Trust/United Kingdom -- G0300329/Medical Research Council/United Kingdom -- G0500289/Medical Research Council/United Kingdom -- G0501573/Medical Research Council/United Kingdom -- G0600676/Medical Research Council/United Kingdom -- G0600974/Medical Research Council/United Kingdom -- G0900688/Medical Research Council/United Kingdom -- MC_G1000733/Medical Research Council/United Kingdom -- Medical Research Council/United Kingdom -- Wellcome Trust/United Kingdom -- New York, N.Y. -- Science. 2009 Feb 27;323(5918):1208-11. doi: 10.1126/science.1165942.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Clinical Neuroscience, King's College London, Medical Research Council (MRC) Centre for Neurodegeneration Research, Institute of Psychiatry, London SE5 8AF, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19251628" target="_blank"〉PubMed〈/a〉
    Keywords: Age of Onset ; Amino Acid Sequence ; Amyotrophic Lateral Sclerosis/*genetics/metabolism/pathology ; Animals ; Brain/pathology ; Cell Line ; Cell Nucleus/metabolism ; Cytoplasm/metabolism ; DNA-Binding Proteins/analysis/genetics/metabolism ; Female ; Humans ; Inclusion Bodies/chemistry/ultrastructure ; Male ; Molecular Sequence Data ; Motor Neurons/metabolism ; *Mutation, Missense ; Pedigree ; RNA-Binding Protein FUS/analysis/*genetics/*metabolism ; Rats ; Spinal Cord/pathology ; 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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  • 8
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    Construction and analysis of a human-chimpanzee comparative clone map (2002)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2002-01-05
    Description: The recently released human genome sequences provide us with reference data to conduct comparative genomic research on primates, which will be important to understand what genetic information makes us human. Here we present a first-generation human-chimpanzee comparative genome map and its initial analysis. The map was constructed through paired alignment of 77,461 chimpanzee bacterial artificial chromosome end sequences with publicly available human genome sequences. We detected candidate positions, including two clusters on human chromosome 21 that suggest large, nonrandom regions of difference between the two genomes.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Fujiyama, Asao -- Watanabe, Hidemi -- Toyoda, Atsushi -- Taylor, Todd D -- Itoh, Takehiko -- Tsai, Shih-Feng -- Park, Hong-Seog -- Yaspo, Marie-Laure -- Lehrach, Hans -- Chen, Zhu -- Fu, Gang -- Saitou, Naruya -- Osoegawa, Kazutoyo -- de Jong, Pieter J -- Suto, Yumiko -- Hattori, Masahira -- Sakaki, Yoshiyuki -- New York, N.Y. -- Science. 2002 Jan 4;295(5552):131-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉RIKEN Genomic Sciences Center, 1-7-22 Suehiro-cho, Tsurumi-ku, Yokohama, Kanagawa 230-0045, Japan. afujiyam@gsc.riken.go.jp〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11778049" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Base Sequence ; Chromosomes, Artificial, Bacterial ; Chromosomes, Human, Pair 21/genetics ; Cloning, Molecular ; Contig Mapping ; Female ; Gene Library ; *Genome ; *Genome, Human ; Humans ; Male ; Pan troglodytes/*genetics ; *Physical Chromosome Mapping ; Sequence Alignment ; Sequence Analysis, DNA ; Sequence Tagged Sites ; X Chromosome/genetics ; Y Chromosome/genetics
    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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  • 9
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    Mutations in dynein link motor neuron degeneration to defects in retrograde transport (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-05-06
    Description: Degenerative disorders of motor neurons include a range of progressive fatal diseases such as amyotrophic lateral sclerosis (ALS), spinal-bulbar muscular atrophy (SBMA), and spinal muscular atrophy (SMA). Although the causative genetic alterations are known for some cases, the molecular basis of many SMA and SBMA-like syndromes and most ALS cases is unknown. Here we show that missense point mutations in the cytoplasmic dynein heavy chain result in progressive motor neuron degeneration in heterozygous mice, and in homozygotes this is accompanied by the formation of Lewy-like inclusion bodies, thus resembling key features of human pathology. These mutations exclusively perturb neuron-specific functions of dynein.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hafezparast, Majid -- Klocke, Rainer -- Ruhrberg, Christiana -- Marquardt, Andreas -- Ahmad-Annuar, Azlina -- Bowen, Samantha -- Lalli, Giovanna -- Witherden, Abi S -- Hummerich, Holger -- Nicholson, Sharon -- Morgan, P Jeffrey -- Oozageer, Ravi -- Priestley, John V -- Averill, Sharon -- King, Von R -- Ball, Simon -- Peters, Jo -- Toda, Takashi -- Yamamoto, Ayumu -- Hiraoka, Yasushi -- Augustin, Martin -- Korthaus, Dirk -- Wattler, Sigrid -- Wabnitz, Philipp -- Dickneite, Carmen -- Lampel, Stefan -- Boehme, Florian -- Peraus, Gisela -- Popp, Andreas -- Rudelius, Martina -- Schlegel, Juergen -- Fuchs, Helmut -- Hrabe de Angelis, Martin -- Schiavo, Giampietro -- Shima, David T -- Russ, Andreas P -- Stumm, Gabriele -- Martin, Joanne E -- Fisher, Elizabeth M C -- New York, N.Y. -- Science. 2003 May 2;300(5620):808-12.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurodegenerative Disease, Institute of Neurology, National Hospital for Neurology and Neurosurgery, Queen Square, London WC1N 3BG, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12730604" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Anterior Horn Cells/pathology ; Apoptosis ; *Axonal Transport ; Cell Differentiation ; Cell Movement ; Central Nervous System/embryology ; Chromosome Mapping ; Dimerization ; Dyneins/chemistry/*genetics/*physiology ; Female ; Ganglia, Spinal/pathology ; Golgi Apparatus/metabolism/ultrastructure ; Heterozygote ; Homozygote ; Lewy Bodies/pathology ; Male ; Mice ; Mice, Inbred C3H ; Mice, Inbred C57BL ; Motor Neuron Disease/*genetics/pathology/physiopathology ; Motor Neurons/*physiology/ultrastructure ; Mutation ; Mutation, Missense ; *Nerve Degeneration ; Peptide Fragments/metabolism ; Phenotype ; Point Mutation ; Spinal Nerves/growth & development ; Tetanus Toxin/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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  • 10
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    Role of phosphorylation in regulation of the assembly of endocytic coat complexes (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-08-07
    Description: Clathrin-mediated endocytosis involves cycles of assembly and disassembly of clathrin coat components and their accessory proteins. Dephosphorylation of rat brain extract was shown to promote the assembly of dynamin 1, synaptojanin 1, and amphiphysin into complexes that also included clathrin and AP-2. Phosphorylation of dynamin 1 and synaptojanin 1 inhibited their binding to amphiphysin, whereas phosphorylation of amphiphysin inhibited its binding to AP-2 and clathrin. Thus, phosphorylation regulates the association and dissociation cycle of the clathrin-based endocytic machinery, and calcium-dependent dephosphorylation of endocytic proteins could prepare nerve terminals for a burst of endocytosis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Slepnev, V I -- Ochoa, G C -- Butler, M H -- Grabs, D -- De Camilli, P -- CA46128/CA/NCI NIH HHS/ -- NS36251/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1998 Aug 7;281(5378):821-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute and Department of Cell Biology, Yale University School of Medicine, 295 Congress Avenue, New Haven, CT 06510, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9694653" target="_blank"〉PubMed〈/a〉
    Keywords: Adaptor Protein Complex alpha Subunits ; Adaptor Protein Complex beta Subunits ; Adaptor Proteins, Vesicular Transport ; Adenosine Triphosphate/metabolism ; Animals ; Binding Sites ; Carbazoles/pharmacology ; Chromatography, Affinity ; Clathrin/*metabolism ; Cyclosporine/pharmacology ; Dimerization ; Dynamin I ; Dynamins ; *Endocytosis ; Enzyme Inhibitors/pharmacology ; GTP Phosphohydrolases/*metabolism ; Indole Alkaloids ; Membrane Proteins/*metabolism ; Nerve Tissue Proteins/*metabolism ; Phosphoric Monoester Hydrolases/*metabolism ; Rats ; Recombinant Fusion Proteins/metabolism ; src Homology Domains
    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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