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  • Meteorology and Climatology  (52)
  • Mice  (50)
  • Female  (36)
  • Male  (34)
  • Signal Transduction
  • 2005-2009  (134)
  • 2006  (134)
  • 1
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    The genome of the sea urchin Strongylocentrotus purpuratus (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publikationsdatum: 2006-11-11
    Beschreibung: We report the sequence and analysis of the 814-megabase genome of the sea urchin Strongylocentrotus purpuratus, a model for developmental and systems biology. The sequencing strategy combined whole-genome shotgun and bacterial artificial chromosome (BAC) sequences. This use of BAC clones, aided by a pooling strategy, overcame difficulties associated with high heterozygosity of the genome. The genome encodes about 23,300 genes, including many previously thought to be vertebrate innovations or known only outside the deuterostomes. This echinoderm genome provides an evolutionary outgroup for the chordates and yields insights into the evolution of deuterostomes.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3159423/" 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/PMC3159423/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sea Urchin Genome Sequencing Consortium -- Sodergren, Erica -- Weinstock, George M -- Davidson, Eric H -- Cameron, R Andrew -- Gibbs, Richard A -- Angerer, Robert C -- Angerer, Lynne M -- Arnone, Maria Ina -- Burgess, David R -- Burke, Robert D -- Coffman, James A -- Dean, Michael -- Elphick, Maurice R -- Ettensohn, Charles A -- Foltz, Kathy R -- Hamdoun, Amro -- Hynes, Richard O -- Klein, William H -- Marzluff, William -- McClay, David R -- Morris, Robert L -- Mushegian, Arcady -- Rast, Jonathan P -- Smith, L Courtney -- Thorndyke, Michael C -- Vacquier, Victor D -- Wessel, Gary M -- Wray, Greg -- Zhang, Lan -- Elsik, Christine G -- Ermolaeva, Olga -- Hlavina, Wratko -- Hofmann, Gretchen -- Kitts, Paul -- Landrum, Melissa J -- Mackey, Aaron J -- Maglott, Donna -- Panopoulou, Georgia -- Poustka, Albert J -- Pruitt, Kim -- Sapojnikov, Victor -- Song, Xingzhi -- Souvorov, Alexandre -- Solovyev, Victor -- Wei, Zheng -- Whittaker, Charles A -- Worley, Kim -- Durbin, K James -- Shen, Yufeng -- Fedrigo, Olivier -- Garfield, David -- Haygood, Ralph -- Primus, Alexander -- Satija, Rahul -- Severson, Tonya -- Gonzalez-Garay, Manuel L -- Jackson, Andrew R -- Milosavljevic, Aleksandar -- Tong, Mark -- Killian, Christopher E -- Livingston, Brian T -- Wilt, Fred H -- Adams, Nikki -- Belle, Robert -- Carbonneau, Seth -- Cheung, Rocky -- Cormier, Patrick -- Cosson, Bertrand -- Croce, Jenifer -- Fernandez-Guerra, Antonio -- Geneviere, Anne-Marie -- Goel, Manisha -- Kelkar, Hemant -- Morales, Julia -- Mulner-Lorillon, Odile -- Robertson, Anthony J -- Goldstone, Jared V -- Cole, Bryan -- Epel, David -- Gold, Bert -- Hahn, Mark E -- Howard-Ashby, Meredith -- Scally, Mark -- Stegeman, John J -- Allgood, Erin L -- Cool, Jonah -- Judkins, Kyle M -- McCafferty, Shawn S -- Musante, Ashlan M -- Obar, Robert A -- Rawson, Amanda P -- Rossetti, Blair J -- Gibbons, Ian R -- Hoffman, Matthew P -- Leone, Andrew -- Istrail, Sorin -- Materna, Stefan C -- Samanta, Manoj P -- Stolc, Viktor -- Tongprasit, Waraporn -- Tu, Qiang -- Bergeron, Karl-Frederik -- Brandhorst, Bruce P -- Whittle, James -- Berney, Kevin -- Bottjer, David J -- Calestani, Cristina -- Peterson, Kevin -- Chow, Elly -- Yuan, Qiu Autumn -- Elhaik, Eran -- Graur, Dan -- Reese, Justin T -- Bosdet, Ian -- Heesun, Shin -- Marra, Marco A -- Schein, Jacqueline -- Anderson, Michele K -- Brockton, Virginia -- Buckley, Katherine M -- Cohen, Avis H -- Fugmann, Sebastian D -- Hibino, Taku -- Loza-Coll, Mariano -- Majeske, Audrey J -- Messier, Cynthia -- Nair, Sham V -- Pancer, Zeev -- Terwilliger, David P -- Agca, Cavit -- Arboleda, Enrique -- Chen, Nansheng -- Churcher, Allison M -- Hallbook, F -- Humphrey, Glen W -- Idris, Mohammed M -- Kiyama, Takae -- Liang, Shuguang -- Mellott, Dan -- Mu, Xiuqian -- Murray, Greg -- Olinski, Robert P -- Raible, Florian -- Rowe, Matthew -- Taylor, John S -- Tessmar-Raible, Kristin -- Wang, D -- Wilson, Karen H -- Yaguchi, Shunsuke -- Gaasterland, Terry -- Galindo, Blanca E -- Gunaratne, Herath J -- Juliano, Celina -- Kinukawa, Masashi -- Moy, Gary W -- Neill, Anna T -- Nomura, Mamoru -- Raisch, Michael -- Reade, Anna -- Roux, Michelle M -- Song, Jia L -- Su, Yi-Hsien -- Townley, Ian K -- Voronina, Ekaterina -- Wong, Julian L -- Amore, Gabriele -- Branno, Margherita -- Brown, Euan R -- Cavalieri, Vincenzo -- Duboc, Veronique -- Duloquin, Louise -- Flytzanis, Constantin -- Gache, Christian -- Lapraz, Francois -- Lepage, Thierry -- Locascio, Annamaria -- Martinez, Pedro -- Matassi, Giorgio -- Matranga, Valeria -- Range, Ryan -- Rizzo, Francesca -- Rottinger, Eric -- Beane, Wendy -- Bradham, Cynthia -- Byrum, Christine -- Glenn, Tom -- Hussain, Sofia -- Manning, Gerard -- Miranda, Esther -- Thomason, Rebecca -- Walton, Katherine -- Wikramanayke, Athula -- Wu, Shu-Yu -- Xu, Ronghui -- Brown, C Titus -- Chen, Lili -- Gray, Rachel F -- Lee, Pei Yun -- Nam, Jongmin -- Oliveri, Paola -- Smith, Joel -- Muzny, Donna -- Bell, Stephanie -- Chacko, Joseph -- Cree, Andrew -- Curry, Stacey -- Davis, Clay -- Dinh, Huyen -- Dugan-Rocha, Shannon -- Fowler, Jerry -- Gill, Rachel -- Hamilton, Cerrissa -- Hernandez, Judith -- Hines, Sandra -- Hume, Jennifer -- Jackson, Laronda -- Jolivet, Angela -- Kovar, Christie -- Lee, Sandra -- Lewis, Lora -- Miner, George -- Morgan, Margaret -- Nazareth, Lynne V -- Okwuonu, Geoffrey -- Parker, David -- Pu, Ling-Ling -- Thorn, Rachel -- Wright, Rita -- 2P42 ESO7381/PHS HHS/ -- 5 U54 HG003273/HG/NHGRI NIH HHS/ -- EY11930/EY/NEI NIH HHS/ -- F32 ESO12794/PHS HHS/ -- F32 HD047136/HD/NICHD NIH HHS/ -- F32 HD047136-02/HD/NICHD NIH HHS/ -- F32 HD047136-03/HD/NICHD NIH HHS/ -- F32-HD47136/HD/NICHD NIH HHS/ -- GM058231/GM/NIGMS NIH HHS/ -- GM070840/GM/NIGMS NIH HHS/ -- GM61005/GM/NIGMS NIH HHS/ -- GM61464/GM/NIGMS NIH HHS/ -- HD-37105/HD/NICHD NIH HHS/ -- HD039948/HD/NICHD NIH HHS/ -- HD14483/HD/NICHD NIH HHS/ -- HD66219/HD/NICHD NIH HHS/ -- P30-CA14051/CA/NCI NIH HHS/ -- R01 ES006272/ES/NIEHS NIH HHS/ -- R01 ES006272-13/ES/NIEHS NIH HHS/ -- R01 GM070840/GM/NIGMS NIH HHS/ -- R01 HD028152/HD/NICHD NIH HHS/ -- R01ES006272/ES/NIEHS NIH HHS/ -- R37-HD12896/HD/NICHD NIH HHS/ -- RR-15044/RR/NCRR NIH HHS/ -- S19916/Biotechnology and Biological Sciences Research Council/United Kingdom -- T32 GM007601/GM/NIGMS NIH HHS/ -- U54 HG003273/HG/NHGRI NIH HHS/ -- New York, N.Y. -- Science. 2006 Nov 10;314(5801):941-52.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17095691" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; Calcification, Physiologic ; Cell Adhesion Molecules/genetics/physiology ; Complement Activation/genetics ; Computational Biology ; Embryonic Development/genetics ; Evolution, Molecular ; Gene Expression Regulation, Developmental ; Genes ; *Genome ; Immunity, Innate/genetics ; Immunologic Factors/genetics/physiology ; Male ; Nervous System Physiological Phenomena ; Proteins/genetics/physiology ; *Sequence Analysis, DNA ; Signal Transduction ; Strongylocentrotus purpuratus/embryology/*genetics/immunology/physiology ; Transcription Factors/genetics
    Print ISSN: 0036-8075
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Publiziert von American Association for the Advancement of Science (AAAS)
    Standort Signatur Erwartet Verfügbarkeit
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  • 2
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    Losartan, an AT1 antagonist, prevents aortic aneurysm in a mouse model of Marfan syndrome (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publikationsdatum: 2006-04-08
    Beschreibung: Aortic aneurysm and dissection are manifestations of Marfan syndrome (MFS), a disorder caused by mutations in the gene that encodes fibrillin-1. Selected manifestations of MFS reflect excessive signaling by the transforming growth factor-beta (TGF-beta) family of cytokines. We show that aortic aneurysm in a mouse model of MFS is associated with increased TGF-beta signaling and can be prevented by TGF-beta antagonists such as TGF-beta-neutralizing antibody or the angiotensin II type 1 receptor (AT1) blocker, losartan. AT1 antagonism also partially reversed noncardiovascular manifestations of MFS, including impaired alveolar septation. These data suggest that losartan, a drug already in clinical use for hypertension, merits investigation as a therapeutic strategy for patients with MFS and has the potential to prevent the major life-threatening manifestation of this disorder.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1482474/" 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/PMC1482474/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Habashi, Jennifer P -- Judge, Daniel P -- Holm, Tammy M -- Cohn, Ronald D -- Loeys, Bart L -- Cooper, Timothy K -- Myers, Loretha -- Klein, Erin C -- Liu, Guosheng -- Calvi, Carla -- Podowski, Megan -- Neptune, Enid R -- Halushka, Marc K -- Bedja, Djahida -- Gabrielson, Kathleen -- Rifkin, Daniel B -- Carta, Luca -- Ramirez, Francesco -- Huso, David L -- Dietz, Harry C -- K08 HL067056/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 2006 Apr 7;312(5770):117-21.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute and Department of Pediatrics, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16601194" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Adrenergic beta-Antagonists/administration & dosage/therapeutic use ; Angiotensin II Type 1 Receptor Blockers/administration & dosage/*therapeutic use ; Animals ; Antibodies/immunology ; Aorta/pathology ; Aortic Aneurysm/etiology/*prevention & control ; *Disease Models, Animal ; Elastic Tissue/pathology ; Female ; Losartan/administration & dosage/*therapeutic use ; Lung/pathology ; Lung Diseases/drug therapy/pathology ; Marfan Syndrome/complications/*drug therapy/metabolism/pathology ; Mice ; Microfilament Proteins/genetics ; Mutation ; Neutralization Tests ; Pregnancy ; Pregnancy Complications/drug therapy ; Propranolol/administration & dosage/therapeutic use ; Pulmonary Alveoli/pathology ; Receptor, Angiotensin, Type 1/metabolism ; Signal Transduction ; Transforming Growth Factor beta/antagonists & inhibitors/immunology/*metabolism
    Print ISSN: 0036-8075
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Publiziert von American Association for the Advancement of Science (AAAS)
    Standort Signatur Erwartet Verfügbarkeit
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  • 3
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    Herpes simplex virus encephalitis in human UNC-93B deficiency (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publikationsdatum: 2006-09-16
    Beschreibung: Herpes simplex virus-1 (HSV-1) encephalitis (HSE) is the most common form of sporadic viral encephalitis in western countries. Its pathogenesis remains unclear, as it affects otherwise healthy patients and only a small minority of HSV-1-infected individuals. Here, we elucidate a genetic etiology for HSE in two children with autosomal recessive deficiency in the intracellular protein UNC-93B, resulting in impaired cellular interferon-alpha/beta and -lambda antiviral responses. HSE can result from a single-gene immunodeficiency that does not compromise immunity to most pathogens, unlike most known primary immunodeficiencies. Other severe infectious diseases may also reflect monogenic disorders of immunity.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Casrouge, Armanda -- Zhang, Shen-Ying -- Eidenschenk, Celine -- Jouanguy, Emmanuelle -- Puel, Anne -- Yang, Kun -- Alcais, Alexandre -- Picard, Capucine -- Mahfoufi, Nora -- Nicolas, Nathalie -- Lorenzo, Lazaro -- Plancoulaine, Sabine -- Senechal, Brigitte -- Geissmann, Frederic -- Tabeta, Koichi -- Hoebe, Kasper -- Du, Xin -- Miller, Richard L -- Heron, Benedicte -- Mignot, Cyril -- de Villemeur, Thierry Billette -- Lebon, Pierre -- Dulac, Olivier -- Rozenberg, Flore -- Beutler, Bruce -- Tardieu, Marc -- Abel, Laurent -- Casanova, Jean-Laurent -- G0900867/Medical Research Council/United Kingdom -- New York, N.Y. -- Science. 2006 Oct 13;314(5797):308-12. Epub 2006 Sep 14.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratoire de Genetique Humaine des Maladies Infectieuses, Universite de Paris Rene Descartes, INSERM, U550, Faculte de Medecine Necker, Paris 75015, France.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16973841" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Child, Preschool ; Cytokines/biosynthesis ; Encephalitis, Herpes Simplex/*genetics/immunology ; Female ; *Genetic Predisposition to Disease ; *Herpesvirus 1, Human/immunology ; Humans ; Infant ; Interferon-alpha/biosynthesis/immunology ; Interferon-beta/biosynthesis/immunology ; Interferon-gamma/biosynthesis/immunology ; Interferons/*biosynthesis/immunology ; Leukocytes, Mononuclear/immunology ; Male ; Membrane Transport Proteins/*deficiency/genetics/*physiology ; Mutation ; Pedigree ; Signal Transduction ; Toll-Like Receptor 3/agonists/physiology ; Toll-Like Receptors/agonists/physiology
    Print ISSN: 0036-8075
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Publiziert von American Association for the Advancement of Science (AAAS)
    Standort Signatur Erwartet Verfügbarkeit
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  • 4
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    A genome-wide association study identifies IL23R as an inflammatory bowel disease gene (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publikationsdatum: 2006-10-28
    Beschreibung: The inflammatory bowel diseases Crohn's disease and ulcerative colitis are common, chronic disorders that cause abdominal pain, diarrhea, and gastrointestinal bleeding. To identify genetic factors that might contribute to these disorders, we performed a genome-wide association study. We found a highly significant association between Crohn's disease and the IL23R gene on chromosome 1p31, which encodes a subunit of the receptor for the proinflammatory cytokine interleukin-23. An uncommon coding variant (rs11209026, c.1142G〉A, p.Arg381Gln) confers strong protection against Crohn's disease, and additional noncoding IL23R variants are independently associated. Replication studies confirmed IL23R associations in independent cohorts of patients with Crohn's disease or ulcerative colitis. These results and previous studies on the proinflammatory role of IL-23 prioritize this signaling pathway as a therapeutic target in inflammatory bowel disease.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4410764/" 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/PMC4410764/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Duerr, Richard H -- Taylor, Kent D -- Brant, Steven R -- Rioux, John D -- Silverberg, Mark S -- Daly, Mark J -- Steinhart, A Hillary -- Abraham, Clara -- Regueiro, Miguel -- Griffiths, Anne -- Dassopoulos, Themistocles -- Bitton, Alain -- Yang, Huiying -- Targan, Stephan -- Datta, Lisa Wu -- Kistner, Emily O -- Schumm, L Philip -- Lee, Annette T -- Gregersen, Peter K -- Barmada, M Michael -- Rotter, Jerome I -- Nicolae, Dan L -- Cho, Judy H -- DK62413/DK/NIDDK NIH HHS/ -- DK62420/DK/NIDDK NIH HHS/ -- DK62422/DK/NIDDK NIH HHS/ -- DK62423/DK/NIDDK NIH HHS/ -- DK62429/DK/NIDDK NIH HHS/ -- DK62431/DK/NIDDK NIH HHS/ -- DK62432/DK/NIDDK NIH HHS/ -- P30 DK063491/DK/NIDDK NIH HHS/ -- P30 DK063491-019004/DK/NIDDK NIH HHS/ -- P30 DK063491-029004/DK/NIDDK NIH HHS/ -- P30 DK063491-039004/DK/NIDDK NIH HHS/ -- P30 DK063491-049004/DK/NIDDK NIH HHS/ -- U01 DK062420/DK/NIDDK NIH HHS/ -- U01 DK062422/DK/NIDDK NIH HHS/ -- U01 DK062423/DK/NIDDK NIH HHS/ -- U01 DK062429/DK/NIDDK NIH HHS/ -- U01 DK062432/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 2006 Dec 1;314(5804):1461-3. Epub 2006 Oct 26.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Gastroenterology, Hepatology and Nutrition, Department of Medicine, School of Medicine, University of Pittsburgh, University of Pittsburgh Medical Center Presbyterian, Mezzanine Level, C-Wing, 200 Lothrop Street, Pittsburgh, PA 15213, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17068223" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Alleles ; Case-Control Studies ; Chromosomes, Human, Pair 1/genetics ; Cohort Studies ; Colitis, Ulcerative/genetics ; Crohn Disease/*genetics ; Genetic Markers ; Genetic Predisposition to Disease ; Genetic Testing ; Genome, Human ; Haplotypes ; Humans ; Interleukin-23/metabolism ; Jews/genetics ; Linkage Disequilibrium ; *Polymorphism, Single Nucleotide ; Receptors, Interleukin/*genetics/physiology ; Signal Transduction
    Print ISSN: 0036-8075
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Publiziert von American Association for the Advancement of Science (AAAS)
    Standort Signatur Erwartet Verfügbarkeit
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  • 5
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    Debating sexual selection and mating strategies (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publikationsdatum: 2006-05-09
    Beschreibung: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pizzari, Tommaso -- Birkhead, Tim R -- Blows, Mark W -- Brooks, Rob -- Buchanan, Katherine L -- Clutton-Brock, Tim H -- Harvey, Paul H -- Hosken, Dave J -- Jennions, Michael D -- Kokko, Hanna -- Kotiaho, Janne S -- Lessells, C M -- Macias-Garcia, Constantino -- Moore, Allen J -- Parker, Geoff A -- Partigridge, Linda -- Pitnick, Scott -- Radwan, Jacek -- Ritchie, Mike -- Sheldon, Ben C -- Simmons, Leigh W -- Snook, Rhonda R -- Stockley, Paula -- Zuk, Marlene -- New York, N.Y. -- Science. 2006 May 5;312(5774):689-97; author reply 689-97.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16680817" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; Biological Evolution ; Female ; Male ; Reproduction ; Sex Characteristics ; *Sexual Behavior, Animal ; *Social Behavior
    Print ISSN: 0036-8075
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Publiziert von American Association for the Advancement of Science (AAAS)
    Standort Signatur Erwartet Verfügbarkeit
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  • 6
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    Human lineage-specific amplification, selection, and neuronal expression of DUF1220 domains (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publikationsdatum: 2006-09-02
    Beschreibung: Extreme gene duplication is a major source of evolutionary novelty. A genome-wide survey of gene copy number variation among human and great ape lineages revealed that the most striking human lineage-specific amplification was due to an unknown gene, MGC8902, which is predicted to encode multiple copies of a protein domain of unknown function (DUF1220). Sequences encoding these domains are virtually all primate-specific, show signs of positive selection, and are increasingly amplified generally as a function of a species' evolutionary proximity to humans, where the greatest number of copies (212) is found. DUF1220 domains are highly expressed in brain regions associated with higher cognitive function, and in brain show neuron-specific expression preferentially in cell bodies and dendrites.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Popesco, Magdalena C -- Maclaren, Erik J -- Hopkins, Janet -- Dumas, Laura -- Cox, Michael -- Meltesen, Lynne -- McGavran, Loris -- Wyckoff, Gerald J -- Sikela, James M -- AA11853/AA/NIAAA NIH HHS/ -- New York, N.Y. -- Science. 2006 Sep 1;313(5791):1304-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Human Medical Genetics, University of Colorado at Denver and Health Sciences Center, Aurora, CO 80045, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16946073" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Amino Acid Sequence ; Animals ; *Biological Evolution ; Brain/*metabolism ; Cognition ; Exons ; *Gene Amplification ; Gene Dosage ; Gene Duplication ; Gene Expression ; Genome, Human ; Humans ; Macaca mulatta/genetics ; Mice ; Molecular Sequence Data ; Neocortex/metabolism ; Neurons/*metabolism ; Pan troglodytes/genetics ; Phylogeny ; Polymerase Chain Reaction ; *Protein Structure, Tertiary ; Proteins/*chemistry/genetics ; Rats ; *Selection, Genetic
    Print ISSN: 0036-8075
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Publiziert von American Association for the Advancement of Science (AAAS)
    Standort Signatur Erwartet Verfügbarkeit
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  • 7
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    Symbiotic bacteria direct expression of an intestinal bactericidal lectin (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publikationsdatum: 2006-08-26
    Beschreibung: The mammalian intestine harbors complex societies of beneficial bacteria that are maintained in the lumen with minimal penetration of mucosal surfaces. Microbial colonization of germ-free mice triggers epithelial expression of RegIIIgamma, a secreted C-type lectin. RegIIIgamma binds intestinal bacteria but lacks the complement recruitment domains present in other microbe-binding mammalian C-type lectins. We show that RegIIIgamma and its human counterpart, HIP/PAP, are directly antimicrobial proteins that bind their bacterial targets via interactions with peptidoglycan carbohydrate. We propose that these proteins represent an evolutionarily primitive form of lectin-mediated innate immunity, and that they reveal intestinal strategies for maintaining symbiotic host-microbial relationships.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2716667/" 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/PMC2716667/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cash, Heather L -- Whitham, Cecilia V -- Behrendt, Cassie L -- Hooper, Lora V -- R01 DK070855/DK/NIDDK NIH HHS/ -- R01 DK070855-01/DK/NIDDK NIH HHS/ -- T32-AI007520/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 2006 Aug 25;313(5790):1126-30.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for Immunology, University of Texas Southwestern Medical Center at Dallas, 5323 Harry Hines Boulevard, Dallas, TX 75390, USA. Lora.Hooper@UTSouthwestern.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16931762" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; Antigens, Neoplasm/*metabolism/pharmacology ; Bacteria/growth & development/*immunology ; Biomarkers, Tumor/*metabolism/pharmacology ; Chitin/metabolism ; Colony Count, Microbial ; Germ-Free Life ; Gram-Positive Bacteria/immunology/metabolism ; Homeostasis ; Humans ; *Immunity, Innate ; Immunity, Mucosal ; Intestine, Small/*microbiology ; Lectins, C-Type/*metabolism ; Ligands ; Listeria monocytogenes/ultrastructure ; Mice ; Oligonucleotide Array Sequence Analysis ; Paneth Cells/immunology/*metabolism ; Peptidoglycan/chemistry/*metabolism ; Protein Structure, Tertiary ; Proteins/genetics/*metabolism/pharmacology ; Recombinant Proteins/metabolism ; Secretory Vesicles/metabolism ; Symbiosis
    Print ISSN: 0036-8075
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Publiziert von American Association for the Advancement of Science (AAAS)
    Standort Signatur Erwartet Verfügbarkeit
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  • 8
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    Dissecting the functions of the mammalian clock protein BMAL1 by tissue-specific rescue in mice (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publikationsdatum: 2006-11-25
    Beschreibung: The basic helix-loop-helix (bHLH)-Per-Arnt-Sim (PAS) domain transcription factor BMAL1 is an essential component of the mammalian circadian pacemaker. Bmal1-/- mice lose circadian rhythmicity but also display tendon calcification and decreased activity, body weight, and longevity. To investigate whether these diverse functions of BMAL1 are tissue-specific, we produced transgenic mice that constitutively express Bmal1 in brain or muscle and examined the effects of rescued gene expression in Bmal1-/- mice. Circadian rhythms of wheel-running activity were restored in brain-rescued Bmal1-/- mice in a conditional manner; however, activity levels and body weight were lower than those of wild-type mice. In contrast, muscle-rescued Bmal1-/- mice exhibited normal activity levels and body weight yet remained behaviorally arrhythmic. Thus, Bmal1 has distinct tissue-specific functions that regulate integrative physiology.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3756687/" 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/PMC3756687/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉McDearmon, Erin L -- Patel, Kush N -- Ko, Caroline H -- Walisser, Jacqueline A -- Schook, Andrew C -- Chong, Jason L -- Wilsbacher, Lisa D -- Song, Eun J -- Hong, Hee-Kyung -- Bradfield, Christopher A -- Takahashi, Joseph S -- P50 MH074924/MH/NIMH NIH HHS/ -- R01 ES005703/ES/NIEHS NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2006 Nov 24;314(5803):1304-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Department of Neurobiology and Physiology, Northwestern University, Evanston, IL 60208, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17124323" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): ARNTL Transcription Factors ; Animals ; Basic Helix-Loop-Helix Transcription Factors/genetics/*physiology ; Body Weight ; Brain/*metabolism ; Calcinosis ; Cell Cycle Proteins/genetics ; Chromosomes, Artificial, Bacterial ; *Circadian Rhythm ; Gene Expression ; Longevity ; Mice ; Mice, Inbred C57BL ; Mice, Transgenic ; *Motor Activity ; Muscle, Skeletal/*metabolism ; Nuclear Proteins/genetics ; Organ Specificity ; Period Circadian Proteins ; Suprachiasmatic Nucleus/metabolism ; Tendons/pathology ; Transcription Factors/genetics
    Print ISSN: 0036-8075
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Publiziert von American Association for the Advancement of Science (AAAS)
    Standort Signatur Erwartet Verfügbarkeit
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  • 9
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    Single-Particle Measurements of Midlatitude Black Carbon and Light-Scattering Aerosols from the Boundary Layer to the Lower Stratosphere (2006)
    In:  Other Sources
    Details
    Publikationsdatum: 2019-07-19
    Beschreibung: A single-particle soot photometer (SP2) was flown on a NASA WB-57F high-altitude research aircraft in November 2004 from Houston, Texas. The SP2 uses laser-induced incandescence to detect individual black carbon (BC) particles in an air sample in the mass range of approx.3-300 fg (approx.0.15-0.7 microns volume equivalent diameter). Scattered light is used to size the remaining non-BC aerosols in the range of approx.0.17-0.7 microns diameter. We present profiles of both aerosol types from the boundary layer to the lower stratosphere from two midlatitude flights. Results for total aerosol amounts in the size range detected by the SP2 are in good agreement with typical particle spectrometer measurements in the same region. All ambient incandescing particles were identified as BC because their incandescence properties matched those of laboratory-generated BC aerosol. Approximately 40% of these BC particles showed evidence of internal mixing (e.g., coating). Throughout profiles between 5 and 18.7 km, BC particles were less than a few percent of total aerosol number, and black carbon aerosol (BCA) mass mixing ratio showed a constant gradient with altitude above 5 km. SP2 data was compared to results from the ECHAM4/MADE and LmDzT-INCA global aerosol models. The comparison will help resolve the important systematic differences in model aerosol processes that determine BCA loadings. Further intercomparisons of models and measurements as presented here will improve the accuracy of the radiative forcing contribution from BCA.
    Schlagwort(e): Meteorology and Climatology
    Materialart: Journal of Geophysical Research Atmospheres (ISSN 0148-0227); 111
    Format: text
    Standort Signatur Erwartet Verfügbarkeit
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    NASA TECHNICAL REPORTS
  • 10
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    Prion-induced amyloid heart disease with high blood infectivity in transgenic mice (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publikationsdatum: 2006-07-11
    Beschreibung: We investigated extraneural manifestations in scrapie-infected transgenic mice expressing prion protein lacking the glycophosphatydylinositol membrane anchor. In the brain, blood, and heart, both abnormal protease-resistant prion protein (PrPres) and prion infectivity were readily detected by immunoblot and by inoculation into nontransgenic recipients. The titer of infectious scrapie in blood plasma exceeded 10(7) 50% infectious doses per milliliter. The hearts of these transgenic mice contained PrPres-positive amyloid deposits that led to myocardial stiffness and cardiac disease.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1820586/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1820586/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Trifilo, Matthew J -- Yajima, Toshitaka -- Gu, Yusu -- Dalton, Nancy -- Peterson, Kirk L -- Race, Richard E -- Meade-White, Kimberly -- Portis, John L -- Masliah, Eliezer -- Knowlton, Kirk U -- Chesebro, Bruce -- Oldstone, Michael B A -- 5R01HL66424-04/HL/NHLBI NIH HHS/ -- AGO4342/PHS HHS/ -- NS041219-05/NS/NINDS NIH HHS/ -- P01 AG004342/AG/NIA NIH HHS/ -- New York, N.Y. -- Science. 2006 Jul 7;313(5783):94-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Viral-Immunobiology Laboratory, Departments of Molecular and Integrative Neurosciences and Infectology, Scripps Research Institute, La Jolla, CA 92037, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16825571" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Amyloid/*analysis ; Amyloidosis/blood/etiology/*pathology/physiopathology ; Animals ; Blotting, Western ; Cardiac Catheterization ; Coronary Vessels/chemistry/pathology ; Disease Models, Animal ; Glycosylphosphatidylinositols ; Heart Diseases/blood/etiology/*pathology/physiopathology ; Heart Function Tests ; Immunohistochemistry ; Mice ; Mice, Inbred C57BL ; Mice, Transgenic ; Microcirculation/chemistry/pathology ; Myocardial Contraction ; Myocardium/*chemistry/*pathology ; PrPC Proteins/chemistry ; PrPSc Proteins/*analysis/blood ; Scrapie/blood/*pathology/physiopathology ; Staining and Labeling ; Time Factors
    Print ISSN: 0036-8075
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Publiziert von American Association for the Advancement of Science (AAAS)
    Standort Signatur Erwartet Verfügbarkeit
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