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  • Cell Line  (292)
  • Amino Acid Sequence  (260)
  • 2005-2009  (295)
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  • 1
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    TLR3 deficiency in patients with herpes simplex encephalitis (2007)
    American Association for the Advancement of Science (AAAS)
    Details
    Publikationsdatum: 2007-09-18
    Beschreibung: Some Toll and Toll-like receptors (TLRs) provide immunity to experimental infections in animal models, but their contribution to host defense in natural ecosystems is unknown. We report a dominant-negative TLR3 allele in otherwise healthy children with herpes simplex virus 1 (HSV-1) encephalitis. TLR3 is expressed in the central nervous system (CNS), where it is required to control HSV-1, which spreads from the epithelium to the CNS via cranial nerves. TLR3 is also expressed in epithelial and dendritic cells, which apparently use TLR3-independent pathways to prevent further dissemination of HSV-1 and to provide resistance to other pathogens in TLR3-deficient patients. Human TLR3 appears to be redundant in host defense to most microbes but is vital for natural immunity to HSV-1 in the CNS, which suggests that neurotropic viruses have contributed to the evolutionary maintenance of TLR3.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zhang, Shen-Ying -- Jouanguy, Emmanuelle -- Ugolini, Sophie -- Smahi, Asma -- Elain, Gaelle -- Romero, Pedro -- Segal, David -- Sancho-Shimizu, Vanessa -- Lorenzo, Lazaro -- Puel, Anne -- Picard, Capucine -- Chapgier, Ariane -- Plancoulaine, Sabine -- Titeux, Matthias -- Cognet, Celine -- von Bernuth, Horst -- Ku, Cheng-Lung -- Casrouge, Armanda -- Zhang, Xin-Xin -- Barreiro, Luis -- Leonard, Joshua -- Hamilton, Claire -- Lebon, Pierre -- Heron, Benedicte -- Vallee, Louis -- Quintana-Murci, Lluis -- Hovnanian, Alain -- Rozenberg, Flore -- Vivier, Eric -- Geissmann, Frederic -- Tardieu, Marc -- Abel, Laurent -- Casanova, Jean-Laurent -- G0900867/Medical Research Council/United Kingdom -- New York, N.Y. -- Science. 2007 Sep 14;317(5844):1522-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Human Genetics of Infectious Diseases, Institut National de la Sante et de la Recherche Medicale (INSERM), U550, Faculty Necker, Paris 75015, France.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17872438" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Alleles ; CD8-Positive T-Lymphocytes/immunology ; Cell Line ; Child, Preschool ; Dendritic Cells/immunology ; Encephalitis, Herpes Simplex/*genetics/*immunology ; Female ; Fibroblasts/immunology/metabolism/virology ; Genes, Dominant ; *Herpesvirus 1, Human/physiology ; Heterozygote ; Humans ; Immunity, Innate ; Infant ; Interferons/biosynthesis ; Keratinocytes/immunology ; Killer Cells, Natural/immunology ; Leukocytes, Mononuclear/immunology ; Mutation ; Poly I-C/pharmacology ; Toll-Like Receptor 3/chemistry/*deficiency/*genetics/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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  • 2
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    Isolation and characterization of viruses related to the SARS coronavirus from animals in southern China (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publikationsdatum: 2003-09-06
    Beschreibung: A novel coronavirus (SCoV) is the etiological agent of severe acute respiratory syndrome (SARS). SCoV-like viruses were isolated from Himalayan palm civets found in a live-animal market in Guangdong, China. Evidence of virus infection was also detected in other animals (including a raccoon dog, Nyctereutes procyonoides) and in humans working at the same market. All the animal isolates retain a 29-nucleotide sequence that is not found in most human isolates. The detection of SCoV-like viruses in small, live wild mammals in a retail market indicates a route of interspecies transmission, although the natural reservoir is not known.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Guan, Y -- Zheng, B J -- He, Y Q -- Liu, X L -- Zhuang, Z X -- Cheung, C L -- Luo, S W -- Li, P H -- Zhang, L J -- Guan, Y J -- Butt, K M -- Wong, K L -- Chan, K W -- Lim, W -- Shortridge, K F -- Yuen, K Y -- Peiris, J S M -- Poon, L L M -- New York, N.Y. -- Science. 2003 Oct 10;302(5643):276-8. Epub 2003 Sep 4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Microbiology, The University of Hong Kong, University Pathology Building, Queen Mary Hospital, Hong Kong Special Administrative Region, People's Republic of China. yguan@hkucc.hku.hk〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12958366" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Amino Acid Sequence ; Animals ; Animals, Wild/*virology ; Antibodies, Viral/blood ; Blotting, Western ; Carnivora/*virology ; China ; Coronavirus/classification/genetics/immunology/*isolation & purification ; Coronavirus Infections/veterinary/virology ; Disease Reservoirs ; Feces/virology ; Genome, Viral ; Humans ; Membrane Glycoproteins/chemistry/genetics ; Molecular Sequence Data ; Neutralization Tests ; Nose/virology ; Open Reading Frames/genetics ; Phylogeny ; Polymorphism, Genetic ; Reverse Transcriptase Polymerase Chain Reaction ; SARS Virus/classification/genetics/immunology/*isolation & purification ; Sequence Deletion ; Sequence Homology, Nucleic Acid ; Spike Glycoprotein, Coronavirus ; Viral Envelope Proteins/chemistry/genetics ; Viral Proteins/chemistry/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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  • 3
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    Ethics. The ISSCR guidelines for human embryonic stem cell research (2007)
    American Association for the Advancement of Science (AAAS)
    Details
    Publikationsdatum: 2007-02-03
    Beschreibung: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Daley, George Q -- Ahrlund Richter, Lars -- Auerbach, Jonathan M -- Benvenisty, Nissim -- Charo, R Alta -- Chen, Grace -- Deng, Hong-Kui -- Goldstein, Lawrence S -- Hudson, Kathy L -- Hyun, Insoo -- Junn, Sung Chull -- Love, Jane -- Lee, Eng Hin -- McLaren, Anne -- Mummery, Christine L -- Nakatsuji, Norio -- Racowsky, Catherine -- Rooke, Heather -- Rossant, Janet -- Scholer, Hans R -- Solbakk, Jan Helge -- Taylor, Patrick -- Trounson, Alan O -- Weissman, Irving L -- Wilmut, Ian -- Yu, John -- Zoloth, Laurie -- New York, N.Y. -- Science. 2007 Feb 2;315(5812):603-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Children's Hospital, Boston, Massachusetts, USA. george.daley@childrens.harvard.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17272706" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; Cell Line ; Chimera ; *Embryo Research/ethics/legislation & jurisprudence ; Embryonic Development ; *Embryonic Stem Cells ; *Guidelines as Topic ; Humans ; Informed Consent ; International Cooperation ; Oocyte Donation/economics/ethics ; Pluripotent Stem Cells ; Societies, Scientific ; Tissue Donors/ethics
    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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    DNA double-strand breaks activate a multi-functional genetic program in developing lymphocytes (2008)
    Nature Publishing Group (NPG)
    Details
    Publikationsdatum: 2008-10-14
    Beschreibung: DNA double-strand breaks are generated by genotoxic agents and by cellular endonucleases as intermediates of several important physiological processes. The cellular response to genotoxic DNA breaks includes the activation of transcriptional programs known primarily to regulate cell-cycle checkpoints and cell survival. DNA double-strand breaks are generated in all developing lymphocytes during the assembly of antigen receptor genes, a process that is essential for normal lymphocyte development. Here we show that in murine lymphocytes these physiological DNA breaks activate a broad transcriptional program. This program transcends the canonical DNA double-strand break response and includes many genes that regulate diverse cellular processes important for lymphocyte development. Moreover, the expression of several of these genes is regulated similarly in response to genotoxic DNA damage. Thus, physiological DNA double-strand breaks provide cues that can regulate cell-type-specific processes not directly involved in maintaining the integrity of the genome, and genotoxic DNA breaks could disrupt normal cellular functions by corrupting these processes.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2605662/" 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/PMC2605662/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bredemeyer, Andrea L -- Helmink, Beth A -- Innes, Cynthia L -- Calderon, Boris -- McGinnis, Lisa M -- Mahowald, Grace K -- Gapud, Eric J -- Walker, Laura M -- Collins, Jennifer B -- Weaver, Brian K -- Mandik-Nayak, Laura -- Schreiber, Robert D -- Allen, Paul M -- May, Michael J -- Paules, Richard S -- Bassing, Craig H -- Sleckman, Barry P -- R01 AI047829/AI/NIAID NIH HHS/ -- R01 AI047829-09/AI/NIAID NIH HHS/ -- R01 CA125195/CA/NCI NIH HHS/ -- R01 CA125195-02/CA/NCI NIH HHS/ -- England -- Nature. 2008 Dec 11;456(7223):819-23. doi: 10.1038/nature07392. Epub 2008 Oct 12.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology and Immunology, Washington University School of Medicine, St. Louis, Missouri 63110, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18849970" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; Ataxia Telangiectasia Mutated Proteins ; B-Lymphocytes/drug effects/*metabolism ; Cell Cycle Proteins/drug effects ; Cell Line ; *DNA Breaks, Double-Stranded ; DNA-Binding Proteins/drug effects ; Enzyme Inhibitors/pharmacology ; Gene Expression Profiling ; Gene Expression Regulation, Developmental/drug effects/*genetics ; Homeodomain Proteins/metabolism ; Mice ; Mice, Knockout ; Mice, SCID ; NF-kappa B/metabolism ; Protein-Serine-Threonine Kinases/drug effects ; Tumor Suppressor Proteins/drug effects
    Print ISSN: 0028-0836
    Digitale ISSN: 1476-4687
    Thema: Biologie , Chemie und Pharmazie , Medizin , Allgemeine Naturwissenschaft , Physik
    Publiziert von Nature Publishing Group (NPG)
    Standort Signatur Erwartet Verfügbarkeit
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  • 5
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    A paracrine requirement for hedgehog signalling in cancer (2008)
    Nature Publishing Group (NPG)
    Details
    Publikationsdatum: 2008-08-30
    Beschreibung: Ligand-dependent activation of the hedgehog (Hh) signalling pathway has been associated with tumorigenesis in a number of human tissues. Here we show that, although previous reports have described a cell-autonomous role for Hh signalling in these tumours, Hh ligands fail to activate signalling in tumour epithelial cells. In contrast, our data support ligand-dependent activation of the Hh pathway in the stromal microenvironment. Specific inhibition of Hh signalling using small molecule inhibitors, a neutralizing anti-Hh antibody or genetic deletion of smoothened (Smo) in the mouse stroma results in growth inhibition in xenograft tumour models. Taken together, these studies demonstrate a paracrine requirement for Hh ligand signalling in the tumorigenesis of Hh-expressing cancers and have important implications for the development of Hh pathway antagonists in cancer.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Yauch, Robert L -- Gould, Stephen E -- Scales, Suzie J -- Tang, Tracy -- Tian, Hua -- Ahn, Christina P -- Marshall, Derek -- Fu, Ling -- Januario, Thomas -- Kallop, Dara -- Nannini-Pepe, Michelle -- Kotkow, Karen -- Marsters, James C -- Rubin, Lee L -- de Sauvage, Frederic J -- England -- Nature. 2008 Sep 18;455(7211):406-10. doi: 10.1038/nature07275. Epub 2008 Aug 27.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Genentech Inc., 1 DNA Way, South San Francisco, California 94080, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18754008" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; Cell Line ; Female ; Gene Expression Profiling ; Gene Expression Regulation, Neoplastic ; Hedgehog Proteins/*metabolism ; Humans ; Ligands ; Mice ; Mice, Nude ; Neoplasm Transplantation ; Neoplasms/genetics/*metabolism ; Paracrine Communication/*physiology ; Receptors, G-Protein-Coupled/deficiency/genetics/metabolism ; Stromal Cells/*metabolism
    Print ISSN: 0028-0836
    Digitale ISSN: 1476-4687
    Thema: Biologie , Chemie und Pharmazie , Medizin , Allgemeine Naturwissenschaft , Physik
    Publiziert von Nature Publishing Group (NPG)
    Standort Signatur Erwartet Verfügbarkeit
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  • 6
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    Discovery of insect and human dengue virus host factors (2009)
    Nature Publishing Group (NPG)
    Details
    Publikationsdatum: 2009-04-28
    Beschreibung: Dengue fever is the most frequent arthropod-borne viral disease of humans, with almost half of the world's population at risk of infection. The high prevalence, lack of an effective vaccine, and absence of specific treatment conspire to make dengue fever a global public health threat. Given their compact genomes, dengue viruses (DENV-1-4) and other flaviviruses probably require an extensive number of host factors; however, only a limited number of human, and an even smaller number of insect host factors, have been identified. Here we identify insect host factors required for DENV-2 propagation, by carrying out a genome-wide RNA interference screen in Drosophila melanogaster cells using a well-established 22,632 double-stranded RNA library. This screen identified 116 candidate dengue virus host factors (DVHFs). Although some were previously associated with flaviviruses (for example, V-ATPases and alpha-glucosidases), most of the DVHFs were newly implicated in dengue virus propagation. The dipteran DVHFs had 82 readily recognizable human homologues and, using a targeted short-interfering-RNA screen, we showed that 42 of these are human DVHFs. This indicates notable conservation of required factors between dipteran and human hosts. This work suggests new approaches to control infection in the insect vector and the mammalian host.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3462662/" 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/PMC3462662/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sessions, October M -- Barrows, Nicholas J -- Souza-Neto, Jayme A -- Robinson, Timothy J -- Hershey, Christine L -- Rodgers, Mary A -- Ramirez, Jose L -- Dimopoulos, George -- Yang, Priscilla L -- Pearson, James L -- Garcia-Blanco, Mariano A -- 1R01AI061576-01/AI/NIAID NIH HHS/ -- 1R01AI076442/AI/NIAID NIH HHS/ -- 1SA0RR024572-1/RR/NCRR NIH HHS/ -- 5P30-CA14236/CA/NCI NIH HHS/ -- 5U54-AI057157-05S/AI/NIAID NIH HHS/ -- R01 AI076442/AI/NIAID NIH HHS/ -- R01 AI078997/AI/NIAID NIH HHS/ -- R01 AI078997-01A1/AI/NIAID NIH HHS/ -- R01 AI078997-02/AI/NIAID NIH HHS/ -- R01 GM067761/GM/NIGMS NIH HHS/ -- R21 AI090188/AI/NIAID NIH HHS/ -- R21 AI090188-01/AI/NIAID NIH HHS/ -- R21 NS063845/NS/NINDS NIH HHS/ -- R21-AI64925/AI/NIAID NIH HHS/ -- T32 AI007417/AI/NIAID NIH HHS/ -- U54 AI057157/AI/NIAID NIH HHS/ -- U54 AI057159/AI/NIAID NIH HHS/ -- England -- Nature. 2009 Apr 23;458(7241):1047-50. doi: 10.1038/nature07967.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Genetics and Microbiology, Duke University Medical Center, Durham, North Carolina 27710, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19396146" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Aedes/genetics/virology ; Animals ; Cell Line ; Conserved Sequence/*genetics/physiology ; Dengue Virus/*physiology ; Drosophila melanogaster/*genetics/physiology/*virology ; Gene Knockdown Techniques ; Genome, Insect/genetics ; Host-Pathogen Interactions/*genetics ; Humans ; Insect Vectors/*genetics/*physiology ; RNA Interference ; RNA, Double-Stranded/genetics/metabolism ; Virus Replication
    Print ISSN: 0028-0836
    Digitale ISSN: 1476-4687
    Thema: Biologie , Chemie und Pharmazie , Medizin , Allgemeine Naturwissenschaft , Physik
    Publiziert von Nature Publishing Group (NPG)
    Standort Signatur Erwartet Verfügbarkeit
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  • 7
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    Wnt3a-mediated formation of phosphatidylinositol 4,5-bisphosphate regulates LRP6 phosphorylation (2008)
    American Association for the Advancement of Science (AAAS)
    Details
    Publikationsdatum: 2008-09-06
    Beschreibung: The canonical Wnt-beta-catenin signaling pathway is initiated by inducing phosphorylation of one of the Wnt receptors, low-density lipoprotein receptor-related protein 6 (LRP6), at threonine residue 1479 (Thr1479) and serine residue 1490 (Ser1490). By screening a human kinase small interfering RNA library, we identified phosphatidylinositol 4-kinase type II alpha and phosphatidylinositol-4-phosphate 5-kinase type I (PIP5KI) as required for Wnt3a-induced LRP6 phosphorylation at Ser1490 in mammalian cells and confirmed that these kinases are important for Wnt signaling in Xenopus embryos. Wnt3a stimulates the formation of phosphatidylinositol 4,5-bisphosphates [PtdIns (4,5)P2] through frizzled and dishevelled, the latter of which directly interacted with and activated PIP5KI. In turn, PtdIns (4,5)P2 regulated phosphorylation of LRP6 at Thr1479 and Ser1490. Therefore, our study reveals a signaling mechanism for Wnt to regulate LRP6 phosphorylation.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2532521/" 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/PMC2532521/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pan, Weijun -- Choi, Sun-Cheol -- Wang, He -- Qin, Yuanbo -- Volpicelli-Daley, Laura -- Swan, Laura -- Lucast, Louise -- Khoo, Cynthia -- Zhang, Xiaowu -- Li, Lin -- Abrams, Charles S -- Sokol, Sergei Y -- Wu, Dianqing -- AR051476/AR/NIAMS NIH HHS/ -- CA132317/CA/NCI NIH HHS/ -- DA018343/DA/NIDA NIH HHS/ -- HL080706/HL/NHLBI NIH HHS/ -- NS36251/NS/NINDS NIH HHS/ -- P30 DA018343/DA/NIDA NIH HHS/ -- R01 AR051476/AR/NIAMS NIH HHS/ -- R01 AR051476-01A1/AR/NIAMS NIH HHS/ -- R01 AR051476-02/AR/NIAMS NIH HHS/ -- R01 AR051476-03/AR/NIAMS NIH HHS/ -- R01 CA132317/CA/NCI NIH HHS/ -- R01 CA132317-01A2/CA/NCI NIH HHS/ -- R01 CA139395/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 2008 Sep 5;321(5894):1350-3. doi: 10.1126/science.1160741.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pharmacology, Yale University School of Medicine, New Haven, CT 06510, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18772438" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Adaptor Proteins, Signal Transducing/metabolism ; Animals ; Axin Protein ; Cell Line ; Frizzled Receptors/metabolism ; Humans ; LDL-Receptor Related Proteins/*metabolism ; Low Density Lipoprotein Receptor-Related Protein-6 ; Mice ; Models, Biological ; Phosphatidylinositol 4,5-Diphosphate/*metabolism ; Phosphoproteins/metabolism ; Phosphorylation ; Phosphotransferases (Alcohol Group Acceptor)/metabolism ; RNA, Small Interfering ; Recombinant Proteins/metabolism ; Repressor Proteins/metabolism ; Serine/metabolism ; Signal Transduction ; Threonine/metabolism ; Wnt Proteins/*metabolism ; Wnt3 Protein ; Wnt3A Protein ; Xenopus/embryology ; Xenopus Proteins
    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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    Rare structural variants disrupt multiple genes in neurodevelopmental pathways in schizophrenia (2008)
    American Association for the Advancement of Science (AAAS)
    Details
    Publikationsdatum: 2008-03-29
    Beschreibung: Schizophrenia is a devastating neurodevelopmental disorder whose genetic influences remain elusive. We hypothesize that individually rare structural variants contribute to the illness. Microdeletions and microduplications 〉100 kilobases were identified by microarray comparative genomic hybridization of genomic DNA from 150 individuals with schizophrenia and 268 ancestry-matched controls. All variants were validated by high-resolution platforms. Novel deletions and duplications of genes were present in 5% of controls versus 15% of cases and 20% of young-onset cases, both highly significant differences. The association was independently replicated in patients with childhood-onset schizophrenia as compared with their parents. Mutations in cases disrupted genes disproportionately from signaling networks controlling neurodevelopment, including neuregulin and glutamate pathways. These results suggest that multiple, individually rare mutations altering genes in neurodevelopmental pathways contribute to schizophrenia.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Walsh, Tom -- McClellan, Jon M -- McCarthy, Shane E -- Addington, Anjene M -- Pierce, Sarah B -- Cooper, Greg M -- Nord, Alex S -- Kusenda, Mary -- Malhotra, Dheeraj -- Bhandari, Abhishek -- Stray, Sunday M -- Rippey, Caitlin F -- Roccanova, Patricia -- Makarov, Vlad -- Lakshmi, B -- Findling, Robert L -- Sikich, Linmarie -- Stromberg, Thomas -- Merriman, Barry -- Gogtay, Nitin -- Butler, Philip -- Eckstrand, Kristen -- Noory, Laila -- Gochman, Peter -- Long, Robert -- Chen, Zugen -- Davis, Sean -- Baker, Carl -- Eichler, Evan E -- Meltzer, Paul S -- Nelson, Stanley F -- Singleton, Andrew B -- Lee, Ming K -- Rapoport, Judith L -- King, Mary-Claire -- Sebat, Jonathan -- HD043569/HD/NICHD NIH HHS/ -- M01 RR000046/RR/NCRR NIH HHS/ -- MH061355/MH/NIMH NIH HHS/ -- MH061464/MH/NIMH NIH HHS/ -- MH061528/MH/NIMH NIH HHS/ -- NS052108/NS/NINDS NIH HHS/ -- R01 HD043569/HD/NICHD NIH HHS/ -- RR000046/RR/NCRR NIH HHS/ -- RR025014/RR/NCRR NIH HHS/ -- U01 MH061355/MH/NIMH NIH HHS/ -- U01 MH061464/MH/NIMH NIH HHS/ -- U01 MH061528/MH/NIMH NIH HHS/ -- U24 NS052108/NS/NINDS NIH HHS/ -- UL1 RR025014/RR/NCRR NIH HHS/ -- Howard Hughes Medical Institute/ -- Intramural NIH HHS/ -- New York, N.Y. -- Science. 2008 Apr 25;320(5875):539-43. doi: 10.1126/science.1155174. Epub 2008 Mar 27.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine, University of Washington, Seattle, WA 98195, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18369103" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Adolescent ; Adult ; Age of Onset ; Amino Acid Sequence ; Brain/cytology/*growth & development/metabolism ; Case-Control Studies ; Child ; Excitatory Amino Acid Transporter 1/chemistry/genetics/physiology ; Female ; *Gene Deletion ; *Gene Duplication ; Genetic Predisposition to Disease ; Genome, Human ; Humans ; Male ; Molecular Sequence Data ; *Mutation ; Neurons/cytology/physiology ; Oligonucleotide Array Sequence Analysis ; Polymorphism, Single Nucleotide ; Receptor, Epidermal Growth Factor/chemistry/genetics/physiology ; Receptor, ErbB-4 ; Schizophrenia/*genetics/physiopathology ; 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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  • 9
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    Mutations in a human ROBO gene disrupt hindbrain axon pathway crossing and morphogenesis (2004)
    American Association for the Advancement of Science (AAAS)
    Details
    Publikationsdatum: 2004-04-24
    Beschreibung: The mechanisms controlling axon guidance are of fundamental importance in understanding brain development. Growing corticospinal and somatosensory axons cross the midline in the medulla to reach their targets and thus form the basis of contralateral motor control and sensory input. The motor and sensory projections appeared uncrossed in patients with horizontal gaze palsy with progressive scoliosis (HGPPS). In patients affected with HGPPS, we identified mutations in the ROBO3 gene, which shares homology with roundabout genes important in axon guidance in developing Drosophila, zebrafish, and mouse. Like its murine homolog Rig1/Robo3, but unlike other Robo proteins, ROBO3 is required for hindbrain axon midline crossing.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1618874/" 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/PMC1618874/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Jen, Joanna C -- Chan, Wai-Man -- Bosley, Thomas M -- Wan, Jijun -- Carr, Janai R -- Rub, Udo -- Shattuck, David -- Salamon, Georges -- Kudo, Lili C -- Ou, Jing -- Lin, Doris D M -- Salih, Mustafa A M -- Kansu, Tulay -- Al Dhalaan, Hesham -- Al Zayed, Zayed -- MacDonald, David B -- Stigsby, Bent -- Plaitakis, Andreas -- Dretakis, Emmanuel K -- Gottlob, Irene -- Pieh, Christina -- Traboulsi, Elias I -- Wang, Qing -- Wang, Lejin -- Andrews, Caroline -- Yamada, Koki -- Demer, Joseph L -- Karim, Shaheen -- Alger, Jeffry R -- Geschwind, Daniel H -- Deller, Thomas -- Sicotte, Nancy L -- Nelson, Stanley F -- Baloh, Robert W -- Engle, Elizabeth C -- DC00162/DC/NIDCD NIH HHS/ -- DC05524/DC/NIDCD NIH HHS/ -- EY12498/EY/NEI NIH HHS/ -- EY13583/EY/NEI NIH HHS/ -- EY15298/EY/NEI NIH HHS/ -- EY15311/EY/NEI NIH HHS/ -- MH60233/MH/NIMH NIH HHS/ -- P30 HD 18655/HD/NICHD NIH HHS/ -- R01 EY008313/EY/NEI NIH HHS/ -- R01 EY008313-14/EY/NEI NIH HHS/ -- R01 HL066251/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 2004 Jun 4;304(5676):1509-13. Epub 2004 Apr 22.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurology, University of California, Los Angeles, CA 90095, USA. jjen@ucla.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15105459" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Adult ; Alternative Splicing ; Amino Acid Motifs ; Amino Acid Sequence ; Axons/*physiology ; Evoked Potentials, Motor ; Evoked Potentials, Somatosensory ; Female ; Functional Laterality ; Genetic Linkage ; Humans ; In Situ Hybridization ; Magnetic Resonance Imaging ; Male ; Medulla Oblongata/growth & development/pathology ; Microsatellite Repeats ; Molecular Sequence Data ; Morphogenesis ; Mutation ; Neural Pathways ; Ophthalmoplegia/*genetics/pathology/physiopathology ; Pedigree ; Protein Structure, Tertiary ; Receptors, Immunologic/chemistry/*genetics/*metabolism ; Reverse Transcriptase Polymerase Chain Reaction ; Rhombencephalon/*growth & development/pathology ; Scoliosis/*genetics/pathology/physiopathology ; Sequence Analysis, DNA ; Syndrome
    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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    Plant cuticular lipid export requires an ABC transporter (2004)
    American Association for the Advancement of Science (AAAS)
    Details
    Publikationsdatum: 2004-10-23
    Beschreibung: A waxy protective cuticle coats all primary aerial plant tissues. Its synthesis requires extensive export of lipids from epidermal cells to the plant surface. Arabidopsis cer5 mutants had reduced stem cuticular wax loads and accumulated sheetlike inclusions in the cytoplasm of wax-secreting cells. These inclusions represented abnormal deposits of cuticular wax and resembled inclusions found in a human disorder caused by a defective peroxisomal adenosine triphosphate binding cassette (ABC) transporter. We found that the CER5 gene encodes an ABC transporter localized in the plasma membrane of epidermal cells and conclude that it is required for wax export to the cuticle.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pighin, Jamie A -- Zheng, Huanquan -- Balakshin, Laura J -- Goodman, Ian P -- Western, Tamara L -- Jetter, Reinhard -- Kunst, Ljerka -- Samuels, A Lacey -- New York, N.Y. -- Science. 2004 Oct 22;306(5696):702-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Botany, University of British Columbia (UBC), 6270 University Boulevard, Vancouver, BC V6T 1Z4, Canada.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15499022" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): ATP-Binding Cassette Transporters/chemistry/genetics/*metabolism ; Amino Acid Motifs ; Amino Acid Sequence ; Arabidopsis/cytology/genetics/*metabolism ; Arabidopsis Proteins/chemistry/genetics/*metabolism ; Biological Transport, Active ; Cell Membrane/metabolism ; Cloning, Molecular ; Dimerization ; Genes, Plant ; Inclusion Bodies/ultrastructure ; *Lipid Metabolism ; Microscopy, Electron ; Molecular Sequence Data ; Mutagenesis, Insertional ; Mutation ; Plant Epidermis/cytology/*metabolism/ultrastructure ; Plant Stems/cytology/metabolism/ultrastructure ; Plants, Genetically Modified ; Recombinant Fusion Proteins/metabolism ; Vacuoles/ultrastructure ; Waxes/*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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