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  • Articles  (197)
  • Cell Line  (197)
  • American Association for the Advancement of Science (AAAS)  (197)
  • Springer
  • 2005-2009  (108)
  • 1985-1989  (89)
  • Computer Science  (197)
  • Electrical Engineering, Measurement and Control Technology
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  • Articles  (197)
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  • American Association for the Advancement of Science (AAAS)  (197)
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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
    Publication Date: 2007-09-18
    Description: 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〉
    Keywords: 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
    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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    Ethics. The ISSCR guidelines for human embryonic stem cell research (2007)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2007-02-03
    Description: 〈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〉
    Keywords: 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
    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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    Neurotoxicity of a fragment of the amyloid precursor associated with Alzheimer's disease (1989)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1989-07-28
    Description: Amyloid deposition in senile plaques and the cerebral vasculature is a marker of Alzheimer's disease. Whether amyloid itself contributes to the neurodegenerative process or is simply a by-product of that process is unknown. Pheochromocytoma (PC12) and fibroblast (NIH 3T3) cell lines were transfected with portions of the gene for the human amyloid precursor protein. Stable PC12 cell transfectants expressing a specific amyloid-containing fragment of the precursor protein gradually degenerated when induced to differentiate into neuronal cells with nerve growth factor. Conditioned medium from these cells was toxic to neurons in primary hippocampal cultures, and the toxic agent could be removed by immunoabsorption with an antibody directed against the amyloid polypeptide. Thus, a peptide derived from the amyloid precursor may be neurotoxic.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Yankner, B A -- Dawes, L R -- Fisher, S -- Villa-Komaroff, L -- Oster-Granite, M L -- Neve, R L -- HD 18655/HD/NICHD NIH HHS/ -- HD 18658/HD/NICHD NIH HHS/ -- NS 01240/NS/NINDS NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1989 Jul 28;245(4916):417-20.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurology, Harvard Medical School, Boston, MA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2474201" target="_blank"〉PubMed〈/a〉
    Keywords: Alzheimer Disease/*etiology/pathology ; Amyloid/genetics/*physiology ; Blotting, Northern ; Cell Line ; Fibroblasts ; Gene Expression Regulation ; Humans ; Immunoblotting ; Neurons/pathology ; Nucleic Acid Hybridization ; Pheochromocytoma ; Protein Precursors/genetics/*physiology ; RNA/analysis/genetics ; Restriction Mapping ; Transfection ; Tumor Cells, Cultured
    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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    Wnt3a-mediated formation of phosphatidylinositol 4,5-bisphosphate regulates LRP6 phosphorylation (2008)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2008-09-06
    Description: 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〉
    Keywords: 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
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 5
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    HIN-200 proteins regulate caspase activation in response to foreign cytoplasmic DNA (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-01-10
    Description: The mammalian innate immune system is activated by foreign nucleic acids. Detection of double-stranded DNA (dsDNA) in the cytoplasm triggers characteristic antiviral responses and macrophage cell death. Cytoplasmic dsDNA rapidly activated caspase 3 and caspase 1 in bone marrow-derived macrophages. We identified the HIN-200 family member and candidate lupus susceptibility factor, p202, as a dsDNA binding protein that bound stably and rapidly to transfected DNA. Knockdown studies showed p202 to be an inhibitor of DNA-induced caspase activation. Conversely, the related pyrin domain-containing HIN-200 factor, AIM2 (p210), was required for caspase activation by cytoplasmic dsDNA. This work indicates that HIN-200 proteins can act as pattern recognition receptors mediating responses to cytoplasmic dsDNA.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Roberts, Tara L -- Idris, Adi -- Dunn, Jasmyn A -- Kelly, Greg M -- Burnton, Carol M -- Hodgson, Samantha -- Hardy, Lani L -- Garceau, Valerie -- Sweet, Matthew J -- Ross, Ian L -- Hume, David A -- Stacey, Katryn J -- New York, N.Y. -- Science. 2009 Feb 20;323(5917):1057-60. doi: 10.1126/science.1169841. Epub 2009 Jan 8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉The University of Queensland, Institute for Molecular Bioscience, QLD 4072, Australia.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19131592" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Caspase 1/*metabolism ; Caspase 3/*metabolism ; Cell Line ; Cytoplasm/*metabolism ; DNA/immunology/*metabolism ; DNA-Binding Proteins/isolation & purification/metabolism ; Enzyme Activation ; Immunity, Innate ; Intracellular Signaling Peptides and Proteins/chemistry/genetics/isolation & ; purification/*metabolism ; Macrophages/immunology/*metabolism ; Membrane Proteins/chemistry/genetics/*metabolism ; Mice ; Mice, Inbred Strains ; RNA, Small Interfering ; Receptors, Pattern Recognition/*metabolism ; Symporters ; Transfection
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 6
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    Purification, cloning, and expression of ciliary neurotrophic factor (CNTF) (1989)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1989-11-24
    Description: Ciliary neurotrophic factor (CNTF) is one of a small number of proteins with neurotrophic activities distinct from nerve growth factor (NGF). CNTF has now been purified and cloned and the primary structure of CNTF from rabbit sciatic nerve has been determined. Biologically active CNTF has been transiently expressed from a rabbit complementary DNA clone. CNTF is a neural effector without significant sequence homologies to any previously reported protein.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lin, L F -- Mismer, D -- Lile, J D -- Armes, L G -- Butler, E T 3rd -- Vannice, J L -- Collins, F -- New York, N.Y. -- Science. 1989 Nov 24;246(4933):1023-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Protein Chemistry Group, Synergen, Inc., Boulder, CO 80301.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2587985" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Cell Line ; Ciliary Neurotrophic Factor ; Cloning, Molecular ; DNA/genetics ; Molecular Sequence Data ; Nerve Growth Factors/*genetics ; Nerve Tissue Proteins/biosynthesis/*genetics/isolation & purification ; Rabbits ; Recombinant Proteins/biosynthesis ; Sciatic Nerve/metabolism ; Transfection
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 7
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    Human CHN1 mutations hyperactivate alpha2-chimaerin and cause Duane's retraction syndrome (2008)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2008-07-26
    Description: Duane's retraction syndrome (DRS) is a complex congenital eye movement disorder caused by aberrant innervation of the extraocular muscles by axons of brainstem motor neurons. Studying families with a variant form of the disorder (DURS2-DRS), we have identified causative heterozygous missense mutations in CHN1, a gene on chromosome 2q31 that encodes alpha2-chimaerin, a Rac guanosine triphosphatase-activating protein (RacGAP) signaling protein previously implicated in the pathfinding of corticospinal axons in mice. We found that these are gain-of-function mutations that increase alpha2-chimaerin RacGAP activity in vitro. Several of the mutations appeared to enhance alpha2-chimaerin translocation to the cell membrane or enhance its ability to self-associate. Expression of mutant alpha2-chimaerin constructs in chick embryos resulted in failure of oculomotor axons to innervate their target extraocular muscles. We conclude that alpha2-chimaerin has a critical developmental function in ocular motor axon pathfinding.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2593867/" 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/PMC2593867/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Miyake, Noriko -- Chilton, John -- Psatha, Maria -- Cheng, Long -- Andrews, Caroline -- Chan, Wai-Man -- Law, Krystal -- Crosier, Moira -- Lindsay, Susan -- Cheung, Michelle -- Allen, James -- Gutowski, Nick J -- Ellard, Sian -- Young, Elizabeth -- Iannaccone, Alessandro -- Appukuttan, Binoy -- Stout, J Timothy -- Christiansen, Stephen -- Ciccarelli, Maria Laura -- Baldi, Alfonso -- Campioni, Mara -- Zenteno, Juan C -- Davenport, Dominic -- Mariani, Laura E -- Sahin, Mustafa -- Guthrie, Sarah -- Engle, Elizabeth C -- G9900837/Medical Research Council/United Kingdom -- G9900989/Medical Research Council/United Kingdom -- R01 EY015298/EY/NEI NIH HHS/ -- R01 EY015298-01/EY/NEI NIH HHS/ -- R01 EY015298-02/EY/NEI NIH HHS/ -- R01 EY015298-03/EY/NEI NIH HHS/ -- R01 EY015298-04/EY/NEI NIH HHS/ -- R01 EY015298-05/EY/NEI NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2008 Aug 8;321(5890):839-43. doi: 10.1126/science.1156121. Epub 2008 Jul 24.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine (Genetics), Children's Hospital Boston, Boston, MA 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18653847" target="_blank"〉PubMed〈/a〉
    Keywords: Abducens Nerve/abnormalities ; Amino Acid Sequence ; Animals ; Axons/physiology ; Cell Line ; Cell Membrane/metabolism ; Chick Embryo ; Chimerin 1/chemistry/*genetics/*metabolism ; Duane Retraction Syndrome/*genetics ; Female ; Gene Expression Profiling ; Heterozygote ; Humans ; Male ; Molecular Sequence Data ; *Mutation, Missense ; Oculomotor Muscles/embryology/innervation/metabolism ; Oculomotor Nerve/abnormalities/embryology ; Pedigree
    Print ISSN: 0036-8075
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  • 8
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    Analysis of Drosophila segmentation network identifies a JNK pathway factor overexpressed in kidney cancer (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-01-24
    Description: We constructed a large-scale functional network model in Drosophila melanogaster built around two key transcription factors involved in the process of embryonic segmentation. Analysis of the model allowed the identification of a new role for the ubiquitin E3 ligase complex factor SPOP. In Drosophila, the gene encoding SPOP is a target of segmentation transcription factors. Drosophila SPOP mediates degradation of the Jun kinase phosphatase Puckered, thereby inducing tumor necrosis factor (TNF)/Eiger-dependent apoptosis. In humans, we found that SPOP plays a conserved role in TNF-mediated JNK signaling and was highly expressed in 99% of clear cell renal cell carcinomas (RCCs), the most prevalent form of kidney cancer. SPOP expression distinguished histological subtypes of RCC and facilitated identification of clear cell RCC as the primary tumor for metastatic lesions.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2756524/" 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/PMC2756524/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Liu, Jiang -- Ghanim, Murad -- Xue, Lei -- Brown, Christopher D -- Iossifov, Ivan -- Angeletti, Cesar -- Hua, Sujun -- Negre, Nicolas -- Ludwig, Michael -- Stricker, Thomas -- Al-Ahmadie, Hikmat A -- Tretiakova, Maria -- Camp, Robert L -- Perera-Alberto, Montse -- Rimm, David L -- Xu, Tian -- Rzhetsky, Andrey -- White, Kevin P -- P50 GM081892/GM/NIGMS NIH HHS/ -- P50 GM081892-01A1/GM/NIGMS NIH HHS/ -- R01 HG003012/HG/NHGRI NIH HHS/ -- R01 HG003012-04/HG/NHGRI NIH HHS/ -- UL1 RR024999/RR/NCRR NIH HHS/ -- UL1 RR024999-02/RR/NCRR NIH HHS/ -- New York, N.Y. -- Science. 2009 Feb 27;323(5918):1218-22. doi: 10.1126/science.1157669. Epub 2009 Jan 22.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute for Genomics and Systems Biology, University of Chicago and Argonne National Laboratory, Chicago, IL 60637, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19164706" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Apoptosis ; Carcinoma, Renal Cell/*genetics/metabolism ; Cell Line ; Compound Eye, Arthropod/embryology/metabolism ; Drosophila Proteins/genetics/metabolism ; Drosophila melanogaster/embryology/*genetics/metabolism ; Embryo, Nonmammalian/metabolism ; Fushi Tarazu Transcription Factors/genetics/metabolism ; Gene Expression Profiling ; Gene Regulatory Networks ; Homeodomain Proteins/genetics/metabolism ; Humans ; Janus Kinases/*metabolism ; Kidney/metabolism ; Kidney Neoplasms/*genetics/metabolism ; Molecular Sequence Data ; Nervous System/embryology ; Nuclear Proteins/*genetics/metabolism ; Phosphoprotein Phosphatases/metabolism ; Phosphorylation ; Repressor Proteins/*genetics/metabolism ; *Signal Transduction ; Transcription Factors/genetics/metabolism ; Transcription, Genetic
    Print ISSN: 0036-8075
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  • 9
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    Treatment of autoimmune neuroinflammation with a synthetic tryptophan metabolite (2005)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2005-11-08
    Description: Local catabolism of the amino acid tryptophan (Trp) by indoleamine 2,3-dioxygenase (IDO) is considered an important mechanism of regulating T cell immunity. We show that IDO transcription was increased when myelin-specific T cells were stimulated with tolerogenic altered self-peptides. Catabolites of Trp suppressed proliferation of myelin-specific T cells and inhibited production of proinflammatory T helper-1 (T(H)1) cytokines. N-(3,4,-Dimethoxycinnamoyl) anthranilic acid (3,4-DAA), an orally active synthetic derivative of the Trp metabolite anthranilic acid, reversed paralysis in mice with experimental autoimmune encephalomyelitis, a model of multiple sclerosis (MS). Trp catabolites and their derivatives offer a new strategy for treating T(H)1-mediated autoimmune diseases such as MS.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Platten, Michael -- Ho, Peggy P -- Youssef, Sawsan -- Fontoura, Paulo -- Garren, Hideki -- Hur, Eun Mi -- Gupta, Rohit -- Lee, Lowen Y -- Kidd, Brian A -- Robinson, William H -- Sobel, Raymond A -- Selley, Michael L -- Steinman, Lawrence -- New York, N.Y. -- Science. 2005 Nov 4;310(5749):850-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurology and Neurological Sciences, Beckman Center for Molecular Medicine, Stanford University, Stanford, CA 94305, USA. michael.platten@uni-tuebingen.de〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16272121" target="_blank"〉PubMed〈/a〉
    Keywords: Adoptive Transfer ; Animals ; Anti-Inflammatory Agents, Non-Steroidal/administration & ; dosage/pharmacology/*therapeutic use ; Antigen-Presenting Cells/drug effects/immunology ; Brain/pathology ; Cell Line ; Cytokines/biosynthesis ; Disease Models, Animal ; Encephalomyelitis, Autoimmune, Experimental/*drug therapy/immunology ; Female ; Histocompatibility Antigens Class II/immunology/metabolism ; Immune Tolerance ; Immunosuppressive Agents/pharmacology/therapeutic use ; Indoleamine-Pyrrole 2,3,-Dioxygenase/genetics/metabolism ; Interferon-gamma/immunology ; Lymphocyte Activation ; Mice ; Mice, Transgenic ; Microglia/drug effects/immunology ; Multiple Sclerosis/drug therapy/immunology/pathology ; Myelin Proteins/immunology ; Signal Transduction ; Spinal Cord/pathology ; T-Lymphocytes/immunology ; Th1 Cells/immunology ; Th2 Cells/immunology ; Tryptophan/*metabolism ; ortho-Aminobenzoates/administration & dosage/pharmacology/*therapeutic use
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  • 10
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    An aneuploid mouse strain carrying human chromosome 21 with Down syndrome phenotypes (2005)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2005-09-24
    Description: Aneuploidies are common chromosomal defects that result in growth and developmental deficits and high levels of lethality in humans. To gain insight into the biology of aneuploidies, we manipulated mouse embryonic stem cells and generated a trans-species aneuploid mouse line that stably transmits a freely segregating, almost complete human chromosome 21 (Hsa21). This "transchromosomic" mouse line, Tc1, is a model of trisomy 21, which manifests as Down syndrome (DS) in humans, and has phenotypic alterations in behavior, synaptic plasticity, cerebellar neuronal number, heart development, and mandible size that relate to human DS. Transchromosomic mouse lines such as Tc1 may represent useful genetic tools for dissecting other human aneuploidies.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1378183/" 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/PMC1378183/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉O'Doherty, Aideen -- Ruf, Sandra -- Mulligan, Claire -- Hildreth, Victoria -- Errington, Mick L -- Cooke, Sam -- Sesay, Abdul -- Modino, Sonie -- Vanes, Lesley -- Hernandez, Diana -- Linehan, Jacqueline M -- Sharpe, Paul T -- Brandner, Sebastian -- Bliss, Timothy V P -- Henderson, Deborah J -- Nizetic, Dean -- Tybulewicz, Victor L J -- Fisher, Elizabeth M C -- 076700/Wellcome Trust/United Kingdom -- MC_U117512674/Medical Research Council/United Kingdom -- New York, N.Y. -- Science. 2005 Sep 23;309(5743):2033-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurodegenerative Disease, Institute of Neurology, Queen Square, London WC1N 3BG, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16179473" target="_blank"〉PubMed〈/a〉
    Keywords: *Aneuploidy ; Animals ; Behavior, Animal ; Brain/pathology ; Cell Count ; Cell Line ; Chimera ; *Chromosomes, Human, Pair 21 ; *Disease Models, Animal ; *Down Syndrome/genetics/physiopathology ; Embryo, Mammalian/cytology ; Facial Bones/pathology ; Female ; Gene Expression ; *Genetic Engineering ; Genetic Markers ; Heart Defects, Congenital/embryology ; Hippocampus/physiopathology ; Humans ; Long-Term Potentiation ; Lymphocyte Activation ; Male ; Maze Learning ; Memory ; Mice ; Mice, Inbred Strains ; *Mice, Transgenic ; Neurons/cytology ; Oligonucleotide Array Sequence Analysis ; Phenotype ; Skull/pathology ; Stem Cells ; Synaptic Transmission ; T-Lymphocytes/immunology
    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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