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  • 1
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    Susceptibility locus for Alzheimer's disease on chromosome 10 (2000)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2000-12-23
    Description: The apolipoprotein E (APOE) gene is the only genetic risk factor that has so far been linked to risk for late-onset Alzheimer's disease (LOAD). However, 50 percent of Alzheimer's disease cases do not carry an APOE4 allele, suggesting that other risk factors must exist. We performed a two-stage genome-wide screen in sibling pairs with LOAD to detect other susceptibility loci. Here we report evidence for an Alzheimer's disease locus on chromosome 10. Our stage one multipoint lod score (logarithm of the odds ratio for linkage/no linkage) of 2.48 (266 sibling pairs) increased to 3.83 in stage 2 (429 sibling pairs) close to D10S1225 (79 centimorgans). This locus modifies risk for Alzheimer's disease independent of APOE genotype.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Myers, A -- Holmans, P -- Marshall, H -- Kwon, J -- Meyer, D -- Ramic, D -- Shears, S -- Booth, J -- DeVrieze, F W -- Crook, R -- Hamshere, M -- Abraham, R -- Tunstall, N -- Rice, F -- Carty, S -- Lillystone, S -- Kehoe, P -- Rudrasingham, V -- Jones, L -- Lovestone, S -- Perez-Tur, J -- Williams, J -- Owen, M J -- Hardy, J -- Goate, A M -- AG16208/AG/NIA NIH HHS/ -- AG5681/AG/NIA NIH HHS/ -- U24 AG021886/AG/NIA NIH HHS/ -- New York, N.Y. -- Science. 2000 Dec 22;290(5500):2304-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Psychiatry, Washington University School of Medicine, 660 S. Euclid, St. Louis, MO 63110, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11125144" target="_blank"〉PubMed〈/a〉
    Keywords: Age of Onset ; Aged ; Alleles ; Alzheimer Disease/*genetics ; Apolipoprotein E4 ; Apolipoproteins E/genetics ; Chromosomes, Human, Pair 10/*genetics ; Genetic Linkage ; Genetic Markers ; *Genetic Predisposition to Disease ; Genotype ; Humans ; Lod Score ; Nuclear Family ; Odds Ratio
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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  • 2
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    GBP5 promotes NLRP3 inflammasome assembly and immunity in mammals (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-03-31
    Description: Inflammasomes are sensory complexes that alert the immune system to the presence of infection or tissue damage. These complexes assemble NLR (nucleotide binding and oligomerization, leucine-rich repeat) or ALR (absent in melanoma 2-like receptor) proteins to activate caspase-1 cleavage and interleukin (IL)-1beta/IL-18 secretion. Here, we identified a non-NLR/ALR human protein that stimulates inflammasome assembly: guanylate binding protein 5 (GBP5). GBP5 promoted selective NLRP3 inflammasome responses to pathogenic bacteria and soluble but not crystalline inflammasome priming agents. Generation of Gbp5(-/-) mice revealed pronounced caspase-1 and IL-1beta/IL-18 cleavage defects in vitro and impaired host defense and Nlrp3-dependent inflammatory responses in vivo. Thus, GBP5 serves as a unique rheostat for NLRP3 inflammasome activation and extends our understanding of the inflammasome complex beyond its core machinery.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Shenoy, Avinash R -- Wellington, David A -- Kumar, Pradeep -- Kassa, Hilina -- Booth, Carmen J -- Cresswell, Peter -- MacMicking, John D -- R01 AI068041-06/AI/NIAID NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2012 Apr 27;336(6080):481-5. doi: 10.1126/science.1217141. Epub 2012 Mar 29.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Boyer Center for Molecular Medicine, 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/22461501" target="_blank"〉PubMed〈/a〉
    Keywords: Alum Compounds ; Animals ; Apoptosis Regulatory Proteins ; Carrier Proteins/genetics/*metabolism ; Caspase 1/metabolism ; Cell Line ; Cytoskeletal Proteins/metabolism ; GTP-Binding Proteins/chemistry/genetics/*metabolism ; Humans ; Inflammasomes/*metabolism ; Interferon-gamma/immunology ; Interleukin-1beta/secretion ; Lipopolysaccharides/immunology ; Listeria monocytogenes ; Listeriosis/immunology ; Macrophages/immunology/*metabolism ; Mice ; Protein Multimerization ; RNA Interference ; Salmonella typhimurium/immunology ; Uric Acid
    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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  • 3
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    Gut microbiota. Antimicrobial peptide resistance mediates resilience of prominent gut commensals during inflammation (2015)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2015-01-13
    Description: Resilience to host inflammation and other perturbations is a fundamental property of gut microbial communities, yet the underlying mechanisms are not well understood. We have found that human gut microbes from all dominant phyla are resistant to high levels of inflammation-associated antimicrobial peptides (AMPs) and have identified a mechanism for lipopolysaccharide (LPS) modification in the phylum Bacteroidetes that increases AMP resistance by four orders of magnitude. Bacteroides thetaiotaomicron mutants that fail to remove a single phosphate group from their LPS were displaced from the microbiota during inflammation triggered by pathogen infection. These findings establish a mechanism that determines the stability of prominent members of a healthy microbiota during perturbation.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4388331/" 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/PMC4388331/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cullen, T W -- Schofield, W B -- Barry, N A -- Putnam, E E -- Rundell, E A -- Trent, M S -- Degnan, P H -- Booth, C J -- Yu, H -- Goodman, A L -- AI064184/AI/NIAID NIH HHS/ -- AI76322/AI/NIAID NIH HHS/ -- DK089121/DK/NIDDK NIH HHS/ -- DP2 GM105456/GM/NIGMS NIH HHS/ -- GM103574/GM/NIGMS NIH HHS/ -- GM105456/GM/NIGMS NIH HHS/ -- R01 GM103574/GM/NIGMS NIH HHS/ -- T32 AI007640/AI/NIAID NIH HHS/ -- UL1 TR000142/TR/NCATS NIH HHS/ -- New York, N.Y. -- Science. 2015 Jan 9;347(6218):170-5. doi: 10.1126/science.1260580.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Microbial Pathogenesis, Yale University School of Medicine, New Haven, CT 06520, USA. Microbial Sciences Institute, Yale University School of Medicine, New Haven, CT 06520, USA. ; Department of Microbial Pathogenesis, Yale University School of Medicine, New Haven, CT 06520, USA. ; Department of Molecular Biosciences and Institute of Cell and Molecular Biology, University of Texas, Austin, TX 78712, USA. ; Department of Microbiology, University of Illinois at Urbana-Champaign, Urbana, IL 61801, USA. ; Section of Comparative Medicine, Yale University School of Medicine, New Haven, CT 06520, USA. ; Cancer Epidemiology Program, University of Hawaii Cancer Center, Honolulu, HI 96813, USA. ; Department of Microbial Pathogenesis, Yale University School of Medicine, New Haven, CT 06520, USA. Microbial Sciences Institute, Yale University School of Medicine, New Haven, CT 06520, USA. andrew.goodman@yale.edu.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25574022" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antimicrobial Cationic Peptides ; Bacteroides/*drug effects/genetics/physiology ; Colitis/*microbiology ; Drug Resistance, Bacterial/*genetics ; Escherichia coli/drug effects/physiology ; Gastrointestinal Tract/*microbiology ; Germ-Free Life ; Humans ; Lipid A/metabolism ; Mice ; Microbiota/*drug effects/genetics/physiology ; Phosphoric Monoester Hydrolases/genetics/*physiology ; Polymyxin B/*pharmacology ; Symbiosis
    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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