<?xml version="1.0" encoding="UTF-8"?><xml><records><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Saleh, Maya</style></author><author><style face="normal" font="default" size="100%">Vaillancourt, John P</style></author><author><style face="normal" font="default" size="100%">Graham, Rona K</style></author><author><style face="normal" font="default" size="100%">Huyck, Matthew</style></author><author><style face="normal" font="default" size="100%">Srinivasula, Srinivasa M</style></author><author><style face="normal" font="default" size="100%">Alnemri, Emad S</style></author><author><style face="normal" font="default" size="100%">Steinberg, Martin H</style></author><author><style face="normal" font="default" size="100%">Nolan, Vikki</style></author><author><style face="normal" font="default" size="100%">Baldwin, Clinton T</style></author><author><style face="normal" font="default" size="100%">Hotchkiss, Richard S</style></author><author><style face="normal" font="default" size="100%">Buchman, Timothy G</style></author><author><style face="normal" font="default" size="100%">Zehnbauer, Barbara A</style></author><author><style face="normal" font="default" size="100%">Hayden, Michael R</style></author><author><style face="normal" font="default" size="100%">Farrer, Lindsay A</style></author><author><style face="normal" font="default" size="100%">Roy, Sophie</style></author><author><style face="normal" font="default" size="100%">Nicholson, Donald W</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Differential modulation of endotoxin responsiveness by human caspase-12 polymorphisms.</style></title><secondary-title><style face="normal" font="default" size="100%">Nature</style></secondary-title><alt-title><style face="normal" font="default" size="100%">Nature</style></alt-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">Africa</style></keyword><keyword><style  face="normal" font="default" size="100%">African Americans</style></keyword><keyword><style  face="normal" font="default" size="100%">Alzheimer Disease</style></keyword><keyword><style  face="normal" font="default" size="100%">Animals</style></keyword><keyword><style  face="normal" font="default" size="100%">Apoptosis</style></keyword><keyword><style  face="normal" font="default" size="100%">Base Sequence</style></keyword><keyword><style  face="normal" font="default" size="100%">Case-Control Studies</style></keyword><keyword><style  face="normal" font="default" size="100%">Caspase 12</style></keyword><keyword><style  face="normal" font="default" size="100%">Caspases</style></keyword><keyword><style  face="normal" font="default" size="100%">Concanavalin A</style></keyword><keyword><style  face="normal" font="default" size="100%">Cytokines</style></keyword><keyword><style  face="normal" font="default" size="100%">Endoplasmic Reticulum</style></keyword><keyword><style  face="normal" font="default" size="100%">Gene Frequency</style></keyword><keyword><style  face="normal" font="default" size="100%">Genetic Predisposition to Disease</style></keyword><keyword><style  face="normal" font="default" size="100%">Genotype</style></keyword><keyword><style  face="normal" font="default" size="100%">Humans</style></keyword><keyword><style  face="normal" font="default" size="100%">Inflammation</style></keyword><keyword><style  face="normal" font="default" size="100%">Lipopolysaccharides</style></keyword><keyword><style  face="normal" font="default" size="100%">NF-kappa B</style></keyword><keyword><style  face="normal" font="default" size="100%">Polymorphism, Single Nucleotide</style></keyword><keyword><style  face="normal" font="default" size="100%">Primates</style></keyword><keyword><style  face="normal" font="default" size="100%">Sepsis</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">2004</style></year><pub-dates><date><style  face="normal" font="default" size="100%">2004 May 6</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">429</style></volume><pages><style face="normal" font="default" size="100%">75-9</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;Caspases mediate essential key proteolytic events in inflammatory cascades and the apoptotic cell death pathway. Human caspases functionally segregate into two distinct subfamilies: those involved in cytokine maturation (caspase-1, -4 and -5) and those involved in cellular apoptosis (caspase-2, -3, -6, -7, -8, -9 and -10). Although caspase-12 is phylogenetically related to the cytokine maturation caspases, in mice it has been proposed as a mediator of apoptosis induced by endoplasmic reticulum stress including amyloid-beta cytotoxicity, suggesting that it might contribute to the pathogenesis of Alzheimer&#039;s disease. Here we show that a single nucleotide polymorphism in caspase-12 in humans results in the synthesis of either a truncated protein (Csp12-S) or a full-length caspase proenzyme (Csp12-L). The read-through single nucleotide polymorphism encoding Csp12-L is confined to populations of African descent and confers hypo-responsiveness to lipopolysaccharide-stimulated cytokine production in ex vivo whole blood, but has no significant effect on apoptotic sensitivity. In a preliminary study, we find that the frequency of the Csp12-L allele is increased in African American individuals with severe sepsis. Thus, Csp12-L attenuates the inflammatory and innate immune response to endotoxins and in doing so may constitute a risk factor for developing sepsis.&lt;/p&gt;
</style></abstract><issue><style face="normal" font="default" size="100%">6987</style></issue><custom1><style face="normal" font="default" size="100%">&lt;p&gt;http://www.ncbi.nlm.nih.gov/pubmed/15129283?dopt=Abstract&lt;/p&gt;
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