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10.1016/j.sbi.2014.08.011 http://scihub22266oqcxt.onion/10.1016/j.sbi.2014.08.011 C4268015!4268015!25201319     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=25201319&cmd=llinks): Failed to open stream: HTTP request failed! HTTP/1.1 429 Too Many Requests in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 215 Warning: imagejpeg(C:\Inetpub\vhosts\kidney.de\httpdocs\phplern\25201319.jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117       Curr+Opin+Struct+Biol 2014 ; ä (ä): 17-25 Nephropedia Template TP {{tp|p=25201319|t=2014. Structural Mechanisms in NLR inflammasome signaling |pdf=|usr=}}{{25201319}} gab.com Text Structural Mechanisms in NLR inflammasome signaling JO: Curr Opin Struct Biol http://www.kidney.de/pget.php?&tw=1&pmid=25201319 #FOAvip Members of the NOD-like receptor (NLR) family mediate the innate immune response to a wide range of pathogens, tissue damage and other cellular stresses. They achieve modulation of these signals by forming oligomeric signaling platforms, which in analogy to the apoptosome are predicted to adopt a defined oligomeric architecture and will here be referred to as NLR oligomers. Once formed, oligomers of the NLR proteins NLRP3 or NLRC4 ?recruit? the adaptor protein ASC and the effector caspase-1, whereby NLRC4 can also directly interact with caspase-1. This results in large multi-protein assemblies, termed inflammasomes. Ultimately, the formation of these inflammasomes leads to the activation of caspase-1, which then processes the cytokines IL-1? and IL-18 triggering the immune response. Here we review new insights into NLR structure and implications on NLR oligomer formation as well as the nature of multi-protein inflammasomes. Of note, so dubbed ?canonical inflammasomes? [1] can also be triggered by the NLR NLRP1b and the non-NLR protein AIM2, however the most detailed mechanistic information at hand pertains to NLRC4 while NLRP3 represents the quintessential inflammasome trigger. Thus these two NLRs are mainly used as examples in this article. Twit Text FOAVip Structural Mechanisms in NLR inflammasome signaling ????Curr Opin Struct Biol http://www.kidney.de/pget.php?&tw=1&pmid=25201319 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=25201319 #FOAvip English Wikipedia <ref>{{Cite pmid|25201319}}</ref> Structural Mechanisms in NLR inflammasome signaling #MMPMID25201319 Lechtenberg BC; Mace PD; Riedl SJ Curr Opin Struct Biol 2014[Dec]; ä (ä): 17-25 PMID25201319show ga Members of the NOD-like receptor (NLR) family mediate the innate immune response to a wide range of pathogens, tissue damage and other cellular stresses. They achieve modulation of these signals by forming oligomeric signaling platforms, which in analogy to the apoptosome are predicted to adopt a defined oligomeric architecture and will here be referred to as NLR oligomers. Once formed, oligomers of the NLR proteins NLRP3 or NLRC4 ?recruit? the adaptor protein ASC and the effector caspase-1, whereby NLRC4 can also directly interact with caspase-1. This results in large multi-protein assemblies, termed inflammasomes. Ultimately, the formation of these inflammasomes leads to the activation of caspase-1, which then processes the cytokines IL-1? and IL-18 triggering the immune response. Here we review new insights into NLR structure and implications on NLR oligomer formation as well as the nature of multi-protein inflammasomes. Of note, so dubbed ?canonical inflammasomes? [1] can also be triggered by the NLR NLRP1b and the non-NLR protein AIM2, however the most detailed mechanistic information at hand pertains to NLRC4 while NLRP3 represents the quintessential inflammasome trigger. Thus these two NLRs are mainly used as examples in this article. äStructural Mechanisms in NLR inflammasome signaling (epmc).pdf DeepDyve Pubget Overpricing