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10.1038/s41467-017-01676-0 http://scihub22266oqcxt.onion/10.1038/s41467-017-01676-0 C5691069!5691069!29146903     free     free     free Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Nat+Commun 2017 ; 8 (ä): ä Nephropedia Template TP {{tp|p=29146903|t=2017. Wiskott-Aldrich syndrome protein regulates autophagy and inflammasome activity in innate immune cells |pdf=|usr=}}{{29146903}} gab.com Text Wiskott-Aldrich syndrome protein regulates autophagy and inflammasome activity in innate immune cells JO: Nat Commun http://www.kidney.de/pget.php?&tw=1&pmid=29146903 #FOAvip Dysregulation of autophagy and inflammasome activity contributes to the development of auto-inflammatory diseases. Emerging evidence highlights the importance of the actin cytoskeleton in modulating inflammatory responses. Here we show that deficiency of Wiskott?Aldrich syndrome protein (WASp), which signals to the actin cytoskeleton, modulates autophagy and inflammasome function. In a model of sterile inflammation utilizing TLR4 ligation followed by ATP or nigericin treatment, inflammasome activation is enhanced in monocytes from WAS patients and in WAS-knockout mouse dendritic cells. In ex vivo models of enteropathogenic Escherichia coli and Shigella flexneri infection, WASp deficiency causes defective bacterial clearance, excessive inflammasome activation and host cell death that are associated with dysregulated septin cage-like formation, impaired autophagic p62/LC3 recruitment and defective formation of canonical autophagosomes. Taken together, we propose that dysregulation of autophagy and inflammasome activities contribute to the autoinflammatory manifestations of WAS, thereby identifying potential targets for therapeutic intervention. Twit Text FOAVip Wiskott-Aldrich syndrome protein regulates autophagy and inflammasome activity in innate immune cells ????Nat Commun http://www.kidney.de/pget.php?&tw=1&pmid=29146903 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=29146903 #FOAvip English Wikipedia <ref>{{Cite pmid|29146903}}</ref> Wiskott-Aldrich syndrome protein regulates autophagy and inflammasome activity in innate immune cells #MMPMID29146903 Lee PP; Lobato-Márquez D; Pramanik N; Sirianni A; Daza-Cajigal V; Rivers E; Cavazza A; Bouma G; Moulding D; Hultenby K; Westerberg LS; Hollinshead M; Lau YL; Burns SO; Mostowy S; Bajaj-Elliott M; Thrasher AJ Nat Commun 2017[]; 8 (ä): ä PMID29146903show ga Dysregulation of autophagy and inflammasome activity contributes to the development of auto-inflammatory diseases. Emerging evidence highlights the importance of the actin cytoskeleton in modulating inflammatory responses. Here we show that deficiency of Wiskott?Aldrich syndrome protein (WASp), which signals to the actin cytoskeleton, modulates autophagy and inflammasome function. In a model of sterile inflammation utilizing TLR4 ligation followed by ATP or nigericin treatment, inflammasome activation is enhanced in monocytes from WAS patients and in WAS-knockout mouse dendritic cells. In ex vivo models of enteropathogenic Escherichia coli and Shigella flexneri infection, WASp deficiency causes defective bacterial clearance, excessive inflammasome activation and host cell death that are associated with dysregulated septin cage-like formation, impaired autophagic p62/LC3 recruitment and defective formation of canonical autophagosomes. Taken together, we propose that dysregulation of autophagy and inflammasome activities contribute to the autoinflammatory manifestations of WAS, thereby identifying potential targets for therapeutic intervention. äWiskott-Aldrich syndrome protein regulates autophagy and inflammasome (epmc).pdf DeepDyve Pubget Overpricing