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10.1016/j.chom.2017.04.001 http://scihub22266oqcxt.onion/10.1016/j.chom.2017.04.001 C5478421!5478421!28494242     free     free     free Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Cell+Host+Microbe 2017 ; 21 (5): 611-618.e5 Nephropedia Template TP {{tp|p=28494242|t=2017. Pseudomonas aeruginosa effector ExoS inhibits ROS production in human neutrophils |pdf=|usr=}}{{28494242}} gab.com Text Pseudomonas aeruginosa effector ExoS inhibits ROS production in human neutrophils JO: Cell Host Microbe http://www.kidney.de/pget.php?&tw=1&pmid=28494242 #FOAvip Neutrophils are the first line of defense against bacterial infections, and the generation of reactive oxygen species is a key part of their arsenal. Pathogens use detoxification systems to avoid the bactericidal effects of reactive oxygen species. Here we demonstrate that the Gram-negative pathogen Pseudomonas aeruginosa is susceptible to reactive oxygen species but actively blocks the reactive oxygen species burst using two type III secreted effector proteins, ExoS and ExoT. ExoS ADP-ribosylates Ras and prevents it from interacting with and activating phosphoinositol-3-kinase (PI3K), which is required to stimulate the phagocytic NADPH-oxidase that generates reactive oxygen species. ExoT also affects PI3K signaling via its ADP-ribosyltransferase activity but does not act directly on Ras. A non-ribosylatable version of Ras restores reactive oxygen species production and results in increased bacterial killing. These findings demonstrate that subversion of the host innate immune response requires ExoS-mediated ADP-ribosylation of Ras in neutrophils. Twit Text FOAVip Pseudomonas aeruginosa effector ExoS inhibits ROS production in human neutrophils ????Cell Host Microbe http://www.kidney.de/pget.php?&tw=1&pmid=28494242 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=28494242 #FOAvip English Wikipedia <ref>{{Cite pmid|28494242}}</ref> Pseudomonas aeruginosa effector ExoS inhibits ROS production in human neutrophils #MMPMID28494242 Vareechon C; Zmina SE; Karmakar M; Pearlman E; Rietsch A Cell Host Microbe 2017[May]; 21 (5): 611-618.e5 PMID28494242show ga Neutrophils are the first line of defense against bacterial infections, and the generation of reactive oxygen species is a key part of their arsenal. Pathogens use detoxification systems to avoid the bactericidal effects of reactive oxygen species. Here we demonstrate that the Gram-negative pathogen Pseudomonas aeruginosa is susceptible to reactive oxygen species but actively blocks the reactive oxygen species burst using two type III secreted effector proteins, ExoS and ExoT. ExoS ADP-ribosylates Ras and prevents it from interacting with and activating phosphoinositol-3-kinase (PI3K), which is required to stimulate the phagocytic NADPH-oxidase that generates reactive oxygen species. ExoT also affects PI3K signaling via its ADP-ribosyltransferase activity but does not act directly on Ras. A non-ribosylatable version of Ras restores reactive oxygen species production and results in increased bacterial killing. These findings demonstrate that subversion of the host innate immune response requires ExoS-mediated ADP-ribosylation of Ras in neutrophils. äPseudomonas aeruginosa effector ExoS inhibits ROS production in human (epmc).pdf DeepDyve Pubget Overpricing