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10.1371/journal.pcbi.1004582 http://scihub22266oqcxt.onion/10.1371/journal.pcbi.1004582 C4642971!4642971 !26562652     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=26562652 &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\26562652 .jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117       PLoS+Comput+Biol 2015 ; 11 (11 ): e1004582 Nephropedia Template TP {{tp|p=26562652 |t=2015. Dynamic Redox Regulation of IL-4 Signaling |pdf=|usr=}}{{26562652 }} gab.com Text Dynamic Redox Regulation of IL-4 Signaling JO: PLoS Comput Biol http://www.kidney.de/pget.php?&tw=1&pmid=26562652 #FOAvip Quantifying the magnitude and dynamics of protein oxidation during cell signaling is technically challenging. Computational modeling provides tractable, quantitative methods to test hypotheses of redox mechanisms that may be simultaneously operative during signal transduction. The interleukin-4 (IL-4) pathway, which has previously been reported to induce reactive oxygen species and oxidation of PTP1B, may be controlled by several other putative mechanisms of redox regulation; widespread proteomic thiol oxidation observed via 2D redox differential gel electrophoresis upon IL-4 treatment suggests more than one redox-sensitive protein implicated in this pathway. Through computational modeling and a model selection strategy that relied on characteristic STAT6 phosphorylation dynamics of IL-4 signaling, we identified reversible protein tyrosine phosphatase (PTP) oxidation as the primary redox regulatory mechanism in the pathway. A systems-level model of IL-4 signaling was developed that integrates synchronous pan-PTP oxidation with ROS-independent mechanisms. The model quantitatively predicts the dynamics of IL-4 signaling over a broad range of new redox conditions, offers novel hypotheses about regulation of JAK/STAT signaling, and provides a framework for interrogating putative mechanisms involving receptor-initiated oxidation. Twit Text FOAVip Dynamic Redox Regulation of IL-4 Signaling ????PLoS Comput Biol http://www.kidney.de/pget.php?&tw=1&pmid=26562652 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26562652 #FOAvip English Wikipedia <ref>{{Cite pmid|26562652 }}</ref> Dynamic Redox Regulation of IL-4 Signaling #MMPMID26562652 Dwivedi G ; Gran MA ; Bagchi P ; Kemp ML PLoS Comput Biol 2015[Nov]; 11 (11 ): e1004582 PMID26562652 show ga Quantifying the magnitude and dynamics of protein oxidation during cell signaling is technically challenging. Computational modeling provides tractable, quantitative methods to test hypotheses of redox mechanisms that may be simultaneously operative during signal transduction. The interleukin-4 (IL-4) pathway, which has previously been reported to induce reactive oxygen species and oxidation of PTP1B, may be controlled by several other putative mechanisms of redox regulation; widespread proteomic thiol oxidation observed via 2D redox differential gel electrophoresis upon IL-4 treatment suggests more than one redox-sensitive protein implicated in this pathway. Through computational modeling and a model selection strategy that relied on characteristic STAT6 phosphorylation dynamics of IL-4 signaling, we identified reversible protein tyrosine phosphatase (PTP) oxidation as the primary redox regulatory mechanism in the pathway. A systems-level model of IL-4 signaling was developed that integrates synchronous pan-PTP oxidation with ROS-independent mechanisms. The model quantitatively predicts the dynamics of IL-4 signaling over a broad range of new redox conditions, offers novel hypotheses about regulation of JAK/STAT signaling, and provides a framework for interrogating putative mechanisms involving receptor-initiated oxidation. |Algorithms [MESH] |Humans [MESH] |Interleukin-4/*metabolism [MESH] |Jurkat Cells [MESH] |Models, Biological [MESH] |Oxidation-Reduction [MESH] |Protein Tyrosine Phosphatases [MESH] |Signal Transduction/*physiology [MESH]Dynamic Redox Regulation of IL-4 Signaling (epmc).pdf DeepDyve Pubget Overpricing