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10.1371/journal.pone.0136633 http://scihub22266oqcxt.onion/10.1371/journal.pone.0136633 C4552301!4552301!26312487     free     free     free Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       PLoS+One 2015 ; 10 (8): ä Nephropedia Template TP {{tp|p=26312487|t=2015. Activation of p38 Mitogen-Activated Protein Kinase in Gaucher?s Disease |pdf=|usr=}}{{26312487}} gab.com Text Activation of p38 Mitogen-Activated Protein Kinase in Gaucher s Disease JO: PLoS One http://www.kidney.de/pget.php?&tw=1&pmid=26312487 #FOAvip Gaucher?s disease is caused by defects in acid ?-glucosidase 1 (GBA1) and has been also proposed as an inflammatory disease. GBA1 cleaves glucosylceramide to form ceramide, an established bioactive lipid, and defects in GBA1 lead to aberrant accumulation in glucosylceramide and insufficient formation of ceramide. We investigated if the pro-inflammatory kinase p38 is activated in Gaucher?s disease, since ceramide has been proposed to suppress p38 activation. Three Gaucher?s disease mouse models were employed, and p38 was found to be activated in lung and liver tissues of all Gaucher?s disease mice. Most interestingly, neuronopathic Gaucher?s disease type mice, but not non-neuronopathic ones, displayed significant activation of p38 and up-regulation of p38-inducible proinflammatory cytokines in brain tissues. In addition, all type of Gaucher?s disease mice also showed increases in serum IL-6. As cellular signalling is believed to represent an in vivo inflammatory phenotype in Gaucher?s disease, activation of p38 and possibly its-associated formation of proinflammatory cytokines were assessed in fibroblasts established from neuronopathic Gaucher?s disease mice. In mouse Gaucher?s disease cells, p38 activation and IL-6 formation by TNF-? treatment were enhanced as compared to those of wild type. Furthermore, human fibroblasts from Gaucher?s disease patients also displayed increases in p38 activation and IL-6 formation as comparison to healthy counterpart. These results raise the potential that proinflammatory responses such as p38 activation and IL-6 formation are augmented in Gaucher?s disease. Twit Text FOAVip Activation of p38 Mitogen-Activated Protein Kinase in Gaucher s Disease ????PLoS One http://www.kidney.de/pget.php?&tw=1&pmid=26312487 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26312487 #FOAvip English Wikipedia <ref>{{Cite pmid|26312487}}</ref> Activation of p38 Mitogen-Activated Protein Kinase in Gaucher?s Disease #MMPMID26312487 Kitatani K; Wada M; Perry D; Usui T; Sun Y; Obeid LM; Yaegashi N; Grabowski GA; Hannun YA PLoS One 2015[]; 10 (8): ä PMID26312487show ga Gaucher?s disease is caused by defects in acid ?-glucosidase 1 (GBA1) and has been also proposed as an inflammatory disease. GBA1 cleaves glucosylceramide to form ceramide, an established bioactive lipid, and defects in GBA1 lead to aberrant accumulation in glucosylceramide and insufficient formation of ceramide. We investigated if the pro-inflammatory kinase p38 is activated in Gaucher?s disease, since ceramide has been proposed to suppress p38 activation. Three Gaucher?s disease mouse models were employed, and p38 was found to be activated in lung and liver tissues of all Gaucher?s disease mice. Most interestingly, neuronopathic Gaucher?s disease type mice, but not non-neuronopathic ones, displayed significant activation of p38 and up-regulation of p38-inducible proinflammatory cytokines in brain tissues. In addition, all type of Gaucher?s disease mice also showed increases in serum IL-6. As cellular signalling is believed to represent an in vivo inflammatory phenotype in Gaucher?s disease, activation of p38 and possibly its-associated formation of proinflammatory cytokines were assessed in fibroblasts established from neuronopathic Gaucher?s disease mice. In mouse Gaucher?s disease cells, p38 activation and IL-6 formation by TNF-? treatment were enhanced as compared to those of wild type. Furthermore, human fibroblasts from Gaucher?s disease patients also displayed increases in p38 activation and IL-6 formation as comparison to healthy counterpart. These results raise the potential that proinflammatory responses such as p38 activation and IL-6 formation are augmented in Gaucher?s disease. äActivation of p38 Mitogen-Activated Protein Kinase in Gaucher?s Diseas(epmc).pdf DeepDyve Pubget Overpricing