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10.1016/j.bbrc.2014.09.068 http://scihub22266oqcxt.onion/10.1016/j.bbrc.2014.09.068 C4278587!4278587 !25261722     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=25261722 &cmd=llinks): Failed to open stream: HTTP request failed! 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Inflammatory cytokines, interleukin-1 beta and tumor necrosis factor-alpha, upregulated in glioblastoma multiforme, raise the levels of CRYAB in exosomes secreted by U373 glioma cells |pdf=|usr=}}{{25261722 }} gab.com Text Inflammatory cytokines, interleukin-1 beta and tumor necrosis factor-alpha, upregulated in glioblastoma multiforme, raise the levels of CRYAB in exosomes secreted by U373 glioma cells JO: Biochem Biophys Res Commun http://www.kidney.de/pget.php?&tw=1&pmid=25261722 #FOAvip In the brain, levels of inflammatory cytokines, interleukin-1 beta (IL-1?) and tumor necrosis factor-alpha (TNF-?), are elevated under traumatic brain injury, neuroinflammatory conditions and glioblastoma multiforme (GBM). In GBM, the levels of small heat shock protein, CRYAB (HspB5) are also reported to be elevated, where it has been shown to exert anti-apoptotic activity. Interestingly, CRYAB is secreted via exosomes by various cells. In order to understand the relation between inflammatory cytokines and CRYAB, U373 glioma cells, were stimulated with proinflammatory cytokines, IL-1? and TNF-?, and their effect on CRYAB levels in cells and secreted exosomes was studied. Our results show that U373 cells produce and secrete CRYAB via exosomes and that stimulation with IL-1? and TNF-? significantly increase the levels of CRYAB in not only the cells but also in the secreted exosomes. In addition, cytokine stimulation of U373 cells brings about changes in the secreted exosomal proteome, many of which are involved in cancer progression. Twit Text FOAVip Inflammatory cytokines, interleukin-1 beta and tumor necrosis factor-alpha, upregulated in glioblastoma multiforme, raise the levels of CRYAB in exosomes secreted by U373 glioma cells ????Biochem Biophys Res Commun http://www.kidney.de/pget.php?&tw=1&pmid=25261722 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=25261722 #FOAvip English Wikipedia <ref>{{Cite pmid|25261722 }}</ref> Inflammatory cytokines, interleukin-1 beta and tumor necrosis factor-alpha, upregulated in glioblastoma multiforme, raise the levels of CRYAB in exosomes secreted by U373 glioma cells #MMPMID25261722 Kore RA ; Abraham EC Biochem Biophys Res Commun 2014[Oct]; 453 (3 ): 326-31 PMID25261722 show ga In the brain, levels of inflammatory cytokines, interleukin-1 beta (IL-1?) and tumor necrosis factor-alpha (TNF-?), are elevated under traumatic brain injury, neuroinflammatory conditions and glioblastoma multiforme (GBM). In GBM, the levels of small heat shock protein, CRYAB (HspB5) are also reported to be elevated, where it has been shown to exert anti-apoptotic activity. Interestingly, CRYAB is secreted via exosomes by various cells. In order to understand the relation between inflammatory cytokines and CRYAB, U373 glioma cells, were stimulated with proinflammatory cytokines, IL-1? and TNF-?, and their effect on CRYAB levels in cells and secreted exosomes was studied. Our results show that U373 cells produce and secrete CRYAB via exosomes and that stimulation with IL-1? and TNF-? significantly increase the levels of CRYAB in not only the cells but also in the secreted exosomes. In addition, cytokine stimulation of U373 cells brings about changes in the secreted exosomal proteome, many of which are involved in cancer progression. |Brain Neoplasms/*metabolism/pathology [MESH] |Cell Line, Tumor [MESH] |Cytokines/metabolism [MESH] |Exosomes/*metabolism [MESH] |Glioblastoma/*metabolism/pathology [MESH] |Humans [MESH] |Inflammation Mediators/metabolism [MESH] |Interleukin-1beta/*metabolism [MESH] |Tumor Necrosis Factor-alpha/*metabolism [MESH]Inflammatory cytokines, interleukin-1 beta and tumor necrosis factor-a(epmc).pdf DeepDyve Pubget Overpricing