Direct gene transfer of adenoviral-mediated interferon a into @entity1 @entity150 cells but not the bystander factors produced induces endoplasmic reticulum stress-related XXXX .

@entity1 @entity137 @entity589 @entity5 @entity3726 @entity5594 @entity281 @entity150 @entity14920 @entity24765 @entity4020 @entity1284
We have previously shown that adenoviral-mediated interferon a (Ad- @entity4020 ) is cytotoxic both to cells that are sensitive to recombinant interferon a ( @entity4020 ) and to cells which are resistant to @entity4020 . The @entity5 cell-specific cytotoxic effects of Ad- @entity4020 involve three different mechanisms: 1. The direct effect of @entity4020 production causing @entity5 cell death in @entity4020 sensitive cells (1); 2. The direct effect of Ad- @entity4020 @entity281 and high levels of @entity4020 expression in @entity4020 resistant @entity5 cells (2); and 3. The indirect effect of the Ad- @entity4020 bystander factors produced (2-4). After Ad- @entity4020 @entity281 , the cells produce a large amount of perinuclear localized IFN protein. This protein over-load could be a major factor in the direct @entity5 cell death of those cells infected with Ad- @entity4020 compared with the indirect cytotoxic effects of the bystander factors produced. Here, we investigated whether a component of Ad-IFN-induced cell death involves @entity1284 -induced endoplasmic reticulum (ER) stress, using an @entity4020 -resistant @entity1 @entity150 cell line (KU7), and the normal @entity1 urothelial cell line, TERT-NHUC, as preclinical models. We found that the two ER stress response pathways examined were activated in KU7 cells. In contrast, following treatment of the normal TERT-NHUC cells with Ad- @entity4020 , no ER stress signals were observed. In addition, no ER stress related changes were seen, when KU7 cells were exposed to conditioned medium from Ad- @entity4020 -treated KU7 cells, indicating that bystander produced @entity137 did not involve ER stress. After 24   h of Ad- @entity4020 @entity281 , the KU7 @entity5 cells produced spliced @entity5594 and @entity14920 protein ( @entity14920 ), evoking an ER stress response that could contribute to Ad- @entity4020 induced apoptosis in these @entity5 cells. In addition, @entity3726 / @entity3726 , @entity24765 and @entity589 were also subsequently modified following activation of the ER stress pathways, thereby signaling downstream effectors in a pro-apoptotic manner.
