Browsing by Author "Szegezdi, E."
Now showing items 1-3 of 3
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Cytokine-induced β-cell apoptosis is no-dependent, mitochondria-mediated and inhibited by bcl-xl
Holohan, C.; Szegezdi, E.; Ritter, T.; O'Brien, T.; Samali, A. (Wiley-Blackwell, 2008-04-01)Pro-inflammatory cytokines are implicated as the main mediators of beta-cell death during type 1 diabetes but the exact mechanisms remain unknown. This study examined the effects of interleukin-1 beta (IL-1 beta), ... -
Designed tumor necrosis factor-related apoptosis-inducing ligand variants initiating apoptosis exclusively via the dr5 receptor
van der Sloot, A. M.; Tur, V.; Szegezdi, E.; Mullally, M. M.; Cool, R. H.; Samali, A.; Serrano, L.; Quax, W. J. (Proceedings of the National Academy of Sciences, 2006-05-26)Tumor necrosis factor-related apoptosis-inclucing ligand (TRAIL) is a potential anticancer drug that selectively induces apoptosis in a variety of cancer cells by interacting with death receptors DR4 and DR5. TRAIL can ... -
Nerve growth factor blocks thapsigargin-induced apoptosis at the level of the mitochondrionviaregulation of bim
Szegezdi, E.; Reed Herbert, K.; Kavanagh, E. T.; Samali, A.; Gorman, A. M. (Wiley-Blackwell, 2008-02-06)This study examined how the neurotrophin, nerve growth factor (NGF), protects PC12 cells against endoplasmic reticulum (ER) stress-induced apoptosis. ER stress was induced using thapsigargin (TG) that inhibits the ...