Article Abstract:
Mitochondrial holocytochrome c release mediates c-Myc-induced apoptosis sensitization. c-Myc is a protein encoded by the c-myc proto-oncogene and it is a potent cell-proliferation and apoptosis inducer. Ability of cytochrome c to activate apoptosis is entirely dependent on other signals. Both CD95/Fas and p53 signaling have been implicated in c-Myc-induced apoptosis. Neither was needed for c-Myc-induced cytochrome c release, but inhibition of CD95 signaling in fibroblasts prevented c-Myc-induced apoptosis. It seemed to do so by obstructing ability of cytosolic cytochrome c to activate caspases.
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Article Abstract:
Previous studies revealed that the Drosophila epidermal growth factor receptor/reticular activating system signaling pathway suppresses apoptosis. A critical target of the pathway is the death-inducing protein hid. The disseminated expression of an active Ras mutant suppressed the widespread cell death that accompanies normal embryonic development in the fly. This developmental death required genes within a region of the Drosophila chromosome that contains apoptotic effectors reaper, hid and grim. Thus, the product of the genes is the initiator of cell death.
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Article Abstract:
Apoptosis or programmed cell death continues to intrigue researchers with its signaling and suppression systems. Oncoproteins, tumor suppressor proteins and signaling pathways can both trigger and suppress apoptosis. A breakthrough in research is the direct connection between the signal emanating from the TNF (tumor necrosis factor)/CD95 (cytotoxic T cell ligand effector) system and the apoptosis system.
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