c-Myc-induced sensitization to apoptosis is mediated through cytochrome c release

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.

United Kingdom, Genetic disorders, Cytochrome c

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Dying like flies

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.

Drosophila, Epidermal growth factor, Epidermal growth factors

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A license to kill

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.

T cell antigen receptors, T cells, Tumor necrosis factor

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