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E2F1 and c-Myc in cell growth and death Matsumura I; Tanaka H; Kanakura YCell Cycle 2003[Jul]; 2 (4): 333-8Cell cycle machinery controls not only cell growth but also cell survival and death. For example, overexpression of c-Myc or E2F1, which are involved in G1/S transition, causes apoptosis under certain conditions. Furthermore, endogenous E2F1 also participates in apoptosis, as evidenced by the defect of apoptosis in E2F1-deficient mice. Candidate molecules that mediate c-Myc- and E2F1-enhanced apoptosis include p14/p19ARF, ornithine decarboxylase and lactate dehydrogenase-A (for c-Myc) as well as p14/p19ARF, p73, Apaf-1 and caspase-3 (for E2F1). c-Myc also activates the CD95/Fas-FADD-mediated death signal. c-Myc and E2F1 inhibit NF-kappaB activities induced by TNFalpha or reactive oxygen species. Therefore, c-Myc and E2F1 regulate cell growth and death not only by inducing transcription but also by modulating signal transduction pathways.|*Cell Cycle Proteins[MESH]|Animals[MESH]|Apoptosis/*physiology[MESH]|Apoptotic Protease-Activating Factor 1[MESH]|Caspase 3[MESH]|Caspases/metabolism[MESH]|Cell Cycle/physiology[MESH]|Cell Death/physiology[MESH]|Cell Division/*physiology[MESH]|Cell Survival/*physiology[MESH]|Cyclin-Dependent Kinase Inhibitor p16[MESH]|DNA-Binding Proteins/metabolism[MESH]|E2F Transcription Factors[MESH]|E2F1 Transcription Factor[MESH]|Genes, Tumor Suppressor[MESH]|Helminth Proteins/metabolism[MESH]|Mice[MESH]|Muscle Proteins/metabolism[MESH]|NF-kappa B/metabolism[MESH]|Nuclear Proteins/metabolism[MESH]|Protein Interaction Mapping[MESH]|Proteins/metabolism[MESH]|Proto-Oncogene Proteins c-myc/*metabolism[MESH]|S Phase/physiology[MESH]|Signal Transduction[MESH]|Transcription Factors/*metabolism[MESH]|Tumor Protein p73[MESH]|Tumor Suppressor Protein p14ARF/metabolism[MESH]|Tumor Suppressor Proteins[MESH]|fas Receptor/metabolism[MESH] |
