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lüll Elongation factor-1 alpha is a selective regulator of growth factor withdrawal and ER stress-induced apoptosis Talapatra S; Wagner JD; Thompson CBCell Death Differ 2002[Aug]; 9 (8): 856-61To identify genes that contribute to apoptotic resistance, IL-3 dependent hematopoietic cells were transfected with a cDNA expression library and subjected to growth factor withdrawal. Transfected cells were enriched for survivors over two successive rounds of IL-3 withdrawal and reconstitution, resulting in the identification of a full-length elongation factor 1 alpha (EF-1alpha) cDNA. Ectopic EF-1alpha expression conferred protection from growth factor withdrawal and agents that induce endoplasmic reticulum stress, but not from nuclear damage or death receptor signaling. Overexpression of EF-1alpha did not lead to growth factor independent cell proliferation or global alterations in protein levels or rates of synthesis. These findings suggest that overexpression of EF-1alpha results in selective resistance to apoptosis induced by growth factor withdrawal and ER stress.|Animals[MESH]|Apoptosis/*genetics[MESH]|Cell Differentiation/drug effects/genetics[MESH]|Cell Division/drug effects/genetics[MESH]|Cell Survival/drug effects/genetics[MESH]|Cells, Cultured[MESH]|Dose-Response Relationship, Drug[MESH]|Endoplasmic Reticulum/drug effects/*metabolism[MESH]|Enzyme Inhibitors/pharmacology[MESH]|Eukaryotic Cells/drug effects/*metabolism[MESH]|Gene Expression Regulation/drug effects/genetics[MESH]|Humans[MESH]|Interleukin-3/*deficiency/pharmacology[MESH]|Peptide Elongation Factor 1/genetics/*metabolism[MESH]|Protein Synthesis Inhibitors/pharmacology[MESH]|Proto-Oncogene Proteins c-bcl-2/drug effects/genetics/metabolism[MESH]|Stress, Physiological/genetics/*metabolism[MESH]|bcl-X Protein[MESH] |