Abstract
To 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-1α) cDNA. Ectopic EF-1α 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-1α 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-1α results in selective resistance to apoptosis induced by growth factor withdrawal and ER stress.
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Abbreviations
- BH:
-
Bcl-2-homology
- EF-1α:
-
elongation factor 1- alpha
- ER:
-
endoplasmic reticulum
- IL-3:
-
interleukin-3
- PCR:
-
polymerase chain reaction
- PI:
-
propidium iodide
- TNF-α:
-
tumor necrosis factor- alpha
- UPR:
-
unfolded protein response
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We thank members of the Thompson Lab, including Aimee Edinger and David Plas, for their scientific input.
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Talapatra, S., Wagner, J. & Thompson, C. Elongation factor-1 alpha is a selective regulator of growth factor withdrawal and ER stress-induced apoptosis. Cell Death Differ 9, 856–861 (2002). https://doi.org/10.1038/sj.cdd.4401078
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DOI: https://doi.org/10.1038/sj.cdd.4401078
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