2000
DOI: 10.1006/excr.2000.4952
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Rapid Up-Regulation of Peptide Elongation Factor EF-1α Protein Levels Is an Immediate Early Event during Oxidative Stress-Induced Apoptosis

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Cited by 87 publications
(73 citation statements)
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“…For example, increased transcript expression of Eef1␣ is indicative of oxidative stress and the gene product has been demonstrated to take part in apoptosis, especially in response to oxidative stress (Chen et al, 2000;Duttaroy et al, 1998). Mitochondrial isocitrate dehydrogenase 2 (Idh2) is induced by reactive oxygen species (ROS) and has been shown to be affective at combating oxidative stress through its production of NADPH (Jo et al, 2001).…”
Section: Oxidative Stress Ischemia and Hypoxiamentioning
confidence: 99%
“…For example, increased transcript expression of Eef1␣ is indicative of oxidative stress and the gene product has been demonstrated to take part in apoptosis, especially in response to oxidative stress (Chen et al, 2000;Duttaroy et al, 1998). Mitochondrial isocitrate dehydrogenase 2 (Idh2) is induced by reactive oxygen species (ROS) and has been shown to be affective at combating oxidative stress through its production of NADPH (Jo et al, 2001).…”
Section: Oxidative Stress Ischemia and Hypoxiamentioning
confidence: 99%
“…Evidence supporting the presence of distinct non-canonical functions between the two proteins has already started to accumulate. For instance, eEF1A-1/EF-1α exerts pro-apoptotic functions, accelerating the cell death rate, whereas eEF1A-2/S1 protects differentiated myotubes from apoptotic cell death [3,5,15]. Among other non-canonical functions, eEF1A-1/EF-1α cleaves actin cytoskeleton and microtubules [14,16], and interacts with two nuclear proteins, RNA polymerase and zinc finger protein ZPR1, thus enabling cells to successfully cycle through the G 2 /M phase transition [4,6].…”
Section: Introductionmentioning
confidence: 99%
“…The results presented herein show definitely that eEF1A-2/S1 in vivo is only expressed in long-lived, terminally differentiated cells; similar results were obtained in skeletal muscle and heart (data not shown). The switching event is important during development, to maintain long-lived terminally differentiated neurons, cardiomyocytes, and myofibers in a non-replicating stage, protect them from apoptosis, and possibly also from debilitating effects of microtubule severing and myofiber bundling [3][4][5][6][14][15][16].…”
Section: Introductionmentioning
confidence: 99%
“…Furthermore, eEF1A1 mRNA levels remain steady throughout H2O2 treatment, suggesting that the up-regulation of eEF1A1 is mediated post-transcriptionally. Transient depletion of eEF1A1 protects the cells against H2O2-mediated cytotoxicity in proportion to the degree of repression of eEF1A1 protein levels thus suggesting that up-regulation of eEF1A1 plays a role in expediting the execution of the apoptotic program in response to oxidative stress [67]. Interestingly, upon serum deprivation-induced apoptosis, eEF1A2 protein disappears and is replaced by eEF1A1 in dying myotubes.…”
Section: Eukaryotic Elongation Factor 1amentioning
confidence: 99%