Computational Studies of the Metal-Binding Site of the Wild-Type and the H46R Mutant of the Copper, Zinc Superoxide Dismutase

2012 ◽  
Vol 51 (10) ◽  
pp. 5561-5568 ◽  
Author(s):  
Raúl Mera-Adasme ◽  
Fernando Mendizábal ◽  
Mauricio Gonzalez ◽  
Sebastián Miranda-Rojas ◽  
Claudio Olea-Azar ◽  
...  
Keyword(s):  
Superoxide Dismutase ◽  
Binding Site ◽  
Metal Binding ◽  
Computational Studies ◽  
Wild Type ◽  
Metal Binding Site ◽  
Copper Zinc Superoxide Dismutase ◽  
Zinc Superoxide Dismutase ◽  
Copper Zinc

scholarly journals Human Bcl-2 Reverses Survival Defects in Yeast Lacking Superoxide Dismutase and Delays Death of Wild-Type Yeast

1997 ◽  
Vol 137 (7) ◽  
pp. 1581-1588 ◽  
Author(s):  
Valter D. Longo ◽  
Lisa M. Ellerby ◽  
Dale E. Bredesen ◽  
Joan S. Valentine ◽  
Edith B. Gralla
Keyword(s):  
Superoxide Dismutase ◽  
Stationary Phase ◽  
Mammalian Cells ◽  
Antioxidant Protection ◽  
Wild Type ◽  
Copper Zinc Superoxide Dismutase ◽  
Zinc Superoxide Dismutase ◽  
Apoptotic Protein ◽  
Copper Zinc ◽  
Wild Type Yeast

We expressed the human anti-apoptotic protein, Bcl-2, in Saccharomyces cerevisiae to investigate its effects on antioxidant protection and stationary phase survival. Yeast lacking copper-zinc superoxide dismutase (sod1Δ) show a profound defect in entry into and survival during stationary phase even under conditions optimal for survival of wild-type strains (incubation in water after stationary phase is reached). Expression of Bcl-2 in the sod1Δ strain caused a large improvement in viability at entry into stationary phase, as well as increased resistance to 100% oxygen and increased catalase activity. In addition, Bcl-2 expression reduced mutation frequency in both wild-type and sod1Δ strains. In another set of experiments, wild-type yeast incubated in expired minimal medium instead of water lost viability quickly; expression of Bcl-2 significantly delayed this stationary phase death. Our results demonstrate that Bcl-2 has activities in yeast that are similar to activities it is known to possess in mammalian cells: (a) stimulation of antioxidant protection and (b) delay of processes leading to cell death.

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