E. I. Rachenko
Russian Academy of Sciences
14 Papers
51 Citations
E. I. Rachenko is an academic researcher from Russian Academy of Sciences. The author has contributed to research in topics: Sodium azide & Saccharomyces cerevisiae. The author has an hindex of 5, co-authored 14 publications.
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Papers
Do mitochondria regulate the heat-shock response in Saccharomyces cerevisiae ?
E. G. Rikhvanov,N. N. Varakina,T. M. Rusaleva,E. I. Rachenko,Dmitry A. Knorre,Victor K. Voinikov +5 more
TL;DR: The results obtained clearly indicate that a mild heat shock elicits a hyperpolarization of the inner mitochondrial membrane and such an event is one of several signals triggering the chain of reactions that activates the expression of the HSP104 gene and probably theexpression of other heat shock-regulated genes in S. cerevisiae.
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[Heat shock-induced changes in the respiration of the yeast Saccharomyces cerevisiae].
E. G. Rikhvanov,N. N. Varakina,T. M. Rusaleva,E. I. Rachenko,V. A. Kiseleva,Victor K. Voinikov +5 more
TL;DR: It is suggested that the enhanced respiration of yeast cells at 45°C leads to an intense accumulation of reactive oxygen species, which may be one of the reasons for the heat shock–induced cell death.
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Sodium Azide Reduces the Thermotolerance of Respiratively Grown Yeasts
TL;DR: It was suggested that the decreasing effect of sodium azide on thermotolerance takes place only when the yeast cell is incapable of using fermentation for ATP synthesis and obtains energy via oxidative phosphorylation.
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The Effect of Sodium Azide on the Thermotolerance of the Yeasts Saccharomyces cerevisiae and Candida albicans
TL;DR: It is suggested that azide exerts a protective effect on the thermotolerance of yeast cells when their energy requirements are met by the fermentation of glucose, but when cells obtain energy through respiratory metabolism, the azide inhibition of mitochondria enhances the damage inflicted on the cells by heat shock.
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The effect of sodium malonate on yeast thermotolerance
TL;DR: The suggestion is made that cell tolerance to heat shock depends on the normal functioning of mitochondria, and their increased activity at elevated temperatures may accelerate the formation of cytotoxic reactive oxygen species and, hence, is not beneficial to cells.
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