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. 2010 Dec;42(6):483-9.
doi: 10.1007/s10863-010-9315-6. Epub 2010 Nov 12.

VDAC contributes to mRNA levels in Saccharomyces cerevisiae cells by the intracellular reduction/oxidation state dependent and independent mechanisms

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VDAC contributes to mRNA levels in Saccharomyces cerevisiae cells by the intracellular reduction/oxidation state dependent and independent mechanisms

Hanna Gałgańska et al. J Bioenerg Biomembr. 2010 Dec.

Abstract

Available data suggest that voltage-dependent anion selective channel (VDAC) constitutes an important component of a cellular regulatory mechanism based on the intracellular reduction/oxidation (redox) state. Here, using quantitative RT-PCR, we demonstrated that depletion of VDAC1 (termed here VDAC) in Saccharomyces cerevisiae cells distinctly affected levels of mRNAs encoding nuclear proteins sensitive to changes of the intracellular redox state including the nuclear transcription factors important for adaptation to the redox state and proteins involved in communication between mitochondria and the nucleus. We also revealed that the changes of the studied protein transcript levels generally correlated with changes of the intracellular redox state although VDAC appears also to affect mRNA levels by a mechanism not based on changes of the intracellular redox states. Thus, VDAC seems to be an important element of the intracellular signaling network.

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References

    1. Curr Opin Plant Biol. 2007 Dec;10(6):600-6 - PubMed
    1. BMC Genomics. 2008 Jan 23;9:34 - PubMed
    1. FEBS Lett. 2007 Jun 19;581(15):2802-10 - PubMed
    1. Mol Cell Biol. 1997 Oct;17(10):5727-38 - PubMed
    1. Nat Rev Genet. 2008 May;9(5):383-95 - PubMed

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