High impact information on Ubiquinone 30

• Coenzyme Q6 and iron reduction are responsible for the extracellular ascorbate stabilization at the plasma membrane of Saccharomyces cerevisiae [1].
• This observation suggests that this cytosolic effector may be translocated to the inner membrane of the mitochondria, the intracellular site for ubiquinone-6 biosynthesis [2].
• Increasing concentrations of glucose (1-5%) in the growth medium depressed ubiquinone-6 biosynthesis in continuously cultured wild type Saccharomyces cerevisiae [2].
• Addition of succinate and either coenzyme Q6 or DB to mitochondria from the Q-deficient yeast cells resulted in the initial reduction of cytochrome b followed by a slow reduction of cytochrome c1 with a reoxidation of cytochrome b [3].
• Identification of 3,4-dihydroxy-5-hexaprenylbenzoic acid as an intermediate in the biosynthesis of ubiquinone-6 by Saccharomyces cerevisiae [4].

Biological context of Ubiquinone 30

• Both coenzyme Q6 and NADH-ascorbate free radical reductase were rescued in plasma membranes derived from a strain obtained by transformation of the coq3delta strain with a single-copy plasmid bearing the wild type COQ3 gene and in plasma membranes isolated form the coq3delta strain grown in the presence of coenzyme Q6 [5].

Anatomical context of Ubiquinone 30

• In contrast, the lack of coenzyme Q6 in these membranes resulted in only a partial inhibition of either the ferricyanide or cytochrome-c reductase [5].

Associations of Ubiquinone 30 with other chemical compounds

• Synthesis of 5-demethoxyubiquinone-6 and ubiquinone-6 from 3-hexaprenyl-4-hydroxybenzoate in yeast mitochondria [6].

References