Respiratory complexes III, IV and V are formed by components of both nuclear and mitochondrial origin and are embedded in the inner mitochondrial membrane.

Expression of iNOS, ARG2, arginine synthetic enzymes, and mitochondrial respiratory complexes III and IV was elevated in asthmatic lung samples compared with healthy controls.

In cytochrome c deficient HeLa1.2 cells, electron transport was compromised due to the lack of electron shuttle between mitochondrial respiratory complexes III and IV.

One spot was identified as a probable ubiquinol-cytochrome c reductase (EC 1.10.2.2) Rieske iron-sulfur protein precursor.

Enzymes of the bc1 complex family power the biosphere through their central role in respiration and photosynthesis.

The controversy stems from the uncertain binding motifs of quinol at the so-called Qo active site of the bc1 complex.

Structures of the 11-subunit mitochondrial bc1 complex were determined with and without the fungicide famoxadone.

We conclude that DBHBM blocks electron transfer at the QN center and thus may be considered a novel group III inhibitor of the bc1 complex.

These results indicate that the aromatic group at position195 of cytochrome b is involved in electron transfer reactions of the bc1 complex.

Many individuals with abnormalities of mitochondrial respiratory chain complex III remain genetically undefined.

This RNA editing is essential for complex III assembly and seed development in maize.

Here we show impaired tumour growth in cancer cells that lack mitochondrial complex III.

Thus, T reg cells require mitochondrial complex III to maintain immune regulatory gene expression and suppressive function.

Ectopically expressed miR-661 inhibited OS cell growth, promoted apoptosis, and reduced the activity of mitochondrial complex III.