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.

Complex I activity was also found in the membranes of mutant strains lacking complexes III or IV.

The amount of non-heme iron sulphur protein of complex III was low in skeletal muscle, liver, and heart.

Some of the Ndi1 associations took place with complexes III and IV, suggesting the formation of respirasome-like structures.

The shedding was also blocked in microvessels after knockdown of a complex III component and after mitochondria-targeted catalase overexpression.

Ethanol also caused a leak of electrons, primarily from complex III, with generation of mitochondrial ROS and reverse electron transport.

Consistent changes in H(2)O(2) production from Complex III in programmed animals were not found.

Electron transfer from complex I to complex III, which requires quinones, is severely depressed, whereas the individual complexes are fully active.

We observed that the concomitant decrease in the level of two respiratory enzymes, complexes III and IV, led to their repression.

In all three patients the major biochemical defect was in complex III of the mitochondrial respiratory chain, a relatively uncommon defect.

Mechanistically, it is thought to act as a potent and selective OXPHOS inhibitor, by targeting the CoQ10-dependence of mitochondrial complex III.

Mutant analysis in Caenorhabditis elegans reveals that complex III affects supercomplex I·III·IV formation by acting as an assembly or stabilizing factor.