Anti-MTCO2 antibody [12C4F12]

Supplementary info

This supplementary information is collated from multiple sources and compiled automatically.

Activity summary

'MTCO2' also known as 'mt-co2' or 'mtco2e' is a mitochondrial gene that encodes for a component of the cytochrome c oxidase complex referred to as Complex IV in the electron transport chain. The protein plays a mechanical role in facilitating electron transfer within mitochondria an essential process in cellular respiration. MTCO2 is predominantly expressed in tissues with high energy demands such as muscle and neurons. The known mass of the MTCO2 protein is approximately 25 kDa. It sits in the mitochondrial inner membrane where it contributes to creating the proton gradient driving ATP synthesis.

Biological function summary

MTCO2 (or cytochrome c oxidase subunit II) serves as an important player in aerobic respiration. It is part of the cytochrome c oxidase complex which forms the last enzyme complex of the electron transport chain. As part of this complex MTCO2 facilitates the transfer of electrons from cytochrome c to oxygen resulting in the reduction of oxygen to water. This electron transfer is paired with proton translocation across the mitochondrial membrane which is critical for ATP production.

Pathways

MTCO2 contributes significantly to the oxidative phosphorylation pathway which is essential for ATP production in eukaryotic cells. It directly interacts with other components of the mitochondrial electron transport chain like cytochrome c and NADH dehydrogenase which are critical for maintaining the flow of electrons and the integrity of the energy production process. Another pathway it is part of is the apoptosis pathway regulated by non-lethal stress conditions where controlled release of cytochrome c can trigger programmed cell death.

Associated diseases and disorders

MTCO2 mutations and dysfunctions have been linked with mitochondrial disorders especially those affecting energy-demanding tissues leading to conditions such as mitochondrial myopathy and Leber's hereditary optic neuropathy. These disorders result from compromised oxidative phosphorylation leading to inadequate energy supply. The dysfunction of cytochrome c oxidase which contains the MTCO2 subunit is a central aspect of these diseases often tying this protein to other complexes within the electron transport chain that also underpin mitochondrial diseases.