Anti-Complex I Immunocapture antibody [18G12BC2]

Supplementary info

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

Activity summary

Complex I also known as NADH:ubiquinone oxidoreductase is a large enzyme complex in the mitochondrial inner membrane. It weighs approximately 980 kDa and plays an important role in the electron transport chain. Complex I is responsible for transferring electrons from NADH to ubiquinone initiating the production of ATP. This complex contains multiple subunits and constitutes the largest component of the mitochondrial respiratory chain. Researchers distinguish it with names like Complex I or mitochondrial Complex 1. It is ubiquitously expressed in the mitochondria of eukaryotic cells.

Biological function summary

Complex I plays an integral role in cellular energy production. It forms the first part of the oxidative phosphorylation system and is essential for ATP synthesis. Complex I is part of a larger structure called the mitochondrial complex which includes several other enzyme complexes working in concert. The electrons move through the complexes generating a proton gradient that the ATP synthase uses to produce ATP. Disruption in Complex I's function can lead to disturbed energy balance within the cell.

Pathways

Complex I contributes significantly to the oxidative phosphorylation pathway. This pathway is fundamental for aerobic respiration and the production of cellular ATP. Complex I interacts with other components such as cytochrome c and Complex III. Electron flow through these complexes facilitates the conversion of energy stored in NADH into a usable form driving metabolic processes. Dysfunction in this pathway can affect energy extraction from nutrients and overall cellular performance.

Associated diseases and disorders

Defective Complex I has links to neurodegenerative diseases such as Parkinson's disease and mitochondrial disorders like Leigh syndrome. Mutations in the components of Complex I can disrupt electron transport leading to decreased ATP production and increased reactive oxygen species. This damage affects tissues with high energy demands especially neurons. For example Complex I abnormalities may compromise the scavenging activity of related proteins like superoxide dismutase which exacerbates oxidative stress and neuronal damage.