Anti-NDUFA7 antibody

Supplementary info

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

Activity summary

The NDUFA7 protein also known as NADH dehydrogenase [ubiquinone] 1 alpha subcomplex subunit 7 is an integral part of the mitochondrial respiratory chain. It has a molecular weight of approximately 12 kDa. This protein is expressed mostly in the mitochondria of various cells and tissues such as muscle liver and brain. It plays a significant role in the electron transport chain where it contributes to the transfer of electrons from NADH to ubiquinone therefore contributing to ATP production.

Biological function summary

The NDUFA7 protein operates as a component of the mitochondrial complex I also referred to as NADH:ubiquinone oxidoreductase. This complex which includes around 45 different subunits is the first and largest enzyme of the mitochondrial respiratory chain. NDUFA7 does not directly catalyze the electron transfer but stabilizes the structure of the complex necessary for efficient electron flow. Proper functioning of complex I is essential for maintaining cellular energy homeostasis and normal metabolic activity.

Pathways

NDUFA7 plays an important role within the oxidative phosphorylation pathway which is important for aerobic energy production. This protein is closely related to other proteins in complex I such as NDUFA9 which together ensure efficient functioning of the electron transfer process. Moreover NDUFA7 indirectly influences other metabolic networks that rely on ATP including the TCA cycle and fatty acid oxidation highlighting its fundamental contribution to cellular metabolism.

Associated diseases and disorders

Mutations in the NDUFA7 gene can lead to mitochondrial disorders such as Leigh syndrome and mitochondrial complex I deficiency. These are serious conditions that may result in motor disability developmental challenges and other systemic problems. In the context of these disorders NDUFA7 interacts with proteins like NDUFS1 which also constitutes a part of complex I and defects in these proteins can amplify mitochondrial dysfunction highlighting the interconnectedness of protein actions within the cell.