Anti-ATP5A antibody [7H10BD4F9] - Mitochondrial Marker

Supplementary info

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

Activity summary

ATP5A also known as ATP synthase F1 subunit alpha is a protein important for cellular energy production. As part of the ATP synthase complex it plays a mechanical role in synthesizing ATP from ADP and inorganic phosphate. The ATP5A protein has a molecular weight of approximately 55 kDa and is widely expressed in the inner mitochondrial membrane across different cell types. Its central function lies in its ability to harness the energy of the proton gradient generated by the electron transport chain to catalyze ATP synthesis.

Biological function summary

ATP5A is essential in cellular respiration serving as a catalytic core of the F1 component of ATP synthase. As part of the multi-subunit enzyme complex ATP synthase is responsible for ATP production the primary energy currency in cells. The ATP5A subunit works in conjunction with other subunits of the enzyme oligomer to facilitate the conversion of energy released during oxidative phosphorylation into a usable form. The protein's efficiency in this biological role underpins its importance in sustaining cellular energy homeostasis.

Pathways

ATP5A plays a pivotal role in oxidative phosphorylation and the electron transport chain integral components of cellular respiration. The oxidative phosphorylation pathway depends on this protein to manage the synthesis of ATP molecules while the electron transport chain creates the proton gradient necessary for ATP production. ATP5A is functionally connected to other proteins in these pathways such as ATP5B and cytochrome c oxidase working in a coordinated manner to ensure efficient energy transfer and maintenance.

Associated diseases and disorders

ATP5A is implicative in mitochondrial disorders and neurodegenerative diseases such as Leigh syndrome and Parkinson's disease. These conditions often arise from deficits in ATP production where ineffective ATP synthase activity can contribute to cellular energy failures. In the context of Parkinson’s disease for instance ATP5A interactions with other proteins like Parkin can contribute to mitochondrial dysfunction an important pathological feature of the disorder. Through such associations alterations in ATP5A activity can significantly impact disease progression and symptomatology.