Anti-ATP1A3 antibody [EPR14138]

Supplementary info

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

Activity summary

ATP1A3 also known as the alpha3 subunit of the sodium-potassium ATPase is an ion pump that functions to maintain the electrochemical gradients of sodium and potassium ions across the plasma membrane. It is a protein with a molecular mass of approximately 110 kDa. ATP1A3 expression is found mainly in neurons of the central nervous system. By actively transporting three sodium ions out of the cell and two potassium ions into the cell ATP1A3 helps sustain the resting potential essential for neuronal excitability and signaling.

Biological function summary

The sodium-potassium ATPase where ATP1A3 serves acts as a vital component in maintaining ion homeostasis. This protein resides in cell membranes and forms a part of the larger complex required for normal neuron function. Its activity also influences other cell functions like cell volume regulation and signal transduction processes. The alpha3 subunit specifically exhibits specialized roles in neuronal tissues where rapid Na+ and K+ exchange is necessary contributing significantly to nerve impulse transmission.

Pathways

The function of ATP1A3 is integral in the maintenance of the membrane potential which is an important part of many physiological pathways including the action potential propagation in neurons. Another pathway where its activity is significant involves synaptic vesicle cycling which depends on ATP1A3 to maintain ionic conditions for synaptic transmission. Proteins such as the beta subunit of the sodium-potassium ATPase ATP1B1 closely associate with ATP1A3 and modulate its activity and stability.

Associated diseases and disorders

Mutations in ATP1A3 have associations with neurological conditions such as Alternating Hemiplegia of Childhood (AHC) and Rapid-Onset Dystonia-Parkinsonism (RDP). These disorders are characterized by sudden severe disruptions in motor function that relate to impaired ion gradients caused by dysfunctional ATP1A3. In AHC the disrupted interaction of ATP1A3 with other ion pumps like ATP1A2 exacerbates neurological function deficits.