Anti-NCX1 antibody [EPR12739]

Supplementary info

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

Activity summary

NCX1 also known as the Sodium-Calcium Exchanger 1 plays a critical role in removing calcium ions from cells by exchanging them for sodium ions. It operates as an antiporter mechanism facilitating the transport of three sodium ions into the cell in exchange for one calcium ion being transported out. The protein has a molecular mass of approximately 120 kDa. NCX1 is widely expressed in various tissues including heart brain kidney and skeletal muscle indicating its importance in multiple physiological processes.

Biological function summary

NCX1 contributes significantly to controlling intracellular calcium levels important for muscle contraction and neuronal function. The protein forms part of a larger complex that includes several regulatory proteins which modulate its activity according to the cellular environment. By managing calcium ion concentration inside cells NCX1 influences various cellular processes such as muscle relaxation and excitatory signaling in neurons.

Pathways

NCX1 integrates itself into the cellular calcium homeostasis and cardiac excitation-contraction coupling pathways. In the cardiac tissue it works alongside other proteins like the L-type calcium channel contributing to the regulation of the heart’s rhythm and contraction force. Another pathway involves its interaction with the sodium-potassium ATPase which helps maintain the cell's electrochemical gradient essential for proper muscle and nerve function.

Associated diseases and disorders

NCX1 has been linked to cardiovascular diseases such as heart failure and arrhythmias. Abnormal NCX1 function can disrupt calcium balance leading to these conditions. Moreover the protein's relationship with the L-type calcium channel is important because alterations in their interaction can exacerbate such cardiovascular disorders. Additionally NCX1 has connections to disorders like epilepsy where other ion channels and transporters also play critical roles in maintaining neural excitability and preventing seizure activities.