Anti-Kir2.1/KCNJ2 antibody [EPR4530]

Supplementary info

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

Activity summary

The Kir2.1 protein also known as KCNJ2 belongs to a family of inward-rectifier potassium channels. Kir2.1 is important for setting and stabilizing the resting membrane potential. It has a molecular mass of approximately 48 kDa. Kir2.1 is mainly expressed in the heart and brain tissues and it facilitates the flow of potassium ions across the cell membrane with high efficiency. This modulation of potassium ion movement is critical for maintaining membrane potential and is vital for the normal electrical activity in excitable tissues.

Biological function summary

This process aids in the regulation of cellular excitability. Kir2.1 is an integral part of cell membranes and often associates with other proteins to form a functional channel complex. This complex plays a role in neuronal signaling and cardiac rhythm regulation contributing to various physiological functions in muscle and nerve tissue. Its roles underpin how potassium currents modulate nerve impulses and heartbeats reflecting its participation in the body's complex communication and control systems.

Pathways

The Kir2.1 channel influences the cardiac action potential and is involved in maintaining the stability of the heart’s electrical signaling. It is part of the cardiac conduction pathway. The channel interacts with other cardiac proteins like KCNJ3 and KCNJ5 complementing their function in the repolarization phase of the cardiac action potential. Kir2.1's presence in pathways responsible for repolarization highlights the precision needed for effective cardiac and neurological functions.

Associated diseases and disorders

Mutations in the Kir2.1 gene KCNJ2 relate to Andersen-Tawil syndrome and cardiac arrhythmias. Andersen-Tawil syndrome characterized by periodic paralysis cardiac arrhythmias and developmental anomalies highlights the multifaceted role Kir2.1 plays in cellular function. Kir2.1 mutations disrupt electrical stability in heart and skeletal muscle tissues. Similar mutations associate with connections to other membrane proteins like KCNH2 often exacerbating arrhythmic risk a critical factor in heart-related conditions.