Recombinant Human Junctional Sarcoplasmic Reticulum protein (His tag N-Terminus)

Supplementary information

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

The junctional sarcoplasmic reticulum (JSR) also known as the triad junction is a specialized region of the sarcoplasmic reticulum in muscle cells. It plays key role in excitation-contraction coupling. JSR contains proteins that facilitate the rapid release of calcium ions. It often mentioned in context of its interaction with the ryanodine receptor (RyR) and the dihydropyridine receptor (DHPR). The molecular weight of various JSR-associated proteins can differ widely with the ryanodine receptor weighing approximately 565 kDa. JSR is mostly found in skeletal and cardiac muscle tissues where it links with transverse tubules to create the triad structure essential for muscle function.

Biological function summary

The JSR ensures efficient calcium signalling necessary for muscle contractions. This region acts as main calcium storage in muscle cells and releases calcium upon stimulation which is critical for muscle contraction. The JSR forms complex with other protein components such as the ryanodine receptor and calsequestrin that buffer calcium ions and regulate their release. Calcium ions rapidly diffuse from the sarcoplasmic reticulum into the cytoplasm to bind to the myofilaments triggering contraction.

Pathways

Calcium release from the JSR influences muscle contraction and protocols including excitation-contraction coupling. It connects to the calcium signaling pathway and plays an important part in the contraction mechanism in both skeletal and cardiac muscle. The JSR involves important interactions with proteins like the dihydropyridine receptor located in the transverse tubule initiating calcium ion release from the ryanodine receptor. This release forms a link between electrical signals and mechanical contractions in muscle fibers.

Improper function or mutations affecting the JSR lead to conditions like malignant hyperthermia and cardiac arrhythmias. Malignant hyperthermia a genetic disorder is often triggered by mutations in the ryanodine receptor part of the JSR causing abnormal calcium release and resulting in deadly muscle rigidity and heat production. Cardiac arrhythmias can emerge from disruptions in calcium handling within the JSR particularly when irregular calcium releases affect normal heart rhythm. The dysregulation can involve interactions with proteins such as calsequestrin which plays role in maintaining proper calcium storage and release dynamics within the JSR.