These authors concluded that the ER calcium pump might be a target of mefloquine.

When it is time for the muscle to relax, a "calcium pump" protein in the internal membrane sucks calcium back into storage.

PKG also activates the sarcolemma calcium pump to remove activating calcium.

This effect was exacerbated by treatment with thapsigargin, a specific inhibitor of the ER calcium pump [ 6 ] .

Sarcalumenin is partially responsible for calcium buffering in the lumen of the sarcoplasmic reticulum and helps out calcium pump proteins.

This gradient is maintained through various plasma membrane calcium pumps that utilize ATP for energy, as well as a sizable storage within intracellular compartments.

This causes the calcium pump between the muscle lumen and sarcoplasmic reticulum to short circuit; the calcium ions remain bound to the troponin, continuing muscle contraction.

The molecular target of artemisinin is controversial, although recent studies suggest that SERCA, a calcium pump in the endoplasmic reticulum may be associated with artemisinin resistance.

On the other hand, cytokines are likely to activate ER stress by decreasing the calcium pump Serca2b (also known as Atp2a2), leading to subsequent depletion in the ER calcium stores.

In some cells, calcium entry is stimulated when the ER stores are artificially emptied by applying the calcium pump inhibitors thapsigargin or 2,5-di- tert- butylhydroquinone, or the calcium ionophore ionomycin.

The antagonisation by mefloquine of the ER calcium release induced by thapsigargin, a specific inhibitor of the ER calcium pump, suggests that mefloquine mobilizes ER calcium stores.

The structure of the PMCA is similar to that of the SERCA calcium pumps, which are responsible for removing calcium from the cytoplasm into the lumen of the sarcoplasmic reticulum.

Calbindin is a vitamin D-dependent calcium-binding protein inside intestinal epithelial cells which functions together with TRPV6 and calcium pumps (PMCA1) in the basal membrane to actively transport calcium into the body.

He has led teams that defined the genetic basis for the human skeletal muscle diseases, malignant hyperthermia, central core disease and Brody disease and he has demonstrated that mutations in phospholamban, a regulator of the calcium pump, can cause cardiomyopathy.

Calbindin-D9k mediates the transport of calcium across the enterocytes from the apical side, where entry is regulated by the calcium channel TRPV6, to the basolateral side, where calcium pumps such as PMCA1 utilize intracellular adenosine triphosphate to pump calcium into the blood.

PCr generated by mtCK in mitochondria is shuttled to cytosolic CK that is coupled to ATP-dependent processes, e.g. ATPases, like acto-myosin ATPase for muscle contraction, or ion pumps, like the calcium pump for muscle relaxation.

MacLennan has made fundamental contributions to our understanding of the mechanism of ion transport by SR calcium pumps, the storage of calcium in the SR by acidic lumenal proteins and the release of calcium from the SR by calcium release channels.