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Calcium binds to the messenger protein Calmodulin. The calcium-calmodulin complex then activates myosin light chain kinase (MLCK), which phosphorylates myosin to allow it to bind to actin - producing contraction.
Calcium binds to troponin, which moves the tropomyosin out of the way so that myosin can bind to actin; this ultimately causes a power-stroke.
Yes, calcium is necessary for the release of neurotransmitters that cause a muscle to initiate a contraction. Calcium is also needed to bind to the troponin-tropomyosin complex causing it to change position so the myosin head can attach to the actin molecule which results in contraction.
Calcium ions bind to the thin filament ( actin ), turn it and expose the binding site to the thick filament (myosin ).
Muscle contraction results
An action potential. It is the nerve impulse that enters into sarcomeres from the sarcoplasmic reticulum and provides the energy for the calcium ions to briefly bind to the troponin on the actin myofilament to allow for contraction to occur by bringing the Z-lines closer together.
Actin changes shape.
Calcium ions bind to troponin and change its shape.
They bind to regulatory sites on troponin to remove contraction inhibition
The tropomyosin molecule blocks the active sites of the actin. Troponin is a molecule that is bound to the tropomyosin. Troponin needs CA+ (calcium ions) to bind to it in order to rotate the tropomyosin molecule and expose the actin molecules for the myosin heads to interact for muscle contraction.
Calcium ions bind to troponin and change its shape.
Calcium is released from the sarcoplasm to bind with the troponin which allows the tropomyosin the reveal the binding sites on the actin so the muscle can contract