form a muscle cell
When a muscle is at rest, the active sites on the actin are blocked by tropomyosin. Tropomyosin prevents myosin binding to actin, which helps to keep the muscle relaxed. In order for muscle contraction to occur, tropomyosin must be moved out of the way to expose the active sites on actin.
Before contraction:1) no nerve impulse to myoneural junction.2) Ca++ in the sarcoplasmic reticulum3) combining of actin and myosin is prevented by a tropomyosin-troponin complex that attatches to the actin.Contraction:1) an action potential (nerve impulse) travels along a neural axon to a myoneural junction (synapse)2) Acetylcholine (neurotransmitter) is released from the synaptic vesicles of the neuron.3) acetylcholine diffuses over into the sacrolemma and the t-tubules.4) Ca++mis released from the sarcoplasmic reticulum.5) the Ca++ then binds to the actin degrading the tropomyosin-troponin complex to expose myosin attatchment sights6) the heads of the myosin myofilaments attatch to the exposed attatchment sights on actin filament7) ATP binds to the heads of the myosin filaments. breakdown of the ATP to ADP+p releases energy and causes a bending of myosin heads.8) another ATP binds to the myosin head causing it to release the actin filament then attatch again with the head unbent. again the ATP breaks down and the process continues.To relax:1) nerve impulse stops2) active transport returns Ca++ to the sarcoplasmic reticulum3) ATP's are reformed (ADP+P+energy=ATP)4) Tropomyosin-troponin complex reforms causing the myosin to release the actin5) when the filaments release each other they slide back to the resting position.
the function of a muscle cell is, by definition, to move. this can be accomplished when the cell contracts. contracting makes it denser, which is why when you feel a relaxed muscle in your arm suddenly tense up, it hardens.A muscle cell expands and contracts in order to allow the human body to control the movement of it's limbs.
Homologous chromosomes are pairs of chromosomes that have genes for the same traits arranged in the same order. They are inherited from each parent and are involved in genetic variation during reproduction.
The sliding filament theory is the explanation for how muscles produce force (or, usually, shorten). It explains that the thick and thin filaments within the sarcomere slide past one another, shortening the entire length of the sarcomere. In order to slide past one another, the myosin heads will interact with the actin filaments and, using ATP, bend to pull past the actin.
ATP
There are many regulatory proteins in the human body, such as transcription factors, kinases, and G-proteins. It would depend on the specific context or system you are referring to in order to determine the name of the regulatory protein.
In order for myosin to connect to actin's active sites, Ca ions must be released from storage in the sarcoplasmic reticulum into the sarcoplasm. A nerve impulse stimulates the release of Ca ions from the sarcoplasmic reticulum. Once the Ca ions are released into the sarcoplasm, they bind to troponin. Once they bind to troponin, troponin no longer is bound to tropomyosin. Tropomyosin is now no longer covering up actin's active sites, thus allowing myosin to attach to actin's active sites.
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.
The cross-bridge must bind to ATP in order to disconnect from actin. When ATP binds to the cross-bridge, it allows for the power stroke to occur, leading to the dissociation of the cross-bridge from actin.
When a muscle is at rest, the active sites on the actin are blocked by tropomyosin. Tropomyosin prevents myosin binding to actin, which helps to keep the muscle relaxed. In order for muscle contraction to occur, tropomyosin must be moved out of the way to expose the active sites on actin.
The filaments of myofibrils constructed from proteins, myofilaments, consist of 2 types, thick and thin. Thin filaments consist primarily of the protein actin; thick filaments consist primarily of the protein myosin. The protein complex composed of actin and myosin is sometimes referred to as "actomyosin." In striated muscle, such as skeletal and cardiac muscle, the actin and myosin filaments each have a specific and constant length on the order of a few micrometers, far less than the length of the elongated muscle cell (a few millimeters in the case of human skeletal muscle cells). The filaments are organized into repeated subunits along the length of the myofibril. These subunits are called sarcomeres.
Before contraction:1) no nerve impulse to myoneural junction.2) Ca++ in the sarcoplasmic reticulum3) combining of actin and myosin is prevented by a tropomyosin-troponin complex that attatches to the actin.Contraction:1) an action potential (nerve impulse) travels along a neural axon to a myoneural junction (synapse)2) Acetylcholine (neurotransmitter) is released from the synaptic vesicles of the neuron.3) acetylcholine diffuses over into the sacrolemma and the t-tubules.4) Ca++mis released from the sarcoplasmic reticulum.5) the Ca++ then binds to the actin degrading the tropomyosin-troponin complex to expose myosin attatchment sights6) the heads of the myosin myofilaments attatch to the exposed attatchment sights on actin filament7) ATP binds to the heads of the myosin filaments. breakdown of the ATP to ADP+p releases energy and causes a bending of myosin heads.8) another ATP binds to the myosin head causing it to release the actin filament then attatch again with the head unbent. again the ATP breaks down and the process continues.To relax:1) nerve impulse stops2) active transport returns Ca++ to the sarcoplasmic reticulum3) ATP's are reformed (ADP+P+energy=ATP)4) Tropomyosin-troponin complex reforms causing the myosin to release the actin5) when the filaments release each other they slide back to the resting position.
micrometer,centimeter,millimeter,meter
Muscle fiber contraction is a complex process involving a number of cell parts and chemical substances that result in the sliding movement of the actin and myosin filaments and causes a contraction. A myosin filament is composed of protein strands with globular ends called cross-bridges that extend outward along the length of the filament. The actin filaments have ADP molecules attached to its surface that serve as active sites for linking the cross-bridges of the myosin filaments. Although the process is not completely understood, the sliding filament theory suggests that the myosin cross-bridge attaches to an actin active site and bends slightly, pulling the actin with it. It releases its attachment, straightens, and combines with another active site further down the actin filament, causing the sarcomere to shorten. When the nerve impulse reaches the distal end of its branch, acetylcholine is released into the gap. The acetylcholine diffuses rapidly across the motor end plate and combines with protein receptors in the sarcolemma. This causes a muscle impulse to be generated and pass in all directions over the entire sarcolemma, and through the T-tubules deep into the fiber. The S.R., which contains a high concentration of calcium ions, becomes more permeable and allows the ions to diffuse into the sarcoplasm. When a high enough concentration is present in the sarcoplasm, the linkages between the actin and myosin filaments occur and contraction takes place. The calcium ions are moved quickly back into the S.R. by an active transport system (calcium pump). When enough calcium ions have been removed from the sarcoplasm, the muscle relaxes. At the same time, the acetylcholine is rapidly decomposed by the enzyme cholinesterase. This prevents a single nerve impulse from causing a sustained contraction.
micrometer,centimeter,millimeter,meter
If atoms are arranged in a repeated order they are negatively charged