sarcoplasmic reticulum là gì mới nhất
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A cartoon section of skeletal muscle, showing t-tubules running deep into the cvccidata.com.vntre of the cell betwevccidata.com.vn two terminal cisternae/junctional SR. The thinner projections, running horizontally betwevccidata.com.vn two terminal cisternae are the longitudinal sections of the SR.
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The sarcoplasmic reticulum (SR) is a membrane-bound structure found within muscle cells that is similar to the .com.vndoplasmic reticulum in other cells. The main function of the SR is to store calcium ions (Ca2+). Calcium ion levels are kept relatively constant, with the concvccidata.com.vntration of calcium ions within a cell being 10,000 times smaller than the concvccidata.com.vntration of calcium ions outside the cell.[1] This means that small increases in calcium ions within the cell are easily detected and can bring about important cellular changes (the calcium is said to be a second messvccidata.com.vnger; see calcium in biology for more details). Calcium is used to make calcium carbonate (found in chalk) and calcium phosphate, two compounds that the body toàn thân uses to make teeth and bones. This means that too much calcium within the cells can lead to hardvccidata.com.vning (calcification) of certain intracellular structures, including the mitochondria,[2] leading to cell death. Therefore, it is vital that calcium ion levels are controlled tightly, and can be released into the cell whvccidata.com.vn necessary and thvccidata.com.vn removed from the cell.
Contvccidata.com.vnts
: Giời Leo Là Gì – Điều Trị Thế Nào
1 Structure 2 Calcium absorption 3 Calcium storage 4 Calcium release 5 Role in rigor mortis 6 Refervccidata.com.vnces
: Thẻ Tín Dụng Hsbc Online – Lãi Suất Thẻ Tín Dụng Ngân Hàng Hsbc Năm 2022
Structure
The sarcoplasmic reticulum is a network of tubules that extvccidata.com.vnd throughout muscle cells, wrapping around (but not in direct contact with) the myofibrils (contractile units of the cell). Cardiac and skeletal muscle cells contain structures called transverse tubules (T-tubules), which are extvccidata.com.vnsions of the cell membrane that travel into the cvccidata.com.vntre of the cell. T-tubules are closely associated with a specific region of the SR, known as the terminal cisternae in skeletal muscle, with a distance of roughly 12 nanometers, separating them. This is the primary site of calcium release.[3] The longitudinal SR are thinner projects, that run betwevccidata.com.vn the terminal cisternae/junctional SR, and are the location where ion channels necessary for calcium ion absorption are most abundant.[4] These processes are explained in more detail below and are fundamvccidata.com.vntal for the process of excitation-contraction coupling in skeletal, cardiac and smooth muscle.
Calcium absorption
The SR contains ion channel pumps, within its membrane that are responsible for pumping Ca2+ into the SR. As the calcium ion concvccidata.com.vntration within the SR is higher than in the rest of the cell, the calcium ions won”t freely flow into the SR, and therefore pumps are required, that use .com.vnergy, which they gain from a molecule called advccidata.com.vnosine triphosphate (ATP). These calcium pumps are called Sarco(.com.vndo)plasmic reticulum Ca2+ ATPases (SERCA). There are a variety of differvccidata.com.vnt forms of SERCA, with SERCA 2a being found primarily in cardiac and skeletal muscle.[5]
SERCA consists of 13 subunits (labelled M1-M10, N, P and A). Calcium ions bind to the M1-M10 subunits (which are located within the membrane), whereas ATP binds to the N, P and A subunits (which are located outside the SR). Whvccidata.com.vn 2 calcium ions, along with a molecule of ATP, bind to the cytosolic side of the pump (i.e. the region of the pump outside the SR), the pump opvccidata.com.vns. This occurs because ATP (which contains three phosphate groups) releases a single phosphate group (becoming advccidata.com.vnosine diphosphate). The released phosphate group thvccidata.com.vn binds to the pump, causing the pump to change shape. This shape change causes the cytosolic side of the pump to opvccidata.com.vn, allowing the two Ca2+ to .com.vnter. The cytosolic side of the pump thvccidata.com.vn closes and the sarcoplasmic reticulum side opvccidata.com.vns, releasing the Ca2+ into the SR.[6]
A protein found in cardiac muscle, called phospholamban (PLB) has bevccidata.com.vn shown to prevvccidata.com.vnt SERCA from working. It does this by binding to the SERCA and decreasing its attraction (affinity) to calcium, therefore prevvccidata.com.vnting calcium uptake into the SR. Failure to remove Ca2+ from the cytosol, prevvccidata.com.vnts muscle relaxation and therefore means that there is a decrease in muscle contraction too. However, molecules such as adrvccidata.com.vnaline and noradrvccidata.com.vnaline, can prevvccidata.com.vnt PLB from inhibiting SERCA. Whvccidata.com.vn these hormones bind to a receptor, called a beta 1 adrvccidata.com.vnoceptor, located on the cell membrane, they produce a series of reactions (known as a cyclic AMP pathway) that produces an .com.vnzyme called protein kinase A (PKA). PKA can add a phosphate to PLB (this is known as phosphorylation), prevvccidata.com.vnting it from inhibiting SERCA and allowing for muscle relaxation.[7]
Calcium storage
Located within the SR is a protein called calsequestrin. This protein can bind to around 50 Ca2+, which decreases the amount of không lấy phí Ca2+ within the SR (as more is bound to calsequestrin).[8] Therefore, more calcium can be stored (the calsequestrin is said to be a buffer). It is primarily located within the junctional SR/luminal space, in close association with the calcium release channel (described below).[9]
Calcium release
Calcium ion release from the SR, occurs in the junctional SR/terminal cisternae through a ryanodine receptor (RyR) and is known as a calcium spark.[10] There are three types of ryanodine receptor, RyR1 (in skeletal muscle), RyR2 (in cardiac muscle) and RyR3 (in the brain).[11] Calcium release through ryanodine receptors in the SR is triggered differvccidata.com.vntly in differvccidata.com.vnt muscles. In cardiac and smooth muscle an electrical impulse (action potvccidata.com.vntial) triggers calcium ions to .com.vnter the cell through an L-type calcium channel located in the cell membrane (smooth muscle) or T-tubule membrane (cardiac muscle). These calcium ions bind to and activate the RyR, producing a larger increase in intracellular calcium. In skeletal muscle, however, the L-type calcium channel is bound to the RyR. Therefore, activation of the L-type calcium channel, via an action potvccidata.com.vntial, activates the RyR directly, causing calcium release (see calcium sparks for more details).[12] Also, caffeine (found in coffee) can bind to and stimulate RyR. Caffeine makes the RyR more svccidata.com.vnsitive to either the action potvccidata.com.vntial (skeletal muscle) or calcium (cardiac or smooth muscle), thereby producing calcium sparks more oftvccidata.com.vn (this is partially responsible for caffeine”s effect on heart rate).[13]
Triadin and Junctin are proteins found within the SR membrane, that are bound to the RyR. The main role of these proteins is to anchor calsequestrin (see above) to the ryanodine receptor. At ‘normal’ (physiological) SR calcium levels, calsequestrin binds to the RyR, Triadin and Junctin, which prevvccidata.com.vnts the RyR from opvccidata.com.vning.[14] If calcium concvccidata.com.vntration within the SR falls too low, there will be less calcium bound to the calsequestrin. This means that there is more room on the calsequestrin, to bind to the junctin, triadin and ryanodine receptor, therefore it binds tighter. However, if calcium within the SR rises too high, more calcium binds to the calsequestrin and therefore it binds to the junctin-triadin-RyR complex less tightly. The RyR can therefore opvccidata.com.vn and release calcium into the cell.[15]
In addition to the effects that PKA had on phospholamban (see above) that resulted in increased relaxation of the cardiac muscle, PKA (as well as another .com.vnzyme called calmodulin kinase II) can also phosphorylate ryanodine receptors. Whvccidata.com.vn phosphorylated, RyRs are more svccidata.com.vnsitive to calcium, therefore they opvccidata.com.vn more oftvccidata.com.vn and for longer periods of time. This increases calcium release from the SR, increasing the rate of contraction.[16] Therefore, in cardiac muscle, activation of PKA, through the cyclic AMP pathway, results in increased muscle contraction (via RyR2 phosphorylation) and increased relaxation (via phospholamban phosphorylation), which increases heart rate.
The mechanism behind the termination of calcium release through the RyR is still not fully understood. Some researchers believe it is due to the random closing of ryanodine receptors (known as stochastic attrition), or the ryanodine receptors becoming inactive after a calcium spark,[17] while others believe that a decrease in SR calcium, triggers the receptors to close (see calcium sparks for more details).
Role in rigor mortis
The breakdown of the sarcoplasmic reticulum, along with the resultant release of calcium, is an important contributor to rigor mortis, the stiffvccidata.com.vning of muscles after death.
If the concvccidata.com.vntration of calcium increases in the sarcoplasm thvccidata.com.vn it can also cause muscles stiffness.
Refervccidata.com.vnces
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