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CTN指的是什么？
2018-07-31 00:00
肌鈣蛋白是肌肉收縮的調(diào)節(jié)蛋白，附在收縮的橫紋肌細微組織上，心肌肌鈣蛋白由肌鈣蛋白T(cTnT)、肌鈣蛋白I(cTnI)及肌鈣蛋白C(cTnC)三種亞單位組成。cTnC有四個能結(jié)合鈣離子的結(jié)合點，當它與細胞內(nèi)的鈣離子結(jié)合時，能導致整個肌鈣蛋白構(gòu)造上的變化。肌鈣蛋白放松了肌動球蛋白，讓肌動球蛋白與肌漿球蛋白互起作用，而造成肌肉收縮。cTnI，不論有鈣無鈣，它都可以阻止肌動蛋白和肌球蛋白的相互作用，并抑制肌動球蛋白的ATP酶活力。cTnT與原肌球蛋白結(jié)合。這三種成分之間存在著鈣依賴性的相互作用，三者結(jié)合通過鈣控制肌肉的收縮。
Troponin is a regulatory protein of muscle contraction and is attached to the subtle tissue of the contractile rhabdomyus muscle. Cardiac troponin is composed of three subunits of troponin T (cTnT), troponin I (cTnI) and troponin C (cTnC). CTnC has four binding sites that bind to calcium ions, and when it binds to calcium ions in cells, it causes structural changes in the whole troponin. Troponin relaxes the action of myosin, which makes myosin interact with sarcoplasmic protein and causes muscle contraction. CTnI, with or without calcium, inhibits the interaction between actin and myosin and the ATPase activity of actin. CTnT is combined with the primary myosin. There is a calcium dependent interaction between the three components. The three combine to control muscle contraction through calcium.
5％-8％的cTnT分布于心肌細胞胞漿，為游離的胞漿蛋白，92％～95％結(jié)合于細肌絲中，為結(jié)合的結(jié)構(gòu)蛋白；3％的cTnI分布于心肌細胞胞漿中，97％與心肌結(jié)構(gòu)蛋白結(jié)合。當心肌細胞因缺血缺氧等因素遭破壞時，游離型cTnI和cTnT可首先迅速從細胞中釋放入血，隨后結(jié)合于心肌結(jié)構(gòu)蛋白中的結(jié)合型cTnI和cTnT逐漸分解，緩慢釋放入循環(huán)血中，從而解釋了以心肌細胞受損為表現(xiàn)的疾病，如急性心肌梗死(AMI)，cTnI和cTnT在循環(huán)血中較早出現(xiàn)并能持續(xù)較長時間的原因。
The cTnT of 5%-8% is distributed in the cytoplasm of cardiac myocytes, which is a free cytoplasmic protein. 92% ~ 95% is combined in the filaments as a binding structural protein; 3% of the cTnI is distributed in the cytoplasm of the cardiac myocytes, and 97% is combined with the cardiac structural protein. When myocardial cells were damaged by ischemic and anoxic factors, the free cTnI and cTnT were first released into the blood rapidly, and then gradually decomposed into the circulating blood in combination with the binding cTnI and cTnT in the cardiac structural protein, which explained the disease, such as acute myocardial infarction (acute myocardial infarction), as manifested in myocardial damage. AMI), cTnI and cTnT appeared in the circulating blood and lasted for a long time.
Troponin is a regulatory protein of muscle contraction and is attached to the subtle tissue of the contractile rhabdomyus muscle. Cardiac troponin is composed of three subunits of troponin T (cTnT), troponin I (cTnI) and troponin C (cTnC). CTnC has four binding sites that bind to calcium ions, and when it binds to calcium ions in cells, it causes structural changes in the whole troponin. Troponin relaxes the action of myosin, which makes myosin interact with sarcoplasmic protein and causes muscle contraction. CTnI, with or without calcium, inhibits the interaction between actin and myosin and the ATPase activity of actin. CTnT is combined with the primary myosin. There is a calcium dependent interaction between the three components. The three combine to control muscle contraction through calcium.
5％-8％的cTnT分布于心肌細胞胞漿，為游離的胞漿蛋白，92％～95％結(jié)合于細肌絲中，為結(jié)合的結(jié)構(gòu)蛋白；3％的cTnI分布于心肌細胞胞漿中，97％與心肌結(jié)構(gòu)蛋白結(jié)合。當心肌細胞因缺血缺氧等因素遭破壞時，游離型cTnI和cTnT可首先迅速從細胞中釋放入血，隨后結(jié)合于心肌結(jié)構(gòu)蛋白中的結(jié)合型cTnI和cTnT逐漸分解，緩慢釋放入循環(huán)血中，從而解釋了以心肌細胞受損為表現(xiàn)的疾病，如急性心肌梗死(AMI)，cTnI和cTnT在循環(huán)血中較早出現(xiàn)并能持續(xù)較長時間的原因。
The cTnT of 5%-8% is distributed in the cytoplasm of cardiac myocytes, which is a free cytoplasmic protein. 92% ~ 95% is combined in the filaments as a binding structural protein; 3% of the cTnI is distributed in the cytoplasm of the cardiac myocytes, and 97% is combined with the cardiac structural protein. When myocardial cells were damaged by ischemic and anoxic factors, the free cTnI and cTnT were first released into the blood rapidly, and then gradually decomposed into the circulating blood in combination with the binding cTnI and cTnT in the cardiac structural protein, which explained the disease, such as acute myocardial infarction (acute myocardial infarction), as manifested in myocardial damage. AMI), cTnI and cTnT appeared in the circulating blood and lasted for a long time.
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