Information om | Engelska ordet TROPONIN

Exempel på hur man kan använda TROPONIN i en mening

• However, troponin C contains an additional alpha-helix at its N-terminus, and is constitutively bound to its target, troponin I.
• In patients with non-severe asymptomatic aortic valve stenosis and no overt coronary artery disease, the increased troponin T (above 14 pg/mL) was found associated with an increased 5-year event rate of ischemic cardiac events (myocardial infarction, percutaneous coronary intervention, or coronary artery bypass surgery).
• The initiation of contraction involves calcium ions binding to troponin, prompting a reaction that displaces tropomyosin from the actin filament binding sites.
• Acute coronary syndrome is subdivided in three scenarios depending primarily on the presence of electrocardiogram (ECG) changes and blood test results (a change in cardiac biomarkers such as troponin levels): ST elevation myocardial infarction (STEMI), non-ST elevation myocardial infarction (NSTEMI), or unstable angina.
• Fifty percent of people with unstable angina will have evidence of necrosis of the heart's muscular cells based on elevated cardiac serum markers such as creatine kinase isoenzyme (CK)-MB and troponin T or troponin I, and thus have a diagnosis of non-ST elevation myocardial infarction.
• JNJ460 also resulted in more structural proteins associated with intercellular growth, such as actin, myosin, and troponin.
• Diagnostic tests includes serum and urine electrophoresis, laboratory testing for the determination of elevated levels of troponin and BNP, and ECGs showing low QRS voltages.
• These muscle contractions are caused by calcium's bonding to troponin and unmasking the binding sites covered by the troponin-tropomyosin complex on the actin myofilament and allowing the myosin cross-bridges to connect with the actin.
• The high sensitive troponin I test is a chemiluminescence microparticle immunoassay, which is used to quantitatively determine cardiac troponin I in human plasma and serum.
• Chemical compounds can bind to troponin C to act as troponin activators (calcium sensitizers) or troponin inhibitors (calcium desensitizers).
• In diastole, the tropomyosin-troponin complex inhibits this interaction, and during systole the rise in intracellular calcium from sarcoplasmic reticulum binds to troponin C and induces a conformational change in the troponin-tropomyosin complex that disinhibits the actomyosin ATPase and permits contraction.
• Troponin I interacts with all major regulatory proteins in the sarcomeric thin filaments of cardiac and skeletal muscles: troponin C, troponin T, tropomyosin and actin.
• In skeletal muscle and cardiac muscle myosins, contraction is activated through thin filament proteins troponin and tropomyosin, whereas in NM-IIB and smooth muscle myosin, contraction initiates via regulatory light chain (MLC20) phosphorylation.
• The seemingly scrambled ssTnI and cTnI gene pair is actually functionally related as they co-express and form troponin complex in the embryonic heart.
• It is the tropomyosin binding and thin filament anchoring subunit of the troponin complex in the sarcomeres of slow twitch skeletal muscle fibers.
• This cytosolic protein belongs to a family of calcium-binding proteins that includes calmodulin, parvalbumin, troponin C, and S100 protein.
• It has been demonstrated that the presence of CapZ at Z-discs modulates the ability of protein phosphatase 1 (PP1) to dephosphorylate cardiac myofilament proteins, including myosin binding protein C, troponin T and myosin regulatory light chain; likely because extraction of CapZ decreased the amount of myofilament-associated PP1.
• The TnI subunit inhibits actomyosin ATPase, the TnT subunit binds tropomyosin and TnC, while the TnC subunit binds calcium and overcomes the inhibitory action of the troponin complex on actin thin filaments.
• Although how perioperative myocardial infarctions should be treated remains under active investigation, it is nonetheless well worth monitoring troponin to screen for infarctions because the prognosis is poor, and infarctions represent opportunities to make sure blood pressure, heart rate, and lipids are controlled.
• It sensitizes and increases the binding efficiency of cardiac troponin in the myofibril to the calcium ions that are already present in systole.

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