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Troponin I (TnI), along with troponin T (TnT) and troponin C (TnC), is one of 3 subunits that form the troponin complex of the thin filaments of striated muscle. Additionally we are shipping Troponin I Type 3 (Cardiac) Antibodies (980) and Troponin I Type 3 (Cardiac) Kits (113) and many more products for this protein.
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In clinical stable patients without known cardiovascular disease, a thorough chest-pain history in combination with hs-TnI (show TNNI2 Proteins) testing can identify a significant low-risk group.
Study showed that in patients who underwent liver transplantation elevation of preoperative high-sensitivity cardiac troponin I level was associated with 1-year mortality and 30-day mortality.
Serial measurement of troponin I revealed a persistent elevation in patients with diabetes mellitus type 2.
Plasma troponin C1 (cTnI) is biomarker of choice for diagnosing acute myocardial infarction (AMI (show CFD Proteins)) because of its high specificity as biomarker for damage to myocardial tissue. Data suggest the "best cut-off" for plasma cTnI is 0.014 micrograms/L in AMI (show CFD Proteins). These studies were conducted in emergency department of a university hospital in Italy using point-of-care testing in patients presenting with chest pain, ages 18-101.
NT-proBNP and hs-cTnI levels were higher in systemic sclerosis patients than controls. Both NT-proBNP and hs-cTnI were associated with the presence of echocardiographic abnormalities.
value of cTnI level assessed 24 hours post-surgery was a reliable predictor of death following liver transplantation with optimal cut-off value of 0.215 ng/mL. The surgery time was the most important predictor of cTnI elevation.
cTnI levels are common in Fabry disease patients, reflecting cardiac involvement.
Report novel troponin I rule-out value below the upper reference limit for acute myocardial infarction.
cTnI determined in hemodynamically stable patients with suspected AMI and wide QRS complex using optimized diagnostic thresholds improves rule-in and rule-out with respect to presence of a significant obstructive CAD
83 preterm infants with Bronchopulmonary dysplasia born <28-wk gestation and still inpatients at 36-wk corrected age received an echocardiogram and blood tests of B-type natriuretic peptide (BNP (show BNP Proteins)), troponin I, and YKL-40 (show CHI3L1 Proteins).
Hyperphosphorylation of this serine199 in cTnI C terminus impacts heart function by depressing diastolic function at baseline and limiting systolic reserve under physiological stresses. Paradoxically, it preserves heart function after ischemia/reperfusion injury, potentially by decreasing proteolysis of cTnI.
The contributions of cardiac myosin binding protein C and troponin I phosphorylation to beta-adrenergic enhancement of in vivo cardiac function
The difference in myosin regulatory light chain phosphorylation between the ventricles of R21C(+/+) in cardiac troponin I mice likely contributes to observed differences in contractile force and the lower tension monitored in the LV of HCM mice
troponin I phosphorylation specifically alters the Ca(2 (show CA2 Proteins)+) sensitivity of isometric tension and the time course of relaxation in cardiac muscle myofibrils
Combined troponin I Ser (show SIGLEC1 Proteins)-150 and Ser (show SIGLEC1 Proteins)-23/24 phosphorylation sustains thin filament Ca(2 (show CA2 Proteins)+) sensitivity playing an adaptive role to preserve contraction during acidic ischemia.
these results indicate that the inability to enhance myofilament relaxation through cTnI phosphorylation predisposes the heart to abnormal diastolic function, reduced accessibility of cardiac reserves, dysautonomia, and hypertrophy.
Dominant negative TnI-TnT interface mutation decreases the binding affinity of cTnI for TnT, causes early ventricular remodeling, and blunts the beta-adrenergic response of cardiac myocytes.
R193H and R205H mutation increase the binding affinity of Troponin I for Troponin T and Troponin C.
Conclude that dilated cardiomyopathy-causing mutations in thin filament proteins abolish the relationship between myofilament Ca(2+) sensitivity and troponin I phosphorylation by PKA.
The pattern of cTnI post-translational modification depends on sex and hypertrophic cardiomyopathy genotype.
An Ala8Val mutation enhances the effect of cardiac troponin I pseudophosphorylation on the rate of dissociation of calcium from reconstituted thin filaments.
Serum cardiac troponin I cannot be used to distinguish cattle with pericarditis from cattle with other primary cardiac diseases or noncardiac, intrathoracic disorders.
Cardiac ANP was increased in horses with mitral regurgitation (MR) and cardiac troponin levels were low in healthy and MR affected horses.
We show that the phosphorylation of cTnI and alphaTm vary in the different chambers of the heart, whereas the phosphorylation of MLC2 and cTnT does not.
hFABP (show FABP3 Proteins) rises faster and correlates better with infarct size and no-reflow than hsTnI in myocardial infarction + reperfusion when measured early after reperfusion.
analysis of expression profiling of porcine troponin I family in three different types of muscles during development
By replacing rat cardiac troponin I (cTnI) in a mammalian cTn complex with trout cTnI it was demonstrated that this protein increases the Ca2+ affinity and reduces the influence of PKA phosphorylation on the Ca2+ affinity of the cTn complex.
Troponin I (TnI), along with troponin T (TnT) and troponin C (TnC), is one of 3 subunits that form the troponin complex of the thin filaments of striated muscle. TnI is the inhibitory subunit\; blocking actin-myosin interactions and thereby mediating striated muscle relaxation. The TnI subfamily contains three genes: TnI-skeletal-fast-twitch, TnI-skeletal-slow-twitch, and TnI-cardiac. This gene encodes the TnI-cardiac protein and is exclusively expressed in cardiac muscle tissues. Mutations in this gene cause familial hypertrophic cardiomyopathy type 7 (CMH7) and familial restrictive cardiomyopathy (RCM).
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, cardiac tropin T
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, troponin 1, type 3