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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 (1006) and Troponin I Type 3 (Cardiac) Proteins (46) and many more products for this protein.
Showing 10 out of 103 products:
Rat (Rattus) TNNI3 ELISA Kit for Sandwich ELISA - ABIN416120
Chai, Liu, Hu: Comparison of femoral and aortic remote ischaemia preconditioning for cardioprotection against myocardial ischaemia/reperfusion injury in a rat model. in Interactive cardiovascular and thoracic surgery 2014
Show all 2 references for ABIN416120
Mouse (Murine) TNNI3 ELISA Kit for Sandwich ELISA - ABIN1000107
Jia, Hao, Guo: Ultrafine carbon black disturbs heart rate variability in mice. in Toxicology letters 2012
Compromised interactions of K206I with actin and hcTnC may lead to impaired relaxation and HCM.
hsTnI at the time of presentation followed by early advanced coronary CTA (show PCYT1A ELISA Kits) assessment improves the risk stratification and diagnostic accuracy for acute coronary syndromes.
These findings showed that a double heterozygous mutation in the TNNI3 gene is involved in the pathogenesis of hypertrophic cardiomyopathy via haploinsufficiency.
The incidence of adverse cardiovascular events was significantly higher in patients with troponin elevation after carotid endarterectomy, which was mainly attributable to silent non-ST segment elevation MIs (show AMH ELISA Kits) that occurred in the early post-operative phase.
Four novel missense variants were identified in TNNI3.
Letter/Case Report: acute decompensated heart failure with troponin I elevation in hereditary hemochromatosis (show HFE ELISA Kits).
In this pilot study, the addition of CACS to hsTnI improves the identification of low-risk subjects in whom CTA (show PCYT1A ELISA Kits) might be avoided.
Exclusion of acute myocardial infarction 2h after presentation in emergency patients with possible acute coronary syndrome can be achieved using hs-cTnT or hs-cTnI assays.
Troponin C (TnC) and the N-terminal helix of Troponin I (TnI N-helix), which occurs in vivo during muscle contraction.
Hybrid coronary revascularization is associated with lower postoperative cTn (show CALCA ELISA Kits) release, compared with off-pump coronary artery bypass surgery.
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 ELISA Kits) 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
Cardiac ANP was increased in horses with mitral regurgitation (MR) and cardiac troponin levels were low in healthy and MR affected horses.
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 ELISA Kits)+) sensitivity of isometric tension and the time course of relaxation in cardiac muscle myofibrils
Combined troponin I Ser (show SIGLEC1 ELISA Kits)-150 and Ser (show SIGLEC1 ELISA Kits)-23/24 phosphorylation sustains thin filament Ca(2 (show CA2 ELISA Kits)+) 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.
A new functional and pathological role of amino acid modifications in the N-terminal acidic domain of cardiac TnI (show TNNI2 ELISA Kits) has been found that is modified by phosphorylations at TnI (show TNNI2 ELISA Kits)(S23 (show RPS23 ELISA Kits)/S24 (show RPS24 ELISA Kits)).
Data show that cardiac TnI (show TNNI2 ELISA Kits) gene transition and the alternatively spliced cardiac TnT isoform switching occur in postnatal pulmonary vein.
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.
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).
troponin I type 3 (cardiac)
, troponin I, cardiac muscle
, troponin IC
, cardiac troponin I
, troponin 1, type 3