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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) Kits (107) and Troponin I Type 3 (Cardiac) Proteins (47) and many more products for this protein.
Showing 10 out of 667 products:
Human Monoclonal TNNI3 Primary Antibody for IHC, ELISA - ABIN1724650
Cummins, Auckland, Cummins: Cardiac-specific troponin-I radioimmunoassay in the diagnosis of acute myocardial infarction. in American heart journal 1987
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Human Polyclonal TNNI3 Primary Antibody for EIA - ABIN318833
Takeda: Crystal structure of troponin and the molecular mechanism of muscle regulation. in Journal of electron microscopy 2005
Show all 2 references for ABIN318833
Human Polyclonal TNNI3 Primary Antibody for IF (p), IHC (p) - ABIN728308
Liu, Li, Sun, Li, Du, Sun, Cao, Li, Jia, Wang, Chang, Yu, Wang, Peng: The use of antibody modified liposomes loaded with AMO-1 to deliver oligonucleotides to ischemic myocardium for arrhythmia therapy. in Biomaterials 2014
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Cow (Bovine) Monoclonal TNNI3 Primary Antibody for EIA, WB - ABIN118970
Marian, Zhao, Seta, Roberts, Yu: Expression of a mutant (Arg92Gln) human cardiac troponin T, known to cause hypertrophic cardiomyopathy, impairs adult cardiac myocyte contractility. in Circulation research 1997
Chicken Polyclonal TNNI3 Primary Antibody for IHC, WB - ABIN2776782
Bos, Theis, Tajik, Gersh, Ommen, Ackerman: Relationship between sex, shape, and substrate in hypertrophic cardiomyopathy. in American heart journal 2008
Amphibian Monoclonal TNNI3 Primary Antibody for EIA, WB - ABIN272322
Laube, Heister, Scholz, Borchardt, Braun: Re-programming of newt cardiomyocytes is induced by tissue regeneration. in Journal of cell science 2006
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 Antibodies) 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 Antibodies) 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 Antibodies).
In this pilot study, the addition of CACS to hsTnI improves the identification of low-risk subjects in whom CTA (show PCYT1A Antibodies) 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 Antibodies) 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 Antibodies) 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 Antibodies)+) sensitivity of isometric tension and the time course of relaxation in cardiac muscle myofibrils
Combined troponin I Ser (show SIGLEC1 Antibodies)-150 and Ser (show SIGLEC1 Antibodies)-23/24 phosphorylation sustains thin filament Ca(2 (show CA2 Antibodies)+) 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 Antibodies) has been found that is modified by phosphorylations at TnI (show TNNI2 Antibodies)(S23 (show RPS23 Antibodies)/S24 (show RPS24 Antibodies)).
Data show that cardiac TnI (show TNNI2 Antibodies) 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