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The protein encoded by TNNT2 is the tropomyosin-binding subunit of the troponin complex, which is located on the thin filament of striated muscles and regulates muscle contraction in response to alterations in intracellular calcium ion concentration. Additionally we are shipping Cardiac Troponin T2 Kits (62) and Cardiac Troponin T2 Proteins (35) and many more products for this protein.
Showing 10 out of 375 products:
Human Polyclonal Cardiac Troponin T2 Primary Antibody for EIA, WB - ABIN951043
Millat, Chanavat, Créhalet, Rousson: Development of a high resolution melting method for the detection of genetic variations in hypertrophic cardiomyopathy. in Clinica chimica acta; international journal of clinical chemistry 2010
Show all 3 references for ABIN951043
Chicken Monoclonal Cardiac Troponin T2 Primary Antibody for IF, IHC (p) - ABIN180606
Malouf, McMahon, Oakeley, Anderson: A cardiac troponin T epitope conserved across phyla. in The Journal of biological chemistry 1992
Chicken Polyclonal Cardiac Troponin T2 Primary Antibody for WB - ABIN2776953
Klaassen, Probst, Oechslin, Gerull, Krings, Schuler, Greutmann, Hürlimann, Yegitbasi, Pons, Gramlich, Drenckhahn, Heuser, Berger, Jenni, Thierfelder: Mutations in sarcomere protein genes in left ventricular noncompaction. in Circulation 2008
Human Monoclonal Cardiac Troponin T2 Primary Antibody for EIA, FACS - ABIN1105666
Hershberger, Pinto, Parks, Kushner, Li, Ludwigsen, Cowan, Morales, Parvatiyar, Potter: Clinical and functional characterization of TNNT2 mutations identified in patients with dilated cardiomyopathy. in Circulation. Cardiovascular genetics 2009
Human Monoclonal Cardiac Troponin T2 Primary Antibody for IA, WB - ABIN265695
Qiao, Tang, Munske, Dutta, Ivory, Dong: Enhanced fluorescence anisotropy assay for human cardiac troponin I and T detection. in Journal of fluorescence 2011
The results presented here have detected important prognostic differences between patients with 1 of the TNNT2 mutations (Arg92Gln) and those with the 5 other TNNT2 mutations. Carriers of the Arg92Gln mutation developed hypertrophic or dilated cardiomyopathy and had a significantly worse prognosis than those with other mutations in TNNT2.
No adverse clinical events or functional changes of the device were noted, even in those with increases in cTnT.
This review summarizes the recent proteomic data on aminoacid sequences of cTnT and cTnI in various species, as well as selected analytical characteristics of human cardiac troponin high-sensitivity assays
High-sensitivity cardiac troponin T could be used as an early biomarker for the risk stratification of patients with type-A acute aortic dissection.
An association between elevated troponin levels and increased mortality was found in critically ill patients.
For patients older than 65 years of age, applications of age-specific troponin T level cut-offs resulted in a decrease in acute myocardial infarction in the entire cohort.
Data show that high-sensitivity cardiac troponin T (hs-cTnT) was detected in 244 (87.1%) type 2 diabetes mellitus patients.
sensitivity and specificity of cardiac specific troponin T levels in detecting cardiac damage are much higher according to telecardiography and electrocardiography
since hs-cTnT levels of non-AMI patients can be over the diagnostic cut-off value, further studies are necessary to define clinically applicable cut-off values of hs-cTnT
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.
Significant changes in thin filament Ca2 (show CA2 Antibodies)+-sensitivity, structure and kinetics are brought about through PKC (show PKC Antibodies) phosphorylation of cardiac troponin T.
The mu-calpain-mediated proteolytic modification of TnT by removing the NH2-terminal variable region of TnT may act as an acute mechanism to adjust muscle contractility under stress conditions.
Substituting smooth muscle caldesmon for skeletal muscle troponin produces a similar decrease and re-increase in fluorescence, but the apparent rate constant for the increase is >10 times that observed with troponin.
In ischemic myocardium, the expression of cTnT showed prominent focal or flaky depletion in myocardial cytoplasm with no expression detected in interstitium.
Data indicate that high-sensitivity troponin T (hs-TnT) levels are influenced by myocardial dysfunction/heart failure (HF) in acute exacerbation of chronic obstructive lung disease (AECOPD), but provide independent prognostic information.
cTnT elevation emerged as a strong, independent predictor of 30-day mortality and remained a modest, but significant, predictor throughout 2 years post transcatheter aortic valve implantation.
MBPC and troponin-I phosphorylation modulate myofilament length-dependent activation
Data indicate that the troponin T Tnnt2(MerCreMer/+) mouse model also provides a useful tool to trace myocardial lineage during development.
TnT (show TNNI1 Antibodies) mutation F72L leads to contractile changes that are linked to dilated cardiomyopathy in the presence of MYH6 (show MYH6 Antibodies) and hypertrophic cardiomyopathy in the presence of MYH7 (show MYH7 Antibodies).
TNT increases slightly during low flux-hemodialysis. High-flux hemodialysis eliminates the biomarker and can mask increases caused by cardiac disease.
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.
Cardiac muscle activation blunted by a mutation to the regulatory component, troponin T.
Study is the first to show that the interplay between the N terminus of cTnT and the overlapping ends of contiguous Tm effectuates different states of Tm on the actin filament.
We conclude that the observed clinical severity of the cTnT Delta160E mutation is caused by a combination of direct sarcomeric disruption coupled to a profound dysregulation of Ca(2 (show CA2 Antibodies)+) homeostasis
Data showed that CXCR4a was significantly more highly expressed in tnnt2 knocked down mutant at 48 and 60 hpf than controls.
We show that the zebrafish silent heart (sih) mutation affects the gene tnnt2.
Tnnt1 (show TNNI1 Antibodies), Tnnt2, and Tnnt3b were conserved in the central tropomyosin (show TPM2 Antibodies)- and C-terminal troponin I-binding domains but the N-terminal hypervariable regions were highly extended and rich in glutamic acid in polypeptides of Tnnt1 (show TNNI1 Antibodies) and Tnnt2, but not Tnnt3b.
The protein encoded by this gene is the tropomyosin-binding subunit of the troponin complex, which is located on the thin filament of striated muscles and regulates muscle contraction in response to alterations in intracellular calcium ion concentration. Mutations in this gene have been associated with familial hypertrophic cardiomyopathy as well as with dilated cardiomyopathy. Transcripts for this gene undergo alternative splicing that results in many tissue-specific isoforms, however, the full-length nature of some of these variants has not yet been determined.
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